University of Chicago Brain Tumors Overcoming Plant Based Diet

Nutritional Preconditioning in Cancer Treatment in Relation to DNA Damage and Aging

Nutritional Preconditioning in Cancer Treatment in Relation to DNA Damage and Aging

Annual Review of Cancer Biology

Vol. 5:161-179 (Volume publication date March 2021)
First published as a Review in Advance on December 2, 2020
https://doi.org/10.1146/annurev-cancerbio-060820-090737

Winnie M.C. van den Boogaard,^1,2 Marry M. van den Heuvel-Eibrink,³ Jan H.J. Hoeijmakers,^1,2,4,5 and Wilbert P. Vermeij^1,2

¹Genome Instability and Nutrition Research Group, Princess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands; email: [email protected]

²Oncode Institute, 3521 AL Utrecht, The Netherlands

³Pediatric Oncology Translational Research Group, Princess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands

⁴Department of Molecular Genetics, Erasmus University Medical Center, 3015 GD Rotterdam, The Netherlands; email: [email protected]

⁵CECAD Forschungszentrum, University of Cologne, 50931 Cologne, Germany

Copyright © 2021 by Annual Reviews. This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See credit lines of images or other third-party material in this article for license information

• Download Citation
• Citation Alerts

Sections

• Abstract
• Keywords
• INTRODUCTION
• THE LINKS BETWEEN DNA DAMAGE, AGING, AND DIETARY RESTRICTION
• CONSERVED RESPONSE OF REDUCED DIETARY INTAKE
• MECHANISTIC INSIGHTS FROM APPLYING DIETARY RESTRICTION TO DNA REPAIR–DEFICIENT MUTANTS
• CHEMOTHERAPY ACCELERATES AGING
• APPLICATIONS OF NUTRITIONAL PRECONDITIONING IN CLINICAL CANCER TREATMENT
• IMPLEMENTATION OF NUTRITIONAL PRECONDITIONING INTO CANCER TREATMENT SCHEDULES
• CLINICAL TRIALS IMPLEMENTING NUTRITIONAL PRECONDITIONING AGAINST CANCER IN HUMANS
• CONCLUDING REMARKS AND PERSPECTIVES
• disclosure statement
• literature cited

Abstract

Dietary restriction (DR) is the most successful nutritional intervention for extending lifespan and preserving health in numerous species. Reducing food intake triggers a protective response that shifts energy resources from growth to maintenance and resilience mechanisms. This so-called survival response has been shown to particularly increase life- and health span and decrease DNA damage in DNA repair–deficient mice exhibiting accelerated aging. Accumulation of DNA damage is the main cause of aging, but also of cancer. Moreover, radiotherapies and most chemotherapies are based on damaging DNA, consistent with their ability to induce toxicity and accelerate aging. Since fasting and DR decrease DNA damage and its effects, nutritional preconditioning holds promise for improving (cancer) therapy and preventing short- and long-term side effects of anticancer treatments. This review provides an overview of the link between aging and cancer, highlights important preclinical studies applying such nutritional preconditioning, and summarizes the first clinical trials implementing nutritional preconditioning in cancer treatment.

INTRODUCTION

Cancer and aging are in many respects each other's counterpart, but they are also intimately interconnected. For both, a set of hallmarks has been identified, with genome instability as a common driving hallmark (Hanahan & Weinberg 2011, López-Otín et al. 2013) (Figure 1). Genome instability can be defined as the accumulation of genetic damage over time, such as structural changes in DNA and chromosomal aberrations. As our DNA is constantly being challenged by a variety of agents and spontaneous reactions, our cells rely on a proper DNA damage response and are equipped with an array of DNA repair processes (Bartek et al. 2007, Hoeijmakers 2001, Lindahl 1993). These DNA maintenance mechanisms are not 100% efficient, which leads to a slow, gradual accumulation of DNA damage with age. Upon DNA replication, damage can yield mutations and chromosomal aberrations, thereby driving tumorigenesis (Hanahan & Weinberg 2011, Hoeijmakers 2001, Negrini et al. 2010). Alternatively, persisting DNA damage can block replication, prompting cell cycle delay or arrest and cellular senescence, or it can trigger transcription stress, resulting in cellular functional decline and cell death, all of which contribute to aging and aging-associated diseases (Hoeijmakers 2009, Lans et al. 2019, López-Otín et al. 2013).

The importance of genome maintenance as a mechanism underlying both cancer and aging was further elucidated by the identification of human genotype-phenotype relationships, as mutations in genes implicated in DNA repair—leading to increased genome instability—enhance cancer susceptibility and/or accelerate aging (Hoeijmakers 2009, Marteijn et al. 2014, Niedernhofer et al. 2018, Vermeij et al. 2014).

Multiple signs of accelerated aging, such as cellular senescence, early graying, cachexia, osteoporosis, liver and kidney aging, and shortened lifespan, were shown for the first time in mice with defective DNA repair caused by mutations identified in rare progeroid diseases in humans (De Boer et al. 2002, Niedernhofer et al. 2006, Weeda et al. 1997). This breakthrough inferred a direct relationship between DNA damage exposure, DNA repair efficiency, and the rate of aging, consistent with the damage accumulation theory of aging (Kirkwood 2005), and it predicted that DNA-damaging chemotherapeutics used in cancer treatment may promote aging, which has now been confirmed in children and adults cured from cancer (Cupit-Link et al. 2017, Maccormick 2006).

Nutritional preconditioning (NP) can boost defense mechanisms and reduce DNA damage levels, which so far have been mostly studied in relation to aging. As genome instability is one of the driving hallmarks of aging and cancer (Figure 1), this review focuses on the relation between DNA damage and (accelerated) aging or cancer, as well as the use of NP as a counteractive measure.

THE LINKS BETWEEN DNA DAMAGE, AGING, AND DIETARY RESTRICTION

DNA damage occurs in every cell at a rapid pace, originating from both endogenous (e.g., reactive metabolites) and exogenous (e.g., UV radiation, X-rays, genotoxins) sources. It is estimated that each mammalian cell experiences up to 10⁵ DNA lesions per day (Gates 2009, Lindahl & Barnes 2000, Swenberg et al. 2011, Tubbs & Nussenzweig 2017), ranging from spontaneous hydrolysis causing abasic (mainly apurinic) sites to deaminated bases, different types of single- and double-stranded breaks, DNA-DNA and DNA-protein cross-links, and about 100 types of oxidative DNA lesions (Cadet et al. 2002, Lindahl 1993, Nakamura & Swenberg 1999). Most of these lesions are removed by an intricate network of complementary DNA repair processes, including mechanisms that resolve damaged bases containing subtle alterations (e.g., oxidative lesions, alkylation damage) by BER (base-excision repair), bulky helix-distorting adducts throughout the genome by GG-NER (global genome nucleotide excision repair), lesions blocking ongoing transcription by TCR (transcription-coupled repair), double-stranded DNA breaks by NHEJ (nonhomologous end-joining) or by HR (homologous recombination), or interstrand DNA cross-links by cross-link repair pathways (Hoeijmakers 2001). Occasionally, however, the damage is unrepairable or not recognized or the repair is simply too late or error prone. This leads to a gradual increase of persisting DNA lesions over time, with genome instability as a consequence (Hoeijmakers 2001, Vijg 2014). Some lesions may occur in actively transcribed genes, causing transcription stress, which leads to altered gene expression (Lans et al. 2019), which in turn may indirectly influence several of the other important hallmarks of aging (Vermeij et al. 2016b) (Figure 1).

The effect of persisting DNA lesions on the process of aging is even more evident when genome integrity mechanisms (e.g., DNA repair systems) are affected. This is the case for a broad variety of rare progeroid syndromes, including Cockayne syndrome (CS), trichothiodystrophy, Werner syndrome, Nijmegen breakage syndrome, and Bloom syndrome, in which patients exhibit multiple features of premature aging (Vermeij et al. 2016b). Virtually all accelerated aging syndromes in humans exhibit this link with genome instability. For many of the genes affected, mouse models have been generated to better understand these progeroid disorders and the biomedical consequences of DNA damage (Carrero et al. 2016, Jaarsma et al. 2013). Several of these mouse models appear to be excellent paradigms of the human syndromes, in which several features were first identified in mice before being confirmed in patients (De Boer et al. 2002, Vermeulen et al. 2001). One such example is the Ercc1 ^Δ/− mouse model (Niedernhofer et al. 2006, Weeda et al. 1997), which is defective in multiple DNA repair pathways (Ahmad et al. 2008, Gillet & Schärer 2006, Kuraoka et al. 2000, Niedernhofer et al. 2004). Consequently, all cells and tissues accumulate many different types of DNA lesions faster than normal, leading to functional decline and widespread accelerated aging in postmitotic and proliferative organs and tissues. This limits their lifespan by 4–6 months, during which they progressively develop frailty and numerous age-related pathologies commonly observed in the elderly (Dollé et al. 2011, Vermeij et al. 2016b).

Besides premature aging, accumulation of DNA damage in the Ercc1 ^Δ/− and other DNA repair–deficient mouse models also triggers a protective response that alters energy metabolism, nutrient sensing, and redox status (Milanese et al. 2019, Niedernhofer et al. 2006). This antiaging survival response resembles dietary restriction (DR), involving the suppression of the GH (growth hormone)/IGF1 somato-, lacto-, and thyrotropic hormonal axes and upregulation of antioxidant defenses and resilience mechanisms, presumably in an attempt to extend lifespan by redirecting resources from growth to cellular maintenance and stress resistance (Niedernhofer et al. 2006, Schumacher et al. 2008, Van Der Pluijm et al. 2006). By limiting the investment of energy resources to organismal growth, this response also explains why progeroid DNA repair–deficient mice and patients remain so small (Laugel 2013). Strikingly, when exposed to agents inducing persistent transcription-blocking DNA lesions, wild-type (WT) mice and normal cells respond in a similar fashion, attenuating growth and supporting maintenance mechanisms, resembling the longevity response induced by DR (Garinis et al. 2009).

CONSERVED RESPONSE OF REDUCED DIETARY INTAKE

The first scientific evidence that reducing food intake prolongs life was provided by two studies from the early 1900s. Osborne and colleagues noted that four rats that were given a restricted diet for various periods of time to retard their growth were among the longest lived in their study (Osborne et al. 1917). More systematically analyzed, a landmark paper for the field of DR (also often termed calorie restriction) was published by McCay and colleagues in 1935 that clearly demonstrated that restriction of food intake by 40% dramatically extended the lifespan of rats (McCay et al. 1935). Over the years, many more species have been examined, ranging from yeast and worms to flies and mice in various genetic backgrounds (Arslan-Ergul et al. 2016, Comfort 1963, Fontana et al. 2010, Goldman et al. 1999, Jönsson 2007, Kenyon 2010, Liao et al. 2010, Pifferi et al. 2018, Weindruch & Sohal 1997, Weindruch et al. 1986). These studies have highlighted the strong evolutionary conservation of the extension of lifespan by reduced dietary intake. For a while, researchers questioned whether this mechanism of extending lifespan only applies to model organisms under laboratory conditions or whether it could also be applied to humans.

The first clear indications arose from DR studies in nonhuman primates by Colman et al. (2009) at the University of Wisconsin (UW) and Mattison et al. (2012) at the National Institute of Aging (NIA). Both research groups used rhesus macaques as experimental animals, subjecting them to 30% DR. Effects on health span confirmed by both research groups include reduced incidence of diabetes and cancer and overall younger appearance of animals subjected to DR. The lifespan of the animals was increased significantly only in the study by Colman et al. (2009), where only 50% of control animals were still alive at the moment of analysis, as opposed to 80% of DR animals. Evaluation of the study protocols revealed important differences between the two studies that might explain why Mattison et al. (2012) did not find a clear effect on lifespan (Austad 2012, Colman et al. 2014, Mattison et al. 2017): The control animals at NIA did not receive bona fide ad libitum (AL) feeding but instead were given a slightly (∼10%) restricted diet, reducing the difference with the 30% DR group (Colman et al. 2014, Mattison et al. 2017). Despite the different outcomes on survival, both UW and NIA studies showed improved health spans and thereby beneficial effects of DR in nonhuman primates.

MECHANISTIC INSIGHTS FROM APPLYING DIETARY RESTRICTION TO DNA REPAIR–DEFICIENT MUTANTS

Despite decades of research, the mechanisms underlying life- and health span extension by DR are still poorly understood. These may involve increased stress resistance and resilience mechanisms; improved antioxidant defenses; alterations in GH, thyroid hormone (TH), and IGF1/insulin signaling; release of appetite-regulating hormones leptin and ghrelin; altered mitochondrial function, including greater utilization of lipids when compared with carbohydrates; activation of NAD⁺ metabolism and enhancement of mitochondrial redox regulation; reduced mammalian target of rapamycin (mTOR)-mediated translation; increased autophagic responses; induced sirtuin regulation; remodeling of fat tissue; and a shift from a pro- to an anti-inflammatory profile of circulating adipokines (Finkel 2015, Hoshino et al. 2018, Madeo et al. 2019, Speakman & Mitchell 2011). Among these mechanisms, the nutrient signaling pathways IGF1 and mTOR are evolutionary most conserved (Fontana et al. 2010), while others might be secondary consequences, dependent on cell type, or influenced by the biological clock, rather than affected by aging itself or, alternatively, regulated during feeding or fasting periods (Barzilai et al. 2012, De Cabo & Mattson 2019, Speakman & Mitchell 2011).

To gain a better understanding of these causes and consequences and to identify essential pathways for promoting longevity through diet, researchers have used model organisms harboring genetic defects. Experiments using Caenorhabditis elegans have highlighted the importance of nutrient-sensing mechanisms and showed the effector genes daf-16/FoxO and aak-2/AMPK to be essential for mediating the longevity effect induced by DR (Greer & Brunet 2009, Mair & Dillin 2008). Applying DR to DNA repair–deficient mice was expected to yield similar outcomes to AL-fed littermates, as they already have an activated DR-like antiaging survival response (Garinis et al. 2009, Schumacher et al. 2008). Unexpectedly, the Ercc1 ^Δ/− progeroid mice responded to an extraordinary degree to the application of DR: Median and maximum remaining lifespans were extended by approximately 200% in both genders (Vermeij et al. 2016a). Similar results were obtained in DNA repair–deficient progeroid Xpg^−/− mice, a model for a severe form of CS combined with the human repair syndrome xeroderma pigmentosum (Barnhoorn et al. 2014, Vermeij et al. 2016a). DR drastically improved health span, retarding all aspects of premature aging examined, including hepato-, nephro-, immuno-, osteo-, and vascular aging, but most notably neurodegeneration: DR preserved 50% more neurons and fully prevented motoric dysfunction, which has major clinical implications. Importantly, this study showed that the already activated survival response was further enhanced by DR, and it identified reduced DNA damage levels and attenuated transcription stress as novel effects of DR that can explain the exaggerated response of DNA repair–deficient mice to DR (Vermeij et al. 2016a).

In the case of laboratory animals, the origin of most of the damage must be endogenous and—in view of the notion that DR has such a strong effect—must be influenced by the amount of food. If food were the sole source of the damage, however, it would be difficult to explain why 30% restriction would exert such a dramatic effect. Therefore, DR must trigger an active program that can delay aging and reduce genome damage. Although improving DNA repair would be an option for reducing genomic injuries, this is unlikely in the case of the Ercc1 ^Δ/− and Xpg ^−/− mice, as multiple repair systems are genetically inactivated in these mutants and effective compensatory pathways are unknown. This suggests that not (or not solely) enhanced damage removal but reduced damage induction and perhaps altered damage responses are the focuses of DR. Indeed, reducing glucose intake and that of other nutritional components leads to a redesign of major metabolic routes (such as glycolysis, oxidative phosphorylation, and pentose phosphate shunt) and alters mitochondrial function. This lowers the respiratory exchange ratio and production of reactive oxygen species (ROS) that could normally damage DNA, but also enhances mitochondrial reducing equivalents that quench ROS. Moreover, it results in a lower body temperature, reducing thermodynamics and decreasing ROS damage to macromolecules (Conti et al. 2006, Finkel 2015, López-Otín et al. 2016, Speakman & Mitchell 2011). Other energy intermediates are directly interacting with nutrient-sensing pathways such as amino acids with mTOR, AMP/ADP with AMPK, NAD⁺/NADH with sirtuins, and fatty acids with PPARs (peroxisome proliferator-activated receptors) (Balasubramanian et al. 2017, Finkel 2015). DR reduces circulating levels of IGF1, insulin, GH, and TH, thereby temporarily suppressing growth, and boosts antioxidant capacities and stress-resistance mechanisms (Bartke 2019, Gillespie et al. 2016), again dampening the induction and negative consequences of DNA damage.

Many of these mechanisms still pop up in DR expression profiles of Ercc1 ^Δ/− mice that actually had this response already activated under AL conditions in response to accumulated DNA damage levels. Surprisingly, Ercc1 ^Δ/− and WT littermates on DR revealed a very similar consistent response: 684 genes out of the 688 common genes upon DR responded concordantly between Ercc1 ^Δ/− and WT mice, including the GH/IGF1 axis and antioxidants (Vermeij et al. 2016a). Therefore, reducing the generation and enhancing the elimination of metabolic byproducts such as ROS that otherwise would wreck the cell's interior, including nuclear and mitochondrial DNA, are likely prime targets of DR.

CHEMOTHERAPY ACCELERATES AGING

The observation that DNA damage is the main driver of aging implies that other instances where DNA damage occurs can benefit from NP. It has become clear that DNA damage–inducing anticancer therapies accelerate aging, most clearly in childhood cancer survivors (Hudson et al. 2013, Maccormick 2006). Since the survival of cancer patients has increased over the last decades, maintaining quality of life is becoming increasingly important. Cancer survivors have, later in life, a higher risk for many pathologies, including frailty, cardiovascular disease, hypertension, stroke, secondary neoplasms, cataracts, low bone mineral density, metabolic syndrome, diabetes, primary hypogonadism, and cognitive decline (Ness et al. 2018), and they develop these at a younger age compared to healthy individuals (Bhakta et al. 2017, Cupit-Link et al. 2017). The clinical phenotype termed frailty (a combination of decreased lean muscle mass, decreased vitality, poor physical activity, and slowness or weakness) in adult childhood cancer survivors reveals an aging tendency comparable with that in the elderly, already two decades earlier than expected (Hayek et al. 2020, Ness & Wogksch 2020, Ness et al. 2017, Smitherman et al. 2018). As with aging, DNA damage is the primary cause of side effects in cancer patients due to intense toxic treatment regimens, which opens possibilities for the use of dietary interventions in cancer treatment (see the sidebar titled Types of Nutritional Preconditioning).

APPLICATIONS OF NUTRITIONAL PRECONDITIONING IN CLINICAL CANCER TREATMENT

NP has the potential to improve quality of life and therapy of cancer patients by preventing short-term toxicities, improving therapeutic efficacy, and reducing late-life effects. DNA-damaging treatments including radio- and most chemotherapies cause local or systemic acute genotoxicity and hence local or systemic accelerated cell death, functional decline, and, therefore, aging. Nutritional strategies have been shown to reduce endogenous DNA damage levels and to boost maintenance and resilience mechanisms (Cabelof et al. 2003, Morselli et al. 2010, Solanas et al. 2017, Vermeij et al. 2016a), which may protect the body from exogenous damages (e.g., chemotherapy) as well. By inducing such a protective survival response prior to DNA-damaging treatments, NP might prevent (part of) these toxicities at least in normal tissues, and probably to a lesser extent or not at all in the tumor, thereby alleviating short- and long-term side effects and the burden experienced by cancer patients. Moreover, NP can be important for other aspects of cancer treatment. In the following sections, different applications relevant for the well-being of cancer patients are discussed.

Over the years, nutritional preconditioning (NP) has been used in aging and cancer research. For the sake of clarity, the interventions frequently referred to in this review are here briefly explained.

Dietary restriction (DR) or caloric restriction (CR) refers to reduced intake without malnutrition. Nutritional intake is allowed during the day, but total caloric intake is generally reduced by 20–40%. More specific forms of DR exist in which the balance of macronutrients is affected or lowered.

The ketogenic diet (KD) has a high fat content, approximately 70%, primarily saturated, and is (very) low in carbohydrate content, but it is usually a normocaloric diet.

Short-term fasting (STF) means no food intake, only water, for a given period, in the range of days. This type of fasting is implemented in intermittent fasting, where periods of normal consumption are alternated with fasting.

Fasting-mimicking diet (FMD) is a diet lower in caloric intake than DR but for a longer period than STF. The most common FMD consists of a 5-day schedule of a plant-based low-calorie and low-protein diet, containing ∼1,100 kcal on the first day, which is lowered to ∼700 kcal on the subsequent 4 days (Wei et al. 2017).

Surgery

NP is highly relevant for surgery. Surgical removal of tumors is an important part of treatment, especially for patients with solid tumors. The blood flow to the tissue surrounding the tumor is temporarily restricted and restored at the end of operation. The temporary lack of oxygen and other nutrients (ischemia), followed by reperfusion, is associated with massive formation of ROS, causing acute tissue damage including oxidative DNA lesions, enhancing cell death and inflammation (Kalogeris et al. 2012), and thereby actually causing local aging. As demonstrated below, both DR and fasting strongly protect against ischemia reperfusion injury (IRI), both in model organisms and patients.

For example, mice subjected to bilateral kidney clamping to induce renal IRI that were preconditioned by 30% DR for 2 or 4 weeks or 2 or 3 days of fasting all survived the surgical procedure and retained superior renal function in comparison to their AL-fed littermates, of which only 40% survived (Mitchell et al. 2010).

Fasting was also shown to reduce damage to the brain after stroke. Sprague-Dawley rats that were subject to a fasting diet for 3 days before receiving cerebral artery occlusion showed significant neuroprotection (Varendi et al. 2014).

Preoperative fasting or DR studied in animal models has also been shown to be beneficial in IRI settings related to, among others, the heart (Shinmura et al. 2005, Wan et al. 2010), liver (Menezes-Filho et al. 2017, Verweij et al. 2011), retina (Kawai et al. 2001), and revascularization (Kondo et al. 2009), indicating the systemic nature of this response.

Clinical trials looking into the effects of preoperative NP are scarce but show promising results. Van Nieuwenhove et al. (2011) studied patients scheduled for laparoscopic gastric bypass surgery in a multicenter, randomized, single-blind study. In total, 273 patients were followed, of which 137 followed a very low-calorie diet (VLCD) for 2 weeks. The main finding of the study was the reduction of postoperative complications for the VLCD group, most clearly for wound infections (Van Nieuwenhove et al. 2011).

Beneficial effects were also shown in patients—of which 94% underwent cancer resection—undergoing liver surgery (Reeves et al. 2013). These patients have a higher risk of complications when having steatosis or steatohepatitis (McCormack et al. 2007, Vauthey et al. 2006). Both pathologies were significantly lowered in patients that performed DR 1 week before surgery, with a caloric intake of 900 kcal/day. Additionally, there was a trend for reduced severity in steatosis and significantly less blood loss in the DR group (Reeves et al. 2013).

Short- and Long-Term Toxicity

The list of side effects caused by radiotherapy and various types of chemotherapy is a very long one. Problems arising during and shortly after therapy hamper normal functioning of patients, affecting quality of life and interfering with therapy regimen, and require ways to reduce suffering without diminishing treatment efficacy. In contrast to many tumor cells, normal cells adapt their metabolism upon nutritional intervention, enhancing stress resistance, making the cells less responsive to harmful agents, which is sometimes termed differential stress resistance (DSR) (Raffaghello et al. 2008).

As most DNA-damaging chemotherapeutics are administered intravenously, toxicity can occur throughout the body. Toxicities induced by DNA damage vary depending on the type of damage (pharmacokinetics and -dynamics of the chemotherapeutic compounds) and the cellular context (such as the proliferation rate, repair capacity, vascularization, etc. of tissues). NP-induced protection against various classes of chemotherapy—i.e., induction of DSR—has been shown using different in vitro and in vivo models.

Doxorubicin, a topoisomerase II inhibitor that blocks the unwinding of DNA (Tewey et al. 1984), thereby inhibiting DNA replication, causes strand breaks. It is also implicated in free radical formation and histone deregulation (Feinstein et al. 1993, Pang et al. 2013). Doxorubicin's main side effect is cardiotoxicity (Lefrak et al. 1973).

Following 48 hours of food deprivation, doxorubicin-treated CD-1 mice showed 100% survival, in contrast to 38% of mice that received Igf1 injections every 12 hours during the fasting period (Lee et al. 2010).

Liver-specific deletion of Igf1r leads to a reduction of 80% of circulating Igf1 levels in mice (LID mice) (Lee et al. 2010), similar to levels established by DR, and can be used to mimic NP. Of the non-tumor-bearing mice, only 25% of control (WT) mice survived two cycles of doxorubicin treatment, whereas all LID mice survived. In melanoma-bearing xenograft mice, 60% of LID mice were still alive 90 days after doxorubicin treatment, whereas none of the treated WT mice survived (Lee et al. 2010). Unfortunately, the authors did not include nontreated controls, making it impossible to determine the effect of only lowered circulating Igf1 levels on survival.

Another topoisomerase II inhibitor, etoposide, prevents religation of DNA strands, thereby causing DNA breaks (Robinson & Osheroff 1991). High-dose treatment was tested in A/J, CD-1, and Nude-nu mice, which were fasted for 2–3 days and subsequently treated with equitoxic doses. In all three models, signs of toxicity, including ruffled hair, kyphosis, and decreased locomotor activity, were clearly present in AL-fed animals but were mild or absent in fasted animals. Etoposide treatment led to weight loss in the first days after treatment, whereas fasted animals gained weight. Survival increased tremendously in fasted mice, as only one mouse from the prefasted group (n = 28) died shortly after treatment from all three backgrounds. From the control mice, 43%, 100%, and 56% had died at 10, 5, and 5 days after treatment for the A/J, CD-1, and Nude-nu groups, respectively (Raffaghello et al. 2008).

Besides toxicity caused by a specific drug, toxicity can be elevated due to interactions between multiple drug treatments. Survival of C57BL/6 mice treated with doxorubicin was significantly lower for mice that received multiple injections of dexamethasone (normally added to treatment to lower nausea and vomiting) before doxorubicin treatment. Two-day fasting before doxorubicin treatment reversed this effect and even increased survival compared to control animals, which were only treated with doxorubicin. At 20 days after treatment, this resulted in 5%, 90%, and 100% survival for animals that received dexamethasone, dexamethasone and fasting, or fasting alone alongside doxorubicin treatment, respectively, whereas doxorubicin treatment alone led to 25% survival. Signs of cardiotoxicity were diminished in animals that were fasted before doxorubicin injection compared to AL-fed animals. No data on cardiotoxicity were available for mice additionally treated with dexamethasone. Dexamethasone causes hyperglycemia, which was shown to be (partially) causal for the increased toxicity, as the addition of insulin alongside dexamethasone (restoration of euglycemia) leads to reduced toxicity; glucose injections before fasting (leading to hyperglycemia) resulted in increased toxicity. Additional experiments showed that fasting leads to increased local concentrations of atrial natriuretic peptides, B-type natriuretic peptides, and cardioprotective peptides, which are probably implicated in reduced cardiotoxicity in fasted animals after doxorubicin treatment (Di Biase et al. 2017).

As a last example, cisplatin is a chemotherapeutic that forms intra- and interstrand cross-links with the DNA, thereby preventing transcription and replication (Siddik 2003). A significant reduction in cisplatin-induced nephrotoxicity was observed in mice that were fasted for 3 days before cisplatin treatment. Histological parameters including tubule damage, glomerular deterioration, brush border degradation, and serum measurements including creatinine and urea levels all indicated less severe kidney damage in fasted mice compared to AL-fed mice (Gunebakan et al. 2020). Together, these findings indicate that NP can induce protection in healthy tissue against multiple types of DNA-damaging chemotherapeutics.

Lastly, NP can be used to reduce long-term toxicity. Especially for childhood cancer survivors, this benefit may be very significant in view of their longer remaining life expectancy and the fact that they experience aging-like pathologies earlier in life compared to the normal population (Armstrong et al. 2014, Hudson et al. 2015, Schuitema et al. 2013). Apart from survival outcomes discussed above, no studies have yet been performed to specifically look at the effects of NP on long-term toxicity, but evidence in the field of aging research supports its potential for delaying aging in general and reduction of DNA damage–driven accelerated aging (Barnhoorn et al. 2014, Vermeij et al. 2016a). Furthermore, the implementation of an NP for acute toxicity might also lead to less accumulation of DNA damage during treatment and therefore prevent or reduce pathologies later in life.

Tumor Growth

Besides preventing toxicities to healthy tissues and organs, NP can also impact the tumor itself. Cancer cells harbor mutations that lead to differentiation arrest, as well as uncontrolled growth due to constitutive activation of proliferative pathways or repression of antigrowth signaling. When the availability of nutrients is reduced, like in NP, many cancer cells cannot easily adapt—in contrast to normal cells—which may render them more vulnerable to damaging agents, a condition termed differential stress sensitization (DSS) (Lee et al. 2012).

This difference in responses between tumor cells that have difficulties in adapting to NP conditions and normal cells that go into defense mode can already result in tumor shrinkage by the NP regimen per se. In vitro, the majority of 17 human and murine cancer cell lines showed decreased survival when starved and treated with doxorubicin or cyclophosphamide compared to either chemotherapeutic alone (Lee et al. 2012). In vivo mouse experiments on various allograft or xenograft models for breast cancer, melanoma, glioma, and ovarian cancer showed reduced tumor growth or tumor shrinkage after 2 days of fasting compared to an AL diet, which was further reduced in combination with chemotherapy (Lee et al. 2012). The effect of fasting on tumor growth was also tested in multiple in vivo metastatic tumor models, including breast cancer, melanoma, and neuroblastoma models. In all cases, mice that were fasted and received chemotherapy showed the longest survival (Lee et al. 2012). Strikingly, even the number of metastatic sites was reduced in several of the tumor models tested.

Similar differential effects of DR on solid tumor growth were found by Kalaany & Sabatini (2009). Six human tumor lines were injected subcutaneously into NOD/SCID (nonobese diabetic/severe combined immunodeficiency) mice, representing prostate, colon, brain, and three different breast cancers. After 2–3 weeks of AL feeding or 40% DR, the colon cancer and two breast cancer tumors were significantly hampered in growth in the DR mice, whereas the prostate cancer, brain cancer, and one of the breast cancer tumors grew to a similar size under AL and DR conditions. As all restricted mice lost equal amounts of body weight and showed a similar decrease in blood plasma Igf1 and insulin levels, the authors hypothesized that the differential response of tumor types should be attributed to a tumor-intrinsic factor. The DR-resistant tumors had aberrant PI3K signaling, either via PTEN loss or mutated PI3K, leading to constitutive PI3K expression. During DR, increased expression of PTEN was required to attenuate tumor volume, as induced expression of PTEN in a PTEN-null model reversed DR resistance. Reduction of tumor size was due to either decreased proliferation or increased apoptosis (Kalaany & Sabatini 2009).

The DSS induced by fasting also applies to hematological cancer types. Mouse models for B cell acute lymphoblastic leukemia (B-ALL) were subjected to four fasting cycles without chemotherapy treatment, alternating between 1–2 days of fasting and 1–2 days of refeeding (Lu et al. 2017). Fasting cycles were performed either 2 days after tumor cell transplantation or at a later time point when a proper tumor was established. Fasting shortly after initiation of B-ALL led to a significant increase in survival, where 75% of fasted animals were still alive at the end of the experiment, at least 61 days longer than fed animals. Survival for animals that were fasted after tumor establishment was at least 62 days longer for 60% of the fasted mice than fed controls. Similar results were obtained for T cell acute lymphoblastic leukemia (T-ALL). Four cycles of fasting after T-ALL induction resulted in 40% survival until the end of the experiment, at least 30 days longer than control animals, of which none survived. When T-ALL was already established, 50% of fasted animals survived for at least 68 days longer than control animals. The authors did not find such an effect of fasting-only on acute myeloid leukemia (AML). The difference in response between ALL and AML was attributed to leptin receptor (LEPR) expression, which was increased after fasting in both B-ALL and T-ALL cells, but was already high in AML and did not increase over time. Overexpression of LEPR drives the differentiation of B-ALL tumor cells into terminal B cells, which are nonmalignant (Lu et al. 2017).

Interestingly, LEPR expression is upstream of PI3K and could interfere with PI3K signaling, consistent with the importance of this pathway in response to DR and fasting, although this does not rule out the relevance of other molecular mechanisms. Due to specific mutations present in different tumor types, the response to NP might depend on the tumor type and mutation (Kanarek et al. 2020). However, independent of tumor status, NP might still have the benefit of reducing therapy-induced side effects.

IMPLEMENTATION OF NUTRITIONAL PRECONDITIONING INTO CANCER TREATMENT SCHEDULES

The health effects of NP alongside standard-of-care cancer therapy are currently being investigated in several clinical trials (Table 1, Supplemental Table 1). The start time, duration, type, and degree of the intervention depend on the specific situation and application and should be compatible with additional therapy (Figure 2). Several additional considerations need to be considered to assure the safety of the patient. First, the physical condition of the patient must be adequate to tolerate a nutritional intervention. Patients that are suitable must be closely monitored and guided by health-care professionals during the whole intervention for parameters such as body weight, food intake, well-being, and physical status. As discussed below, only a few trials have been completed so far, and most evidence for favorable effects of NP has been obtained from mouse studies. More studies with human subjects are required before NP (Figure 2) can become standard practice. The exact schedule and composition of a dietary intervention should be tailored to the treatment schedule and to the specific tumor type to ensure that the survival response is maximally established at the moment damage is occurring and does not enhance tumor growth or toxicity.

CLICK TO VIEW

Table 1

Completed clinical trials studying the implementation of nutritional preconditioning in cancer treatment, including chemotherapy, surgery, and radiotherapy

CLINICAL TRIALS IMPLEMENTING NUTRITIONAL PRECONDITIONING AGAINST CANCER IN HUMANS

The number of trials in which cancer patients undergo any form of NP is limited but has been increasing especially in the last decade (Table 1, Supplemental Table 1). These trials combine different types of NP with chemotherapy, radiotherapy, or surgery in a range of cancer types. The first few trials have been completed, and they confirm the feasibility of implementing adapted feeding strategies into cancer therapy and the safety of patients undergoing NP (Bauersfeld et al. 2018, De Groot et al. 2015, Dorff et al. 2016, Safdie et al. 2009).

Most studies have applied some form of short-term fasting (STF), ranging from 48 to 180 hours. All studies confirm the feasibility and safety of STF alongside chemotherapy. In some cases side effects of fasting were noted, such as dizziness, nausea, and headache, but were considered to be minor (Bauersfeld et al. 2018, Safdie et al. 2009). Overall, the studies showed (a trend towards) reduced side effects attributable to chemotherapy in patients that underwent fasting compared to nonfasted patients. In some studies (De Groot et al. 2015, Dorff et al. 2016), plasma measurements were performed to assess several key metabolic markers, including glucose, insulin, and IGF1. Only IGF1 showed a significant decrease upon fasting (De Groot et al. 2015). Both research groups investigated DNA breaks in peripheral blood mononuclear cells (PBMCs) by either comet assay (Dorff et al. 2016) or γH2AX intensity (De Groot et al. 2015) and revealed lower DNA damage induction following chemotherapy or a faster recovery of PBMCs in fasted patients.

Another diet frequently assessed is the ketogenic diet (KD), mostly studied in patients suffering from brain cancer, but available data are very limited. Besides gliomas, completed trials have also assessed nonbrain tumors (Cohen et al. 2018a,b; Klement & Sweeney 2016; Klement et al. 2019; Martin-McGill et al. 2020; Rieger et al. 2014; Tan-Shalaby et al. 2016; Zahra et al. 2017). Unfortunately, these studies mostly included only a small number of patients or, when started with a larger cohort, experienced dropout during the study (mostly due to scheduling conflicts or other non-diet-related reasons). The main focus of most trials has included the safety and feasibility of KD, as well as the effect of KD on quality of life in cancer patients. The consensus seems to be that KD is feasible and safe in patients with different types of cancer. The combined results suggest that a KD for a maximum of 5–6 weeks consisting of a ratio of fat to other macronutrients of less than 4:1 is most promising as a feasible intervention.

Patients that have been able to stay on a KD mostly reported no severe adverse effects due to the diet and reported that their quality of life was stable or improved (Cohen et al. 2018a, Martin-McGill et al. 2020, Tan-Shalaby et al. 2016). Measurements on body composition have indicated a positive alteration by KD, with a decrease in fat mass and an increase in fat-free mass and skeletal muscle mass (Cohen et al. 2018a, Klement et al. 2019). Taken together, these results might suggest that KD leads to a more beneficial body composition. Use of KD might lead to better treatment response in overweight patients, as it is reported that patients with obesity or low muscle mass might have a lower response to treatment (Calle et al. 2003, Malietzis et al. 2016, Prado et al. 2009, Yip et al. 2015).

An alternative to complete STF is a fasting-mimicking diet (FMD), whose effect has been studied in a few clinical trials. The one FMD trial with published results so far applied FMD to HER2-negative breast cancer patients receiving chemotherapy (De Groot et al. 2019). Unfortunately, the study was terminated due to low compliance, as some patients reported a dislike of the taste of the diet and developed an aversion to food close to chemotherapy treatment. Some of the patients decided to fast instead of undergoing an FMD for part of their chemotherapy cycles or even their whole treatment schedule. Analysis of the FMD group, irrespective of compliance, still showed indications of decreased DNA damage after chemotherapy in lymphocytes compared to the DNA damage levels in the control group (De Groot et al. 2019). Hence, NP appears to improve health parameters and to reduce side effects of chemotherapy treatment.

CONCLUDING REMARKS AND PERSPECTIVES

Although important benefits of DR have already been known for over a century, its potential has still not been fully determined. The relatively recent introduction of NP in cancer treatment already shows promising beneficial effects in different treatment areas (Table 1). Further clinical results await, but preliminary findings hold significant promise for patients. In addition to reduction of tumor volume and treatment-induced side effects, NP might also be of benefit for patients receiving radiotherapy, where DNA damage is inflicted to the healthy tumor environment as well; for patients receiving stem cell transplantation; or in the context of immunotherapy, as numerous immunological parameters also change with DR or fasting.

As the survival response can also be used to reduce or slow down aging-related pathologies, introduction of NP in many more contexts, such as research related to dementia or cardiovascular or autoimmune diseases, could reveal a whole new modality for treatment or prevention (Supplemental Table 2). Of course, in-depth research in these and other areas has to be performed to test this hypothesis. When NP is used, the safety and general health of the patient are of utmost concern, which requires comprehensive analysis of the patient's physical status before starting NP and careful monitoring during NP. When adapted to many characteristics such as the patient's health status, age, activity level, disease, and treatment schedule, NP has the potential to decrease the burden and improve the quality of life for patients at very low costs.

disclosure statement

The authors are not aware of any affiliations, memberships, funding, or financial holdings that might be perceived as affecting the objectivity of this review.

acknowledgments

We acknowledge the support of the European Research Council Advanced Grants DamAge and Dam2Age, ONCODE (Dutch Cancer Society), an NIH grant (PO1 AG017242), the ADPS Longevity Research Award (to W.P.V.), Memorabel and ChemBridge (ZonMw), BBoL (NWO-ENW), and the Deutsche Forschungsgemeinschaft (SFB 829).

literature cited

• 1.

• 2.

  Armstrong GT , Kawashima T , Leisenring W , Stratton K , Stovall M , et al. 2014. Aging and risk of severe, disabling, life-threatening, and fatal events in the childhood cancer survivor study. J. Clin. Oncol. 32(12):1218–27

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Nuclear Genomic Instability and Aging

    Laura J. Niedernhofer, ¹ Aditi U. Gurkar, ^1,2 Yinsheng Wang, ³ Jan Vijg, ⁴ Jan H.J. Hoeijmakers, ⁵ and Paul D. Robbins ^{1 1}Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA; email: [email protected] ²Department of Medicine, Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA³Department of Chemistry, University of California, Riverside, California 92521, USA⁴Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, Bronx, New York 10461, USA⁵Department of Molecular Genetics, Erasmus University Medical Center, 3015 CE Rotterdam, The Netherlands

    Annual Review of Biochemistry Vol. 87: 295 - 322

    • ...have a >2.5-fold increased incidence of severe disabling or life-threatening age-related diseases compared with their siblings (6)....

• 3.

• 4.

• 5.

• 6.

  Barnhoorn S , Uittenboogaard LM , Jaarsma D , Vermeij WP , Tresini M , et al. 2014. Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency. PLOS Genet. 10(10):e1004686

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...TTD, and XFE premature aging phenotypes have been well described (55, 57...

• 7.

  More AR articles citing this reference

  • Cell Cycle–Targeted Cancer Therapies

    Charles J. Sherr ^1,2 and Jiri Bartek ^{3,4 1}Howard Hughes Medical Institute, Chevy Chase, Maryland 20815²Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105; email: [email protected] ³Department of Biochemistry and Biophysics, Division of Translational Medicine and Chemical Biology, Science for Life Laboratory, Karolinska Institute, Stockholm S-171 21, Sweden⁴Danish Cancer Society Research Center, Copenhagen DK 2100, Denmark

    Annual Review of Cancer Biology Vol. 1: 41 - 57

    • ...among them the ATM and CHK2 checkpoint kinases and their prime target, p53 (Ahn et al. 2004, Bartek et al. 2007, Halazonetis et al. 2008)....

  • Pathogenesis and Host Control of Gammaherpesviruses: Lessons from the Mouse

    Erik Barton, ¹ Pratyusha Mandal, ¹ and Samuel H. Speck ^{2 1}Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907;²Department of Microbiology and Immunology, and The Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322; email: [email protected]

    Annual Review of Immunology Vol. 29: 351 - 397

    • ...DNA repair machinery is upregulated and the cell cycle is halted; cells become susceptible to apoptosis if DNA damage cannot be resolved (140)....

• 8.

• 9.

  More AR articles citing this reference

  • Nutrition and Inflammation: Are Centenarians Similar to Individuals on Calorie-Restricted Diets?

    Claudio Franceschi, ¹ Rita Ostan, ² and Aurelia Santoro ^{2 1}IRCCS Institute of Neurological Sciences of Bologna, 40139 Bologna, Italy; email: [email protected] ²Department of Experimental, Diagnostic, and Specialty Medicine (DIMES) and Interdepartmental Centre "L. Galvani" (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; email: [email protected], [email protected]

    Annual Review of Nutrition Vol. 38: 329 - 356

    • ...stress defense mechanisms, and survival pathways, which attenuate proinflammatory responses (6)....

• 10.

  Bauersfeld SP , Kessler CS , Wischnewsky M , Jaensch A , Steckhan N , et al. 2018. The effects of short-term fasting on quality of life and tolerance to chemotherapy in patients with breast and ovarian cancer: a randomized cross-over pilot study. BMC Cancer 18:476

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

• 11.

  Bhakta N , Liu Q , Ness KK , Baassiri M , Eissa H , et al. 2017. The cumulative burden of surviving childhood cancer: an initial report from the St Jude Lifetime Cohort Study (SJLIFE). Lancet 390(10112):2569–82

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Pharmacogenomics in Pediatric Oncology: Mitigating Adverse Drug Reactions While Preserving Efficacy

    Abdelbaset A. Elzagallaai, ¹ Bruce C. Carleton, ^2,3,4 and Michael J. Rieder ^{1 1}Department of Pediatrics, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3M7, Canada; email: [email protected] ²Division of Translational Therapeutics, Department of Pediatrics, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada³Pharmaceutical Outcomes Programme, BC Children's Hospital, Vancouver, British Columbia V5Z 4H4, Canada⁴BC Children's Hospital Research Institute, Vancouver, British Columbia V5Z 4H4, Canada

    Annual Review of Pharmacology and Toxicology Vol. 61: 679 - 699

    • ...22% of children with cancer are admitted to the hospital as a direct result of adverse drug reactions (ADRs) (4...

• 12.

  Cabelof DC , Yanamadala S , Raffoul JJ , Guo Z , Soofi A , Heydari AR . 2003. Caloric restriction promotes genomic stability by induction of base excision repair and reversal of its age-related decline. DNA Repair 2(3):295–307

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 13.

  Cadet J , Douki T , Frelon S , Sauvaigo S , Pouget JP , Ravanat JL . 2002. Assessment of oxidative base damage to isolated and cellular DNA by HPLC-MS/MS measurement. Free Radic. Biol. Med. 33(4):441–49

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 14.

  Calle EE , Rodriguez C , Walker-Thurmond K , Thun MJ . 2003. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N. Engl. J. Med. 348(17):1625–38

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...respectively] are positively associated with risk for at least 12 different cancers (107, 210) and account for 14–20% of all cancer deaths (23)....

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...Eugenia Calle and colleagues (24) published a landmark study confirming the strong links between obesity and cancer mortality....
    • ...The increased risk of NAFLD and NASH likely explains the strong association between obesity and hepatocellular carcinoma (HCC): Obese men were ∼4.5 times more likely to die from liver cancer than controls (24)....
    • ...Obese individuals are approximately twice as likely to die from pancreatic cancer compared with lean individuals (24)....

  • Dietary Fat and Sugar in Promoting Cancer Development and Progression

    Marcus D. Goncalves, ^1,2, Benjamin D. Hopkins, ^1, and Lewis C. Cantley ^{1 1}Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA; email: [email protected], [email protected], [email protected] ²Division of Endocrinology, Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA

    Annual Review of Cancer Biology Vol. 3: 255 - 273

    • ...so the contribution of dietary fat and sugar should be investigated (Calle et al. 2003, Ma et al. 2008)....

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...It is estimated that one in every five US cancer deaths can be attributed to obesity (23), ...

  • The Economics of Obesity and Related Policy

    Julian M. Alston, ¹ Joanna P. MacEwan, ² and Abigail M. Okrent ^{3 1}Department of Agricultural and Resource Economics and the Robert Mondavi Institute Center for Wine Economics, University of California, Davis, California 95616; email: [email protected] ²Precision Health Economics, Los Angeles, California 90025; email: [email protected] ³US Department of Agriculture Economic Research Service, Washington, DC 20250; email: [email protected]

    Annual Review of Resource Economics Vol. 8: 443 - 465

    • ...and obesity is estimated to account for 14% of cancer deaths in men and 20% in women (Calle et al. 2003)....

  • Obesity, Inflammation, and Cancer

    Tuo Deng, ^1,2 Christopher J. Lyon, ¹ Stephen Bergin, ^3,4 Michael A. Caligiuri, ⁴ and Willa A. Hsueh ^{5 1}Diabetes Research Center and Center for Bioenergetics, Houston Methodist Research Institute, Houston, Texas 77030; email: [email protected] ²Department of Medicine, Weill Cornell Medical College at Cornell University, New York, New York 10021³Medical Scientist Training Program and Biomedical Sciences Graduate Program, The Ohio State University, Columbus, Ohio 43210⁴The Comprehensive Cancer Center–Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, Ohio 43210⁵The Diabetes and Metabolism Research Center, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The Ohio State University, Columbus, Ohio 43210; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 11: 421 - 449

    • ...a measure of adiposity, are associated with increased cancer risk (4)....
    • ...and as much as 52% and 62% of the cancer death rate in morbidly obese (BMI > 40 kg/m²) men and women, respectively (4)....

  • Liver Cancer: Connections with Obesity, Fatty Liver, and Cirrhosis

    Andrea Marengo, Chiara Rosso, and Elisabetta BugianesiDivision of Gastroenterology and Hepatology, Department of Medical Sciences, A.O. Città della Salute e della Scienza di Torino, University of Turin, Turin, Italy; email: [email protected], [email protected], [email protected]

    Annual Review of Medicine Vol. 67: 103 - 117

    • ...where the strongest associations are with pancreatic and liver cancer (1)....
    • ...either alone or as cofactor, as highlighted by several large-scale epidemiological studies (1, 8...
    • ...the risk of dying from liver cancer was 4.5 times higher in men with a BMI of 35 kg/m² or above compared to the group with a normal BMI (18.5–25 kg/m²) (1)....

  • Health Benefits of Long-Term Weight-Loss Maintenance

    Christian F. Rueda-Clausen, Ayodele A. Ogunleye, and Arya M. SharmaObesity Research & Management, Clinical Research Unit, Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, T6G 2E1 Canada; email: [email protected], [email protected], [email protected]

    Annual Review of Nutrition Vol. 35: 475 - 516

    • ...95% CI: 1.1–2.1 for women and RR 1.62, 95% CI: 1.4–1.9 for men) (29)....

  • Impact of the Obesity Epidemic on Cancer

    Pamela J. Goodwin ¹ and Vuk Stambolic ^{2 1}Department of Medicine, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X4, Canada; email: [email protected] ²Princess Margaret Cancer Centre and Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2M9, Canada; email: [email protected]

    Annual Review of Medicine Vol. 66: 281 - 296

    • ...During the past decade there has been an explosion of evidence linking obesity with increased cancer incidence and cancer mortality (see Figure 1) (10, 11)....
    • ...Calle et al. (11) estimated that 14% of all cancer deaths in men and 20% of all cancer deaths in women could be avoided if the current patterns of overweight and obesity in the United States could be reversed. ...
    • ...The RRs of mortality from specific types of cancer and all cancers in healthy participants of the American Cancer Society Study II as reported by Calle et al. (11) are shown for men and women on the right side of this figure....

  • Obesity and Cancer: Local and Systemic Mechanisms

    Neil M. Iyengar, ^1,2,3 Clifford A. Hudis, ^1,2 and Andrew J. Dannenberg ^{2 1}Memorial Sloan Kettering Cancer Center, New York, NY 10065; email: [email protected], [email protected] ²Weill Cornell Medical College, New York, NY 10065; email: [email protected] ³Rockefeller University, New York, NY 10065

    Annual Review of Medicine Vol. 66: 297 - 309

    • ...esophagus, colon, prostate, kidney, ovary, uterus, liver, tongue, and others (5...

  • Current Perspective on the Global and United States Cancer Burden Attributable to Lifestyle and Environmental Risk Factors

    David Schottenfeld, ^1,2,3 Jennifer L. Beebe-Dimmer, ^5,6 Patricia A. Buffler, ⁷ and Gilbert S. Omenn ^{1,3,4 1}School of Public Health,²Department of Epidemiology,³Medical School, Department of Internal Medicine,⁴Departments of Computational Medicine and Bioinformatics, Human Genetics, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected], [email protected] ⁵Karmanos Cancer Institute, Division of Population Studies and Disparities Research,⁶Department of Oncology, Wayne State University, Detroit, Michigan 48201; email: [email protected] ⁷School of Public Health, Department of Epidemiology, University of California, Berkeley, California 94720; email: [email protected]

    Annual Review of Public Health Vol. 34: 97 - 117

    • ...which were then applied to the 1999–2000 NHANES of excess body weight prevalence in men and women, 50–69 years of age (14)....

  • Cytokines, Obesity, and Cancer: New Insights on Mechanisms Linking Obesity to Cancer Risk and Progression

    Candace A. Gilbert ¹ and Joyce M. Slingerland ^{1,2,3 1}Braman Family Breast Cancer Institute at Sylvester Comprehensive Cancer Center, Departments of²Medicine and³Biochemistry & Molecular Biology, University of Miami, Miller School of Medicine, Miami, Florida; email: [email protected]

    Annual Review of Medicine Vol. 64: 45 - 57

    • ...There is strong epidemiologic evidence linking obesity with increased incidence of and/or mortality from several types of cancer (2, 3)....
    • ...up to 20% of all cancer deaths in women and 14% in men are currently attributable to obesity (2)....
    • ...obesity is also associated with worse outcome and increased risk of death for individuals diagnosed with colon, kidney, prostate, breast and endometrial cancers, among others (2, 4, 5, 6, 8)....
    • ...several cancers show a worse outcome in obese individuals, suggesting a link between obesity and treatment resistance (2)....

  • Obesity in Cancer Survival

    Niyati Parekh ¹ , Urmila Chandran ^2,3 , and Elisa V. Bandera ^{2,3 1}Department of Nutrition, Food Studies and Public Health, New York University, New York, New York 10003²The Cancer Institute of New Jersey, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903; email: [email protected] ³School of Public Health, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey 08854

    Annual Review of Nutrition Vol. 32: 311 - 342

    • ...Obesity has been shown to be associated with increased cancer mortality (11), ...

  • What Is the Brain-Cancer Connection?

    Lei Cao and Matthew J. DuringCollege of Medicine, The Ohio State University, Columbus, Ohio 43210; email: [email protected], [email protected]

    Annual Review of Neuroscience Vol. 35: 331 - 345

    • ...if both men and women maintained normal weight, 900,000 cancer deaths could be prevented (Calle et al. 2003)....

  • Cancer and Inflammation: An Old Intuition with Rapidly Evolving New Concepts

    Giorgio TrinchieriCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702-1201; email: [email protected]

    Annual Review of Immunology Vol. 30: 677 - 706

    • ...The most obese members of the cohort (BMI > 40) were 52% (men) and 62% (women) more likely to die of cancer than individuals of normal weight (27)....

  • Preventability of Cancer: The Relative Contributions of Biologic and Social and Physical Environmental Determinants of Cancer Mortality

    Graham A. Colditz ¹ and Esther K. Wei ^{2 1}Alvin J. Siteman Cancer Center and Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63108; email: [email protected] ²California Pacific Medical Center, Research Institute, San Francisco, California 94107; email: [email protected]

    Annual Review of Public Health Vol. 33: 137 - 156

    • ...the ACS data indicate that 14–20% of cancer mortality is attributable to obesity (13), ...

  • Biological Mechanisms Linking Obesity and Cancer Risk: New Perspectives

    Darren L. Roberts, ^1,2 Caroline Dive, ¹ and Andrew G. Renehan ^{1,2 1}Clinical and Experimental Pharmacology, Paterson Institute for Cancer Research, The Christie NHS Foundation Trust, Manchester, United Kingdom²School of Cancer, Enabling Sciences and Technology, University of Manchester, Manchester Academic Health Science Centre, United Kingdom; email: [email protected]

    Annual Review of Medicine Vol. 61: 301 - 316

    • ...The media often highlight that obesity is linked to 20% of all cancer deaths in women and 14% in men, quoting the large US Cancer Prevention Study II (11)....

  • The Obesity Epidemic: Current and Future Pharmacological Treatments

    Karl G. Hofbauer, ¹ Janet R. Nicholson, ¹ and Olivier Boss ^{2 1}Applied Pharmacology, Biozentrum/Pharmazentrum, University of Basel, CH 4056 Basel, Switzerland; email: [email protected] ²Sirtris Pharmaceuticals Inc., Cambridge, Massachusetts 02139

    Annual Review of Pharmacology and Toxicology Vol. 47: 565 - 592

    • ...Several epidemiological studies have documented that excessive fat accumulation is associated with serious diseases and leads to increased morbidity and mortality (14...

  • Obesity

    Anthony N. Fabricatore and Thomas A. WaddenUniversity of Pennsylvania, School of Medicine, Department of Psychiatry, Weight and Eating Disorders Program, Philadelphia, Pennsylvania 19104-3309; email: [email protected]; [email protected]

    Annual Review of Clinical Psychology Vol. 2: 357 - 377

    • ...Other studies have suggested that obesity increases the risk of cancer morbidity and mortality (Bergstrom et al. 2001, Calle et al. 2003)....

  • COMPETING DIETARY CLAIMS FOR WEIGHT LOSS: Finding the Forest Through Truculent Trees

    Annual Review of Public Health Vol. 26: 61 - 88

    • ...; and excess body weight is a potent risk factor for most prevalent cancers (26)....

  • ADVANCES IN CANCER EPIDEMIOLOGY: Understanding Causal Mechanisms and the Evidence for Implementing Interventions

    David Schottenfeld ^1,2 and Jennifer L. Beebe-Dimmer ^1,3 Departments of Epidemiology, ¹ Internal Medicine, ² and Urology, ³ School of Public Health, University of Michigan, Ann Arbor, Michigan 48109-2029; email: [email protected], [email protected]

    Annual Review of Public Health Vol. 26: 37 - 60

    • ...the preventive impact of maintaining a recommended BMI below the category of overweight (BMI <25) was 15%–20% of cancer deaths in women and 10%–14% in men, or a total of 90,000 cancer deaths per year (25)....

• 15.

• 16.

  Cohen CW , Fontaine KR , Arend RC , Alvarez RD , Leath CA , et al. 2018a. A ketogenic diet reduces central obesity and serum insulin in women with ovarian or endometrial cancer. J. Nutr. 148(8):1253–60

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 17.

  Cohen CW , Fontaine KR , Arend RC , Soleymani T , Gower BA . 2018b. Favorable effects of a ketogenic diet on physical function, perceived energy, and food cravings in women with ovarian or endometrial cancer: a randomized, controlled trial. Nutrients 10(9):1187

  • Crossref
  • Web of Science ®
  • Google Scholar

• 18.

  More AR articles citing this reference

  • Neuronal Mechanisms that Drive Organismal Aging Through the Lens of Perception

    Christi M. Gendron, ¹ Tuhin S. Chakraborty, ¹ Brian Y. Chung, ¹ Zachary M. Harvanek, ¹ Kristina J. Holme, ¹ Jacob C. Johnson, ¹ Yang Lyu, ¹ Allyson S. Munneke, ² and Scott D. Pletcher ^{1,2 1}Department of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan 48109, USA; email: [email protected] ²Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109, USA

    Annual Review of Physiology Vol. 82: 227 - 249

    • ...and monkeys given a low-calorie diet exhibited decreased overall morbidity as well as decreased incidences of cancer, diabetes, and brain atrophy (8)....

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...a 20-year longitudinal study showed that CR macaques lived longer and had decreased incidences of gastrointestinal cancer, diabetes, cardiovascular disease, and brain atrophy (31)....

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...and the NIA NHP CR studies have highlighted the subtle differences in response to CR (137, 138)....

  • The Roles of Cellular and Organismal Aging in the Development of Late-Onset Maladies

    Filipa Carvalhal Marques, ^1,2, Yuli Volovik, ^1, and Ehud Cohen ^{1 1}Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, Hebrew University School of Medicine, 91120 Jerusalem, Israel; email: [email protected] ²Centre of Ophthalmology and Vision Sciences, Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 1 - 23

    • ...two independent research groups (12, 13) addressed the question of whether the DR-associated longevity and prolonged health span phenotypes are conserved in primates....
    • ...Whereas one group reported that monkeys subjected to a DR regimen exhibited prolonged life span and lower susceptibility to aging-associated maladies (12), ...

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...as well as in rhesus monkeys (5, 6, 7) and in a number of nonmodel organisms....
    • ...and they are protected against brain atrophy, sarcopenia, cardiovascular disease, type 2 diabetes, neoplasia, and endometriosis (6, 14, 15)....
    • ...such as the major advances achieved in developing DR mimetic drugs, with the discovery that DR slows aging in primates (5, 6, 7)...

  • Metabolic and Neuropsychiatric Effects of Calorie Restriction and Sirtuins

    Sergiy Libert and Leonard GuarenteGlenn Laboratory for the Science of Aging, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected]

    Annual Review of Physiology Vol. 75: 669 - 684

    • ...such as yeast (2), worms (3), flies (4), spiders (5, 6), mice (7), and possibly rhesus monkeys (8)....

  • After 65 Years, Research Is Still Fun

    William HanselLiberty Hyde Bailey Emeritus Professor, Cornell University, Ithaca, New York 14853Gordon Cain Professor Emeritus, Louisiana State University, Baton Rouge, Louisiana 70803Professor, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana 70808; email: [email protected]

    

    Annual Review of Animal Biosciences Vol. 1: 1 - 20

    • ...the ability of restricted caloric intake to increase longevity was demonstrated in many species including rhesus monkeys (8), ...

  • HIV Infection, Inflammation, Immunosenescence, and Aging

    Steven G. DeeksDepartment of Medicine, San Francisco General Hospital, University of California San Francisco; email: [email protected]

    Annual Review of Medicine Vol. 62: 141 - 155

    • ...rhesus monkeys randomized to a 30% reduction in caloric intake exhibited a reduced risk of dying from age-associated diseases (although this mortality benefit was not significant when a large number of non-age-associated deaths were included in the analysis) (71)....

• 19.

  Colman RJ , Beasley TM , Kemnitz JW , Johnson SC , Weindruch R , Anderson RM . 2014. Caloric restriction reduces age-related and all-cause mortality in rhesus monkeys. Nat. Commun. 5(7):3557

  • Crossref
  • Medline
  • Google Scholar

  More AR articles citing this reference

  • Repairing Mitochondrial Dysfunction in Disease

    Vincenzo Sorrentino, ¹ Keir J. Menzies, ² and Johan Auwerx ^{1 1}Laboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland; email: [email protected] ²Interdisciplinary School of Health Sciences, University of Ottawa Brain and Mind Research Institute and Centre for Neuromuscular Disease, Ottawa K1H 8M5, Canada; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 58: 353 - 389

    • ...CR improves both age-related and all-cause mortality and morbidity, with accruing evidence demonstrating increases in life span (74)....

  • Senescence in COPD and Its Comorbidities

    Peter J. BarnesNational Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 79: 517 - 539

    • ...AMPK is activated by calorie restriction, which was also shown to extend lifespan (60)....
    • ...Caloric restriction prolongs lifespan in species from yeast to mammals, including primates (60)....

• 20.

  More AR articles citing this reference

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...This may partially stem from some rather controversial claims in the early twentieth century that fish do not age (142), a statement that was later repudiated (143)....

• 21.

  Conti B , Sanchez-Alavez M , Winsky-Sommerer R , Morale MC , Lucero J , et al. 2006. Transgenic mice with a reduced core body temperature have an increased life span. Science 314(5800):825–28

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Metabolic and Neuropsychiatric Effects of Calorie Restriction and Sirtuins

    Sergiy Libert and Leonard GuarenteGlenn Laboratory for the Science of Aging, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected]

    Annual Review of Physiology Vol. 75: 669 - 684

    • ...transgenic mice with a reduced core body temperature have an increased life span (30)....

• 22.

• 23.

  More AR articles citing this reference

  • Nuclear Genomic Instability and Aging

    Laura J. Niedernhofer, ¹ Aditi U. Gurkar, ^1,2 Yinsheng Wang, ³ Jan Vijg, ⁴ Jan H.J. Hoeijmakers, ⁵ and Paul D. Robbins ^{1 1}Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA; email: [email protected] ²Department of Medicine, Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA³Department of Chemistry, University of California, Riverside, California 92521, USA⁴Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, Bronx, New York 10461, USA⁵Department of Molecular Genetics, Erasmus University Medical Center, 3015 CE Rotterdam, The Netherlands

    Annual Review of Biochemistry Vol. 87: 295 - 322

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...TTD, and XFE premature aging phenotypes have been well described (55, 57...

  • Genome Instability and Aging

    Jan Vijg ¹ and Yousin Suh ^{1,2 1}Department of Genetics, Albert Einstein College of Medicine, New York, NY 10461; email: [email protected], [email protected] ²Aging Research Institute, Guangdong Medical College, Dongguan 523808, Guangdong, China

    Annual Review of Physiology Vol. 75: 645 - 668

    • ...are caused by defects in transcription and DNA repair via the nucleotide excision repair (NER) pathway (Figure 2); patients with these disorders show no signs of increased cancer (98)....

  • DNA Repair Defects in Stem Cell Function and Aging

    Youngji Park ¹ and Stanton L. Gerson ^{2 1,2} Division of Hematology and Oncology, ² Comprehensive Cancer Center and Center for Stem Cell Regenerative Medicine, ^1,2 University Hospitals of Cleveland and Case Western Reserve University, Cleveland, Ohio 44106-4937; email: [email protected], [email protected]

    Annual Review of Medicine Vol. 56: 495 - 508

    • ...The link between aging syndromes and HSC defects has been assessed in animal models of human premature aging syndromes. Xpd ^−/− mice are defective in NER owing to loss of the DNA helicase subunit of transcription factor IIH complex, mutations of which cause the human trichothiodystrophy syndrome (3)....
    • ...although human Werner syndrome is associated with striking evidence of premature aging (3, 55...

  • Genetics of Longevity and Aging

    Jan Vijg ^1,2 and Yousin Suh ^{1 1}University of Texas Health Science Center, San Antonio, Texas 78245; email: [email protected], [email protected] ²Geriatric Research Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas 78229

    Annual Review of Medicine Vol. 56: 193 - 212

    • ...symptoms of accelerated aging have been observed in mice with engineered genetic defects in genes involved in genome maintenance, such as p53 (64), the nucleotide excision repair gene Xpd (65), ...

• 24.

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...DER approaches are associated with a prolonged health span and have been implemented in individuals who are normoweight as well as in individuals who are overweight or obese and are seeking to lose weight (38)....
    • ...Biological mechanisms by which DER approaches delay the onset of age-related diseases are expertly reviewed elsewhere (38, 128, 140, 149) and include improved insulin sensitivity, ...

  • Metabolic and Signaling Roles of Ketone Bodies in Health and Disease

    Patrycja Puchalska ¹ and Peter A. Crawford ^{1,2 1}Department of Medicine, Division of Molecular Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA; email: [email protected], [email protected] ²Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, Minnesota 55455, USA

    Annual Review of Nutrition Vol. 41: 49 - 77

    • ...improving health, combatting disease, and offsetting the effects of aging (18, 43, 72, 127, 159)....
    • ...time-restricted eating, caloric restriction, and adherence to low-carbohydrate ketogenic diets (18, 43, 109, 125)....

  • Cardiometabolic Benefits of Intermittent Fasting

    Krista A. Varady, Sofia Cienfuegos, Mark Ezpeleta, and Kelsey GabelDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois 60612, USA; email: [email protected]

    Annual Review of Nutrition Vol. 41: 333 - 361

    • ...Intermittent fasting has emerged as one of the most popular diets for weight loss in recent years (13, 14, 30, 65, 74, 78, 80, 96)....
    • ...Some of the mechanisms by which intermittent fasting may improve metabolic health include reduced free radical production, augmented stress resistance, improved glucose regulation, and suppressed inflammation (21, 30, 74, 78)....
    • ...it has been shown that fasting may upregulate autophagy by decreasing the activity of the mammalian target of rapamycin (mTOR) protein synthesis pathway (4, 25, 30)....

  • Group 2 Innate Lymphoid Cells: Team Players in Regulating Asthma

    Noe Rodriguez-Rodriguez, Mayuri Gogoi, and Andrew N.J. McKenzieMedical Research Council, Laboratory of Molecular Biology, Cambridge, Cambridgeshire, CB2 0QH, United Kingdom; email: [email protected], [email protected], [email protected]

    Annual Review of Immunology Vol. 39: 167 - 198

    • ...and ILC2 responses specifically, but large, carefully controlled trials are required (222)....

• 25.

  De Groot S , Lugtenberg R , Welters M , Ehsan I , Vreeswijk M , et al. 2019. Dietary restriction as an adjunct to neoadjuvant chemotherapy for HER2-negative breast cancer: final results from the DIRECT trial (BOOG 2013–04). Cancer Res. 79(4 Suppl.):P1–15–20 (Abstr.)

  • Google Scholar

• 26.

  De Groot S , Vreeswijk MPG , Welters MJP , Gravesteijn G , Boei JJWA , et al. 2015. The effects of short-term fasting on tolerance to (neo) adjuvant chemotherapy in HER2-negative breast cancer patients: a randomized pilot study. BMC Cancer 15:652

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...and subjects exhibited higher red cell and white cell counts after chemotherapy compared with the nonfasted groups (35)....

• 27.

  Di Biase S , Shim HS , Kim KH , Vinciguerra M , Rappa F , et al. 2017. Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy. PLOS Biol. 15(3):e1002603

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 28.

  Dollé MET , Kuiper RV , Roodbergen M , Robinson J , de Vlugt S , et al. 2011. Broad segmental progeroid changes in short-lived Ercc1 ^−/Δ7 mice. Pathobiol. Aging Age-Relat. Dis. 1(1):7219

  • Crossref
  • Google Scholar

• 29.

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...A FMD was shown to be safe and feasible in a pilot study of patients receiving platinum-based chemotherapies (46)...

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...Dorff et al. (43) prescribed escalating doses of fasting in consecutive subgroups, ...

• 30.

• 31.

  More AR articles citing this reference

  • Development and Therapeutic Potential of Small-Molecule Modulators of Circadian Systems

    Zheng Chen, ¹ Seung-Hee Yoo, ¹ and Joseph S. Takahashi ^{2 1}Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston, Houston, Texas 77030, USA; email: [email protected] ²Department of Neuroscience and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA

    Annual Review of Pharmacology and Toxicology Vol. 58: 231 - 252

    • ...and mTORC1, all of which functionally interact with the clock (32, 137, 139)....

• 32.

  More AR articles citing this reference

  • Neuronal Mechanisms that Drive Organismal Aging Through the Lens of Perception

    Christi M. Gendron, ¹ Tuhin S. Chakraborty, ¹ Brian Y. Chung, ¹ Zachary M. Harvanek, ¹ Kristina J. Holme, ¹ Jacob C. Johnson, ¹ Yang Lyu, ¹ Allyson S. Munneke, ² and Scott D. Pletcher ^{1,2 1}Department of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan 48109, USA; email: [email protected] ²Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109, USA

    Annual Review of Physiology Vol. 82: 227 - 249

    • ...have been shown to extend life span in a range of different species and to improve metabolic health measures in humans (14)....

  • Nutrition and Inflammation: Are Centenarians Similar to Individuals on Calorie-Restricted Diets?

    Claudio Franceschi, ¹ Rita Ostan, ² and Aurelia Santoro ^{2 1}IRCCS Institute of Neurological Sciences of Bologna, 40139 Bologna, Italy; email: [email protected] ²Department of Experimental, Diagnostic, and Specialty Medicine (DIMES) and Interdepartmental Centre "L. Galvani" (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; email: [email protected], [email protected]

    Annual Review of Nutrition Vol. 38: 329 - 356

    • ...Their lower levels of serum insulin-like growth factor (IGF)-1 confirm data from animal models in which the downregulation of IGF-1 and insulin signaling significantly extends survival (31, 138, 139)....

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...are highly conserved across multiple organisms, from yeast to humans (16, 44)....
    • ...The health effects of CR and fasting are conserved in diverse organisms (44)....

  • Senescence in COPD and Its Comorbidities

    Peter J. BarnesNational Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 79: 517 - 539

    • ...reduces the release of insulin and IGF-1, and increases SIRT1 (151)....

  • Signaling Networks Determining Life Span

    Celine E. Riera, ^1,2,3 Carsten Merkwirth, ^1,2,3 C. Daniel De Magalhaes Filho, ^2,4 and Andrew Dillin ^{1,2,3 1}Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; email: [email protected] ²Howard Hughes Medical Institute, Chevy Chase, Maryland 20815³Glenn Center for Research on Aging, University of California, Berkeley, California 94720⁴The Salk Institute for Biological Studies, La Jolla, California 92037

    Annual Review of Biochemistry Vol. 85: 35 - 64

    • ...a more severe DR regimen (30% reduction) increased median life span by up to 50% and drastically delayed the onset of chronic diseases (55)....

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...This evolutionary conservation is most firmly established for the effects of nutrition and of the molecular mechanisms involved in the sensing of nutrients (Figure 1) (2, 3). ...

  • The Ins and Outs of Aging and Longevity

    Thomas A. RandoGlenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA 94305-5235; email: [email protected]

    Annual Review of Physiology Vol. 75: 617 - 619

    • ...the average and maximal life span of individuals within a species (11)....

  • Sensory Perception and Aging in Model Systems: From the Outside In

    Nancy J. Linford, ¹ Tsung-Han Kuo, ² Tammy P. Chan, ³ and Scott D. Pletcher ^{1-3 1}Department of Molecular and Integrative Physiology and Geriatrics Center, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected], [email protected] ²Department of Molecular and Human Genetics and³Developmental Biology Program, Baylor College of Medicine, Houston, Texas 77030 [Erratum]

    Annual Review of Cell and Developmental Biology Vol. 27: 759 - 785

    • ...Direct evidence for the modulation of aging by perception of food cues was first shown in Drosophila using dietary manipulations. Dietary restriction is a reduction in nutrient availability that increases lifespan in many different organisms (Fontana et al. 2010)....
    • ...and humans often exhibit reduced levels of IIS molecules (Fontana et al. 2010, Tatar et al. 2003)....

  • HIV Infection, Inflammation, Immunosenescence, and Aging

    Steven G. DeeksDepartment of Medicine, San Francisco General Hospital, University of California San Francisco; email: [email protected]

    Annual Review of Medicine Vol. 62: 141 - 155

    • ...experimental restriction of caloric intake to levels below that when fed ad libitum but above that which causes starvation is associated with increased longevity (69, 70)....

• 33.

  Garinis GA , Uittenboogaard LM , Stachelscheid H , Fousteri M , van Ijcken W , et al. 2009. Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity. Nat. Cell Biol. 11(5):604–15

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...have been shown to induce distinct gene expression changes that are highly similar to naturally aged organs (55, 60, 104)....
    • ...Hoeijmakers, unpublished results) (55, 85, 87, 104, 106)....

• 34.

  More AR articles citing this reference

  • Mechanisms of Vertebrate DNA Interstrand Cross-Link Repair

    Daniel R. Semlow ^1,2 and Johannes C. Walter ^{1,3 1}Department of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts 02115, USA; email: [email protected] ²Current affiliation: Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, USA³Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA

    Annual Review of Biochemistry Vol. 90: 107 - 135

    • ...purine nucleotides (dG and dA) tend to be more reactive than pyrimidine nucleotides (dT and dC) (5), ...

• 35.

  Gillespie ZE , Pickering J , Eskiw CH . 2016. Better living through chemistry: Caloric restriction (CR) and CR mimetics alter genome function to promote increased health and lifespan. Front. Genet. 7:142

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 36.

  More AR articles citing this reference

  • Revelations About Aging and Disease from Unconventional Vertebrate Model Organisms

    Yang Zhao, Andrei Seluanov, and Vera GorbunovaDepartment of Biology, University of Rochester, Rochester, New York 14627, USA; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 55: 135 - 159

    • ...and HDAC1 and HDAC2 are associated with age-related epigenetic modification (59, 138)....

  • Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions

    Laura Campello, Nivedita Singh, Jayshree Advani, Anupam K. Mondal, Ximena Corso-Díaz, and Anand SwaroopNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; email: [email protected]

    Annual Review of Vision Science Vol. 7: 633 - 664

    • ...DNA double-strand breaks are primarily repaired by HR and NHEJ (Gillet & Scharer 2006)....

• 37.

• 38.

  More AR articles citing this reference

  • Caenorhabditis elegans: A Convenient In Vivo Model for Assessing the Impact of Food Bioactive Compounds on Obesity, Aging, and Alzheimer's Disease

    Peiyi Shen, ^1, Yiren Yue, ^1, Jolene Zheng, ² and Yeonhwa Park ^{1 1}Department of Food Science, University of Massachusetts, Amherst, Massachusetts 01003, USA; email: [email protected] ²CPCRL Inc., Prairieville, Louisiana 70769, USA

    Annual Review of Food Science and Technology Vol. 9: 1 - 22

    • ...Diet restriction–related genes.Dietary restriction without malnutrition has been reported to extend life span and reduce age-dependent decline and diseases in virtually all species tested (Greer & Brunet 2009)....

  • AMP-Activated Protein Kinase: Maintaining Energy Homeostasis at the Cellular and Whole-Body Levels

    D. Grahame HardieDivision of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee, DD1 5EH, Scotland, United Kingdom; email: [email protected]

    Annual Review of Nutrition Vol. 34: 31 - 55

    • ...the AMPK ortholog is required for extension of lifespan in response to dietary restriction and other stresses (4, 43), ...
    • ...whereas the effects of A-769662 to suppress inflammation were impaired if fatty acid oxidation was blocked (43)....

  • The Molecular Basis of Organ Formation: Insights From the C. elegans Foregut

    Susan E. MangoDepartment of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts; email: [email protected]

    Annual Review of Cell and Developmental Biology Vol. 25: 597 - 628

    • ...AMP kinase, and insulin signaling (Greer & Brunet 2009, Greer et al. 2007), ...

• 39.

  Gunebakan E , Yalcin E , Dulger EC , Yigitbasi A , Ates N , et al. 2020. Short-term diet restriction but not alternate day fasting prevents cisplatin-induced nephrotoxicity in mice. Biomedicines 8(2):23

  • Crossref
  • Web of Science ®
  • Google Scholar

• 40.

  More AR articles citing this reference

  • Revelations About Aging and Disease from Unconventional Vertebrate Model Organisms

    Yang Zhao, Andrei Seluanov, and Vera GorbunovaDepartment of Biology, University of Rochester, Rochester, New York 14627, USA; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 55: 135 - 159

    • ...although cancer can occur in young individuals, the incidence of cancer increases steeply at older age (67, 109)....

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...The rapid growth, dysregulated tissue vasculature, and dysregulated metabolism of tumors (77)...
    • ...Chronic inflammation is a hallmark of both cancer (77) and obesity (42)...

  • The Role of Epigenetic Mechanisms in B Cell Lymphoma Pathogenesis

    Leandro Venturutti and Ari M. MelnickDivision of Hematology/Oncology, Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA; email: [email protected], [email protected]

    Annual Review of Cancer Biology Vol. 5: 311 - 330

    • ...GCBs manifest phenotypes resembling the so-called cancer hallmarks (Hanahan & Weinberg 2011) (Figure 1a ), ...

  • Personal Neoantigen Vaccines for the Treatment of Cancer

    Keerthi Shetty ¹ and Patrick A. Ott ^{1,2,3,4 1}Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; email: [email protected] ²Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA³Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA⁴Harvard Medical School, Boston, Massachusetts 02115, USA

    Annual Review of Cancer Biology Vol. 5: 259 - 276

    • ...the relatively small tumor sample that is typically obtained from a metastatic site (selected based mainly on clinical accessibility) almost certainly does not reflect the entire spectrum of targetable mutations in a given patient (Dagogo-Jack & Shaw 2018, Hanahan & Weinberg 2011)....

  • The Bidirectional Relationship Between Cancer Epigenetics and Metabolism

    Luke T. Izzo, Hayley C. Affronti, and Kathryn E. WellenDepartment of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 5: 235 - 257

    • ...The development and progression of cancer involves the acquisition of several hallmark features, including altered metabolism (Hanahan & Weinberg 2011)....

  • The Multifaceted Role of Regulatory T Cells in Breast Cancer

    Kevin Kos ¹ and Karin E. de Visser ^{1,2 1}Division of Tumor Biology and Immunology, Oncode Institute, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; email: [email protected] ²Department of Immunology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands

    Annual Review of Cancer Biology Vol. 5: 291 - 310

    • ...which can profoundly impact the development and progression of cancer (Blomberg et al. 2018, Garner & de Visser 2020, Hanahan & Weinberg 2011)....

  • Ex Vivo Analysis of Primary Tumor Specimens for Evaluation of Cancer Therapeutics

    Cristina E. Tognon, ^1,2 Rosalie C. Sears, ^2,3,4 Gordon B. Mills, ^2,4,5 Joe W. Gray, ^2,4,6 and Jeffrey W. Tyner ^{1,2,5 1}Division of Hematology and Medical Oncology, Oregon Health & Science University, Portland, Oregon 97239, USA; email: [email protected] ²Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon 97239, USA³Department of Molecular and Medical Genetics, Oregon Health & Science University, Portland, Oregon 97239, USA⁴Brenden-Colson Center for Pancreatic Care, Oregon Health & Science University, Portland, Oregon 97201, USA⁵Department of Cell, Developmental, and Cancer Biology, Oregon Health & Science University, Portland, Oregon 97201, USA⁶Department of Biomedical Engineering and Center for Spatial Systems Biomedicine, Oregon Health & Science University, Portland, Oregon 97239, USA

    Annual Review of Cancer Biology Vol. 5: 39 - 57

    • ...and Coussens contributed foundational thought pieces around essential biological hallmarks of cancer (Hanahan & Coussens 2012, Hanahan & Weinberg 2011)....

  • Microbiota Effects on Carcinogenesis: Initiation, Promotion, and Progression

    Lacey R. Lopez, ¹ Rachel M. Bleich, ² and Janelle C. Arthur ^{1,3,4 1}Department of Microbiology and Immunology, The University of North Carolina, Chapel Hill, North Carolina 27599, USA; email: [email protected], [email protected] ²Department of Biology, Appalachian State University, Boone, North Carolina 28608, USA; email: [email protected] ³Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599, USA⁴Center for Gastrointestinal Biology and Disease, The University of North Carolina, Chapel Hill, North Carolina 27599, USA

    Annual Review of Medicine Vol. 72: 243 - 261

    • ...We previously explored this body of knowledge using Hanahan & Weinberg's "hallmarks of cancer" (17) as a framework to classify specific mechanisms by which microbes, ...

  • Monocytes in the Tumor Microenvironment

    Stefano Ugel, Stefania Canè, Francesco De Sanctis, and Vincenzo BronteSection of Immunology, Department of Medicine, University of Verona, Verona 37134, Italy; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 16: 93 - 122

    • ...chronic stress and alterations to cellular homeostasis can steer tumor progression by fueling inflammation, which is among the hallmarks of cancer (92)....

  • Opposing Roles of Type I Interferons in Cancer Immunity

    Giselle M. Boukhaled, ^1,2 Shane Harding, ^1,2,3 and David G. Brooks ^{1,2 1}Princess Margaret Cancer Centre, University Health Network Toronto, Ontario M5G 2M9, Canada; email: [email protected] ²Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada³Departments of Medical Biophysics and Radiation Oncology, University of Toronto, Toronto, Ontario M5S 1A8, Canada

    Annual Review of Pathology: Mechanisms of Disease Vol. 16: 167 - 198

    • ...Hanahan & Weinberg (1) defined the hallmarks of cancer as the pathophysiological events required for tumor growth and survival....

  • The CXCL12/CXCR4/ACKR3 Axis in the Tumor Microenvironment: Signaling, Crosstalk, and Therapeutic Targeting

    Martine J. Smit, ^1,* Géraldine Schlecht-Louf, ^2, Maria Neves, ^3,4,5 Jelle van den Bor, ¹ Petronila Penela, ^3,4,5 Marco Siderius, ¹ Françoise Bachelerie, ^2,* and Federico MayorJr. ^{3,4,5, 1}Department of Medicinal Chemistry, Amsterdam Institute of Molecular and Life Sciences (AIMMS), Faculty of Science, Vrije Universiteit Amsterdam, 1081 HZ Amsterdam, Netherlands; email: [email protected] ²Université Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance, 92140 Clamart, France³Departamento de Biología Molecular and Centro de Biología Molecular Severo Ochoa (CSIC/UAM), 28049 Madrid, Spain⁴Instituto de Investigación Sanitaria La Princesa, 28006 Madrid, Spain⁵CIBER de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain

    Annual Review of Pharmacology and Toxicology Vol. 61: 541 - 563

    • ...Studies in the past decade have provided substantial insight into the highly dynamic nature of the TME and its critical importance for the outcome of cancer, including growth, angiogenesis, progression, and metastasis (124)....

  • Nutrition Regulates Innate Immunity in Health and Disease

    Samuel Philip Nobs, ^1, Niv Zmora, ^1,2, and Eran Elinav ^{1,3 1}Department of Immunology, Weizmann Institute of Science, Rehovot 7610001, Israel; email: [email protected] ²Research Center for Digestive Tract and Liver Diseases and Internal Medicine Division, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6423906, Israel³Cancer-Microbiome Research Division, Deutsches Krebsforschungszentrum (DKFZ), 69120 Heidelberg, Germany; email: [email protected]

    Annual Review of Nutrition Vol. 40: 189 - 219

    • ...aberrant inflammation is seen as a key driving force of carcinogenesis (67); thus, ...

  • Checkpoint Responses to DNA Double-Strand Breaks

    David P. Waterman, ¹ James E. Haber, ^1, and Marcus B. Smolka ^{2, 1}Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA; email: [email protected] ²Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, New York 14853, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 89: 103 - 133

    • ...Mutations in DDC genes such as ATM and TP53 are a central factor in contributing to genomic instability seen in tumors because they allow for the accumulation of more mutations over many cell generations (220, 221)....

  • Cruel to Be Kind: Epithelial, Microbial, and Immune Cell Interactions in Gastrointestinal Cancers

    Shabnam Shalapour ^1,2 and Michael Karin ^{1,2,3 1}Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA; email: [email protected], [email protected] ²Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA³Moores Cancer Center, University of California, San Diego, La Jolla, California 92093, USA

    Annual Review of Immunology Vol. 38: 649 - 671

    • ...inflammation has been recognized as one of the key enablers of the malignant state (1), ...

  • The Neural Regulation of Cancer

    Shawn Gillespie ^1,2 and Michelle Monje ^{2 1}Cancer Biology Graduate Program, Stanford University, Stanford, California 94305, USA²Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 4: 371 - 390

    • ...Only recently has it become clear that this genetic basis of cancer is a necessary but insufficient conceptual framework for understanding and halting cancer growth in complex ecosystems within the body (Hanahan & Weinberg 2011, Martincorena et al. 2015)....

  • Regulatory T Cells in Cancer

    George Plitas ^1,2 and Alexander Y. Rudensky ^{1,3 1}Immunology Program and Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; email: [email protected], [email protected] ²Breast Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA³Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA

    Annual Review of Cancer Biology Vol. 4: 459 - 477

    • ...The TME supports the bioenergetic needs of cancer cells reliant on aerobic glycolysis, fatty acid synthesis, and glutaminolysis (Hanahan & Weinberg 2011)....

  • The Acidic Tumor Microenvironment as a Driver of Cancer

    Ebbe Boedtkjer ¹ and Stine F. Pedersen ^{2 1}Department of Biomedicine, Aarhus University, DK-8000 Aarhus C, Denmark; email: [email protected] ²Department of Biology, University of Copenhagen, DK-2100 Copenhagen, Denmark; email: [email protected]

    Annual Review of Physiology Vol. 82: 103 - 126

    • ...they are key determining factors in the transition from a normal to a preneoplastic state (22)....
    • ...it has been recognized that many cancers exhibit a characteristic metabolic shift toward glycolysis even in the presence of O₂, which has since been denoted the Warburg effect (22, 59)....
    • ...followed by early but still premalignant disruption of tissue organization in the form of dysplasia and metaplasia (22, 83)....
    • ...provides a selection pressure that can give rise to cancer cell populations with more malignant phenotypes (22, 94, 95)....
    • ...Cancer stem cells (CSCs) play essential roles as drivers of tumor growth in at least some cancer types (22)....
    • ...In order for primary tumors to evolve and for cancer cells to invade and establish secondary tumors—directly or through blood or lymphatic vessels—they must be able to avoid immune cell detection and/or immune-mediated cell death (22)....

  • Human Organoids: Tools for Understanding Biology and Treating Diseases

    Frans Schutgens ^1,2 and Hans Clevers ^{1,3 1}Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences, 3584 CT Utrecht, The Netherlands; email: [email protected] ²Department of Pathology, Amsterdam University Medical Centers, Location VU Medical Center, 1081 HV Amsterdam, The Netherlands³Princess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands

    Annual Review of Pathology: Mechanisms of Disease Vol. 15: 211 - 234

    • ...One of the hallmarks of cancer is immune evasion (93), and organoids can be used to study the interaction of the immune system with tumor cells....

  • The Role of the Microbiome in Drug Response

    Rosina Pryor, ^1,2, Daniel Martinez-Martinez, ^1,2, Leonor Quintaneiro, ^1,2,3 and Filipe Cabreiro ^{1,2 1} MRC London Institute of Medical Sciences, London W12 0NN, United Kingdom; email: [email protected] ² Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, United Kingdom³ Institute of Structural and Molecular Biology, University College London and Birkbeck, London WC1E 6BT, United Kingdom

    Annual Review of Pharmacology and Toxicology Vol. 60: 417 - 435

    • ...indirectly via soluble factors (e.g., CC-chemokine ligand 25) (78), and systemically via altered metabolic effects (79)....

  • Liquid–Liquid Phase Separation in Disease

    Simon Alberti ^1,2 and Dorothee Dormann ^{3,4 1}Biotechnology Center (BIOTEC), Center for Molecular and Cellular Bioengineering (CMCB), Technische Universität Dresden, 01307 Dresden, Germany; email: [email protected] ²Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany³BioMedical Center (BMC), Ludwig-Maximilians-University Munich, 82152 Planegg-Martinsried, Germany; email: [email protected] ⁴Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-University Munich, 81377 Munich, Germany

    Annual Review of Genetics Vol. 53: 171 - 194

    • ...resist cell death, induce angiogenesis, and activate invasion and metastasis (61)....
    • ...There is ample genetic evidence that diverse growth factor signaling pathways are hyperactive in cancer cells (61)....

  • The Status and Impact of Clinical Tumor Genome Sequencing

    Kenna R. Mills Shaw and Anirban MaitraKhalifa Bin Zayed Institute for Personalized Cancer Therapy and Sheikh Ahmed Center for Pancreatic Cancer Research, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 20: 413 - 432

    • ...The acquired genomic and epigenetic changes in cancer collectively disrupt healthy cellular biology and drive the hallmark capabilities of cancer cells (44, 45)....

  • Measuring Clonal Evolution in Cancer with Genomics

    Marc J. Williams, ¹ Andrea Sottoriva, ² and Trevor A. Graham ^{1 1}Evolution and Cancer Laboratory, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom; email: [email protected], [email protected] ²Evolutionary Genomics and Modelling Lab, Centre for Evolution and Cancer, The Institute of Cancer Research, London SM2 5NG, United Kingdom

    Annual Review of Genomics and Human Genetics Vol. 20: 309 - 329

    • ...or the ability of cells to evade the homeostatic regulation of physiologically normal tissues (50)....

  • Disease Tolerance as an Inherent Component of Immunity

    Rui Martins, Ana Rita Carlos, Faouzi Braza, Jessica A. Thompson, Patricia Bastos-Amador, Susana Ramos, and Miguel P. SoaresInstituto Gulbenkian de Ciência, 2780–156 Oeiras, Portugal; email: [email protected]

    Annual Review of Immunology Vol. 37: 405 - 437

    • ...This is associated with acquisition of a transcriptional and metabolic profile that supports high cellular proliferative capacity, tissue invasiveness, and metastasis (208)....
    • ...some components of this network can promote tumor progression, as illustrated for NRF2 (211), NFAT5 (212), and mTOR (208), ...

  • Targeting Cancer at the Intersection of Signaling and Epigenetics

    Stephanie Guerra ^1,2 and Karen Cichowski ^{1,2,3 1}Genetics Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA; email: [email protected] ²Harvard Medical School, Boston, Massachusetts 02115, USA³Ludwig Center at Harvard, Harvard Medical School, Boston, Massachusetts 02115, USA

    Annual Review of Cancer Biology Vol. 3: 365 - 384

    • ...or amplifying signals that underlie the basic hallmarks of human cancer (Hanahan & Weinberg 2011)....
    • ...activating invasion and metastasis, and resisting cell death, among others (Hanahan & Weinberg 2000, 2011)....

  • NAD+ Metabolism in Aging and Cancer

    Tyler G. Demarest, ^1,2 Mansi Babbar, ¹ Mustafa N. Okur, ¹ Xiuli Dan, ¹ Deborah L. Croteau, ¹ Nima B. Fakouri, ¹ Mark P. Mattson, ² and Vilhelm A. Bohr ^{1 1}Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA; email: [email protected] ²Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA

    Annual Review of Cancer Biology Vol. 3: 105 - 130

    • ...Hallmarks of aging (Lopez-Otin et al. 2013) and cancer have recently been proposed (Hanahan & Weinberg 2011)....

  • HSP90: Enabler of Cancer Adaptation

    Alex M. Jaeger ¹ and Luke Whitesell ^{2 1}Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA²Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada; email: [email protected]

    Annual Review of Cancer Biology Vol. 3: 275 - 297

    • ...cellular responses to stress have emerged as crucial to supporting the hallmarks of cancer and the malignant state (Hanahan & Weinberg 2011)....
    • ...suggesting that cancer cells do not utilize HSP90 as a driver of aberrant growth but rather as an enabler of the hallmarks of the malignant phenotype (Hanahan & Weinberg 2011, Whitesell & Lindquist 2005). ...

  • The Hallmarks of Ferroptosis

    Scott J. Dixon ¹ and Brent R. Stockwell ^{2 1}Department of Biology, Stanford University, Stanford, California 94305, USA; email: [email protected] ²Department of Biological Sciences and Department of Chemistry, Columbia University, New York, NY 10027, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 3: 35 - 54

    • ...Multicellular organisms must balance cell proliferation and cell death to ensure tissue homeostasis and prevent the onset of neoplastic diseases (Evan & Vousden 2001, Hanahan & Weinberg 2011)....
    • ...Just as the genesis of human cancers requires that all of the hallmarks of cancer be activated (Hanahan & Weinberg 2011), ...

  • Harnessing Tumor Mutations for Truly Individualized Cancer Vaccines

    Mathias Vormehr, ^1,2 Özlem Türeci, ¹ and Ugur Sahin ^{1,2,3 1}Biopharmaceutical New Technologies (BioNTech) Corporation, 55131 Mainz, Germany; email: [email protected], [email protected] ²University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany; email: [email protected] ³TRON – Translational Oncology at the University Medical Center of Johannes Gutenberg University gGmbH, 55131 Mainz, Germany

    Annual Review of Medicine Vol. 70: 395 - 407

    • ...Cancer is associated with genetic and epigenetic alterations (1)....

  • New Cell Cycle Inhibitors Target Aneuploidy in Cancer Therapy

    Masanori Kawakami, ¹ Xi Liu, ¹ and Ethan Dmitrovsky ^{1,2,3 1}Department of Thoracic/Head and Neck Medical Oncology, MD Anderson Cancer Center, The University of Texas, Houston, Texas 77030, USA²Department of Cancer Biology, MD Anderson Cancer Center, The University of Texas, Houston, Texas 77030, USA³Current affiliation: Frederick National Laboratory for Cancer Research, Frederick, Maryland 21701, USA; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 59: 361 - 377

    • ...Cancer cells are frequently genetically unstable, and genomic instability is a hallmark of cancer (1)....
    • ...Aneuploidy is a hallmark of cancer (1)....

  • Heterochromatin: Guardian of the Genome

    Aniek Janssen, ^1,2, Serafin U. Colmenares, ^1,2, and Gary H. Karpen ^{1,2 1}Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA; email: [email protected] ²Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA

    Annual Review of Cell and Developmental Biology Vol. 34: 265 - 288

    • ...oncogenes, tumor suppressors, and DNA repair factors (Hanahan & Weinberg 2011)]....

  • Unconventional Ways to Live and Die: Cell Death and Survival in Development, Homeostasis, and Disease

    Swapna A. Gudipaty, ¹ Christopher M. Conner, ² Jody Rosenblatt, ¹ and Denise J. Montell ^{2 1}Department of Oncological Sciences and Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA²Molecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, California 93106, USA; email: [email protected]

    Annual Review of Cell and Developmental Biology Vol. 34: 311 - 332

    • ...resistance to anoikis is a critical step for tumor cell invasion (Frisch et al. 2013, Hanahan & Weinberg 2011)...

  • Lineage Plasticity in Cancer Progression and Treatment

    Clémentine Le Magnen, ¹ Michael M. Shen, ^1,2,3 and Cory Abate-Shen ^{1,2,4 1}Departments of Urology and Medicine, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY 10032, USA²Department of Systems Biology, Columbia University Medical Center, New York, NY 10032, USA; email: [email protected], [email protected] ³Department of Genetics and Development, Columbia University Medical Center, New York, NY 10032, USA⁴Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA

    Annual Review of Cancer Biology Vol. 2: 271 - 289

    • ...the stresses that promote cellular plasticity are also hallmarks of cancer (Hanahan & Weinberg 2011). ...

  • Harnessing Protease Activity to Improve Cancer Care

    Jaideep S. Dudani, ^1,2 Andrew D. Warren, ^1,3 and Sangeeta N. Bhatia ^{1,3,4,5,6,7 1}Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected], [email protected], [email protected] ²Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA³Harvard–MIT Division of Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA⁴Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA⁵Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA⁶Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02139, USA⁷Howard Hughes Medical Institute, Cambridge, Massachusetts 02139, USA

    Annual Review of Cancer Biology Vol. 2: 353 - 376

    • ...and numerous processes regulated by proteases are broadly dysregulated and functionally distinct in tumors (Hanahan & Weinberg 2011)....

  • The Power Behind the Throne: Senescence and the Hallmarks of Cancer

    Matthew Hoare ^1,2 and Masashi Narita ^{1 1}Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, United Kingdom; email: [email protected], [email protected] ²Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom

    Annual Review of Cancer Biology Vol. 2: 175 - 194

    • ...with the latest iteration (Hanahan & Weinberg 2011) focusing more on the microenvironment....
    • ...Hanahan & Weinberg (2011) subsequently updated their hallmarks of cancer to include two additional hallmarks and two enabling characteristics, ...
    • ... Figure 2 Senescence and the "hallmarks of cancer" (Hanahan & Weinberg 2000, 2011)....
    • ...Hanahan & Weinberg (2011) proposed tumor-promoting inflammation as an enabling characteristic of other hallmarks of carcinogenesis, ...

  • Insights from Large-Scale Cancer Genome Sequencing

    Elaine R. Mardis ^{1,2 1}Institute for Genomic Medicine, Nationwide Children's Hospital, Columbus, Ohio 43205, USA; email: [email protected] ²Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio 43205, USA

    Annual Review of Cancer Biology Vol. 2: 429 - 444

    • ...the idea that disrupted pathways lead to the cancer phenotype has been reinforced by the results of these large-scale studies (Hanahan & Weinberg 2011)....

  • SWI/SNF (BAF) Complexes: Guardians of the Epigenome

    Radhika Mathur ^1,2 and Charles W.M. Roberts ^{3 1}Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, Massachusetts 02215, USA; email: [email protected] ²Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA³Department of Oncology and Comprehensive Cancer Center, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 2: 413 - 427

    • ...each conferring upon cells a selective growth advantage and other hallmark capabilities of cancer (Hanahan & Weinberg 2000, 2011)....

  • New Insights into Lymphoma Pathogenesis

    Kojo S.J. Elenitoba-Johnson ^1,2 and Megan S. Lim ^{1,3 1}Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; email: [email protected], [email protected] ²Center for Personalized Diagnostics and Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA³Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA

    Annual Review of Pathology: Mechanisms of Disease Vol. 13: 193 - 217

    • ...Cellular reprogramming of energy metabolism is a hallmark of cancer (114)....

  • Epigenetic Mechanisms Regulating Adaptive Responses to Targeted Kinase Inhibitors in Cancer

    Steven P. Angus, Jon S. Zawistowski, and Gary L. JohnsonDepartment of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 58: 209 - 229

    • ...Given the essential role of kinases in cell signaling, kinase deregulation underlies many of the hallmarks of cancer (3)....

  • Overcoming Immune Dysregulation with Immunoengineered Nanobiomaterials

    Evan A. Scott, Nicholas B. Karabin, and Punn AugsornworawatDepartment of Biomedical Engineering, Northwestern University, Evanston, Illinois 60208

    Annual Review of Biomedical Engineering Vol. 19: 57 - 84

    • ...This ability to evade immune destruction was recently added to the list of eight essential hallmarks of cancer and is thus considered a vital component of cancer progression and development (32)....

  • Bioinspired Hydrogels to Engineer Cancer Microenvironments

    Kyung Min Park, ^1,2 Daniel Lewis, ¹ and Sharon Gerecht ^{1,3 1}Department of Chemical and Biomolecular Engineering, Johns Hopkins Physical Sciences–Oncology Center and Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, Maryland 21218; email: [email protected] ²Division of Bioengineering, Incheon National University, Incheon 22012, Republic of Korea³Department of Materials Science and Engineering, Johns Hopkins University, Baltimore, Maryland 21218

    Annual Review of Biomedical Engineering Vol. 19: 109 - 133

    • ...and dynamic nature, play a critical role in cancer development and progression (122)....

  • Glutaminolysis: A Hallmark of Cancer Metabolism

    Lifeng Yang, ^1,2 Sriram Venneti, ³ and Deepak Nagrath ^{1,2,4,5,6,7 1}Laboratory for Systems Biology of Human Diseases, Rice University, Houston, Texas 77005²Department of Chemical and Biomolecular Engineering, Rice University, Houston, Texas 77005³Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected] ⁴Department of Bioengineering, Rice University, Houston, Texas 77005⁵Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected] ⁶Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109⁷Comprehensive Cancer Center, University of Michigan Health Systems, Ann Arbor, Michigan 48109

    Annual Review of Biomedical Engineering Vol. 19: 163 - 194

    • ...activation of invasion and metastasis, reprogramming of energy metabolism, and evasion of immune destruction (1)....

  • Noncoding RNAs in Cancer Development

    Chao-Po Lin and Lin HeDivision of Cellular and Developmental Biology, Department of Molecular and Cell Biology, University of California, Berkeley, California 94705; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 163 - 184

    • ...and immune surveillance to yield metastatic tumor growth (Hanahan & Weinberg 2011)....

  • How Tumor Virology Evolved into Cancer Biology and Transformed Oncology

    Harold VarmusMeyer Cancer Center, Weill Cornell Medicine, New York, NY 10065; email: [email protected]

    

    Annual Review of Cancer Biology Vol. 1: 1 - 18

    • ...the ones I now hear most often discussed are Hanahan & Weinberg's (2000, 2011) two highly cited essays on the "hallmarks of cancer," certainly not anything from tumor virology....
    • ...A less obvious and less mutant-centric approach is through the phenotypic commonalities summarized in the review articles by Hanahan & Weinberg (2000, 2011)....

  • Multiple Roles for the MLL/COMPASS Family in the Epigenetic Regulation of Gene Expression and in Cancer

    Joshua J. Meeks and Ali ShilatifardDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 425 - 446

    • ...which ultimately result in uncontrolled proliferation or loss of cell death mechanisms (Hanahan & Weinberg 2000, 2011)....

  • The Role of Autophagy in Cancer

    Naiara Santana-Codina, ^1, Joseph D. Mancias, ^1, and Alec C. Kimmelman ^{2 1}Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215²Department of Radiation Oncology, Perlmutter Cancer Center, New York University School of Medicine, New York, NY 10016; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 19 - 39

    • ...These hallmarks of cancer have been identified during the past 30 years of cancer biology research (Hanahan & Weinberg 2011)....

  • Overcoming On-Target Resistance to Tyrosine Kinase Inhibitors in Lung Cancer

    Ibiayi Dagogo-Jack ¹ , Jeffrey A. Engelman ² , and Alice T. Shaw ^{1 1}Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114; email: [email protected], [email protected] ²Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 257 - 274

    • ...and activation of programs that enhance invasive and metastatic capabilities (Hanahan & Weinberg 2011)....

  • Apoptosis and Cancer

    Anthony LetaiDana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 275 - 294

    • ...Evading apoptosis or resisting cell death has been proposed as a hallmark of cancer (Hanahan & Weinberg 2000, 2011)....

  • Analyzing Tumor Metabolism In Vivo

    Brandon Faubert ¹ and Ralph J. DeBerardinis ^{1,2,3 1}Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8502²Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8502³McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8502; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 99 - 117

    • ...altered metabolism is still considered a hallmark of cancer and a potential source of therapeutic targets (Hanahan & Weinberg 2011)....

  • Extracellular Matrix Remodeling and Stiffening Modulate Tumor Phenotype and Treatment Response

    Jennifer L. Leight, ^1, Allison P. Drain, ^2, and Valerie M. Weaver ^{3 1}Department of Biomedical Engineering and The James Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210; email: [email protected] ²University of California, Berkeley–University of California, San Francisco Graduate Program in Bioengineering, Center for Bioengineering and Tissue Regeneration, Department of Surgery, University of California, San Francisco, California 94143; email: [email protected] ³Center for Bioengineering and Tissue Regeneration, Department of Surgery, Department of Anatomy, Department of Bioengineering and Therapeutic Sciences, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, and Helen Diller Comprehensive Cancer Center, University of California, San Francisco, California 94143; email: [email protected]

    Annual Review of Cancer Biology Vol. 1: 313 - 334

    • ...whereas malignant progression and metastasis are fostered by dynamic interactions among the transformed tumor cells and their cellular and noncellular tissue microenvironment (Hanahan & Weinberg 2011, Pickup et al. 2014)....

  • The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer

    Silvia Affo, Le-Xing Yu, and Robert F. SchwabeDepartment of Medicine, Columbia University, New York, NY 10032; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 12: 153 - 186

    • ...activating invasion and metastasis, reprogramming energy metabolism, and evading immune destruction (9)....
    • ...represented in the liver by quiescent hepatic stellate cells (HSCs), and normal epithelia suppress growth via contact inhibition (9, 20)....

  • Signaling and Immune Regulation in Melanoma Development and Responses to Therapy

    William M. Lin ¹ and David E. Fisher ^{1,2 1}Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts 02114²Cutaneous Biology Research Center, Massachusetts General Hospital, Boston, Massachusetts 02114; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 12: 75 - 102

    • ...and signaling pathways is depicted in the context of Hanahan & Weinberg's 2011 updated hallmarks of cancer (14), ...
    • ...Telomerase maintains the telomere length on chromosomal ends and is thought to be a critical target in cancer biology (14, 15)....
    • ...are categorized in the context of Hanahan & Weinberg's revised hallmarks of cancer (Figure 1) (14)....
    • ...The p53 and PI3K/AKT pathways enable evasion of apoptosis and autophagy, respectively (Figure 1) (14)....
    • ...expel waste, and acquire the capacity for invasion and metastasis (14)....
    • ...Otto Warburg first recognized that cancers reprogram glucose metabolism toward aerobic glycolysis (14)....
    • ...RAS can increase rates of glycolysis through upregulation of HIF-1α and HIF-2α. MYC and TP53 are two other melanoma genes associated with glycolytic fueling (14, 80)....

  • Lymphangioleiomyomatosis: A Monogenic Model of Malignancy

    Vera P. Krymskaya ¹ and Francis X. McCormack ^{2 1}Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104²Department of Internal Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio 45267; email: [email protected]

    Annual Review of Medicine Vol. 68: 69 - 83

    • ...A fundamental hallmark of cancer cells is sustained proliferative capacity (28)....

  • Critical Functions of the Lysosome in Cancer Biology

    Shawn M. Davidson ^1,2 and Matthew G. Vander Heiden ^{1,2,3 1}Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected], [email protected] ²Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139³Dana-Farber Cancer Institute, Boston, Massachusetts 02215

    Annual Review of Pharmacology and Toxicology Vol. 57: 481 - 507

    • ...or are the consequence of, lysosomal function or dysfunction (11) (Figure 1)....
    • ... Figure 1 Relationship of the lysosome to the classic hallmarks of cancer (11)....

  • The Ecology and Evolution of Cancer: The Ultra-Microevolutionary Process

    Chung-I Wu, ^1,3,4, Hurng-Yi Wang, ² Shaoping Ling, ^1,3 and Xuemei Lu ^{3, 1}State Key Laboratory of Biocontrol, College of Ecology and Evolution, Sun Yat-Sen University, Guangzhou 510275, China; email: [email protected] ²Graduate Institute of Clinical Medicine and Hepatitis Research Center, National Taiwan University and Hospital, Taipei 106, Taiwan; email: [email protected] ³CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; email: [email protected] ⁴Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637; email: [email protected]

    Annual Review of Genetics Vol. 50: 347 - 369

    • ...Because genome instability in tumors is frequently observed (31, 57, 150), whether the instability is necessary for tumorigenesis has been a contentious issue (14, 43, 146)...
    • ...Hanahan & Weinberg (57) defined a number of convergent phenotypes that they referred to as cancer hallmarks....
    • ...two lists of cancer driver genes do not overlap at all (57)....
    • ...the convergence in phenotypes is manifested in the many cancer hallmarks (57)....

  • Aneuploidy in Cancer and Aging

    Ryan M. Naylor ¹ and Jan M. van Deursen ^{1,2 1}Department of Biochemistry and Molecular Biology,²Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota 55905; email: [email protected]

    Annual Review of Genetics Vol. 50: 45 - 66

    • ...Tumorigenesis is a multistep process in which normal cells progress toward a transformed state through the acquisition of cancer hallmarks (46)....
    • ...Among these hallmarks are the abilities to sustain proliferative signaling, evade cell cycle inhibition, and resist cell death (46)....
    • ...Hanahan & Weinberg (46) solidified genome instability as an enabling characteristic of cancer....

  • An Evolutionary Genetic Perspective on Cancer Biology

    Max Shpak ^1,2,3 and Jie Lu ^{1, 1}NeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas 78705; email: [email protected] ²Center for Systems and Synthetic Biology, University of Texas, Austin, Texas 78712³Fresh Pond Research Institute, Cambridge, Massachusetts 02140

    Annual Review of Ecology, Evolution, and Systematics Vol. 47: 25 - 49

    • ...We begin with a brief review of the genetic mechanisms and cellular basis of cancer (Hanahan & Weinberg 2000, 2011)....

  • Structure and Function of the Mitochondrial Ribosome

    Basil J. Greber ^1, * and Nenad Ban ^{1 1}Department of Biology, Institute of Molecular Biology and Biophysics, ETH Zurich, CH-8093 Zurich, Switzerland; email: [email protected]*Present address: California Institute for Quantitative Biosciences (QB3), University of California, Berkeley, California 94720-3220

    Annual Review of Biochemistry Vol. 85: 103 - 132

    • ...Even though ATP production in cancer cells has long been thought to occur mostly by glycolysis in the cytoplasm (143), ...
    • ...explaining why the inhibition of mitochondrial protein synthesis also affects cancer cells that depend on glycolysis in the cytoplasm for their metabolism (47, 143)....

  • Obesity, Inflammation, and Cancer

    Tuo Deng, ^1,2 Christopher J. Lyon, ¹ Stephen Bergin, ^3,4 Michael A. Caligiuri, ⁴ and Willa A. Hsueh ^{5 1}Diabetes Research Center and Center for Bioenergetics, Houston Methodist Research Institute, Houston, Texas 77030; email: [email protected] ²Department of Medicine, Weill Cornell Medical College at Cornell University, New York, New York 10021³Medical Scientist Training Program and Biomedical Sciences Graduate Program, The Ohio State University, Columbus, Ohio 43210⁴The Comprehensive Cancer Center–Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, Ohio 43210⁵The Diabetes and Metabolism Research Center, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The Ohio State University, Columbus, Ohio 43210; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 11: 421 - 449

    • ...develop replicative immortality, induce angiogenesis, and stimulate invasion and metastasis (40)....
    • ...inflammation promotes several steps in the process of metastasis, which is a major mechanism of cancer death (40)....

  • Cancer Stem Cells: Basic Concepts and Therapeutic Implications

    Dany Nassar ¹ and Cédric Blanpain ^{1,2 1}IRIBHM, Université Libre de Bruxelles, Brussels B-1070, Belgium; email: [email protected] ²WELBIO, Université Libre de Bruxelles, Brussels B-1070, Belgium

    Annual Review of Pathology: Mechanisms of Disease Vol. 11: 47 - 76

    • ...as well as the ability to evade growth suppression and apoptosis, collectively described as the hallmarks of cancer cells (1)....

  • Mechanisms and Consequences of Cancer Genome Instability: Lessons from Genome Sequencing Studies

    June-Koo Lee, ¹ Yoon-La Choi, ^2,3 Mijung Kwon, ^4,5 and Peter J. Park ^{6 1}Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, South Korea; email: [email protected] ²Department of Pathology and Translational Genomics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, South Korea³Department of Health Sciences and Technology, Samsung Advanced Institute of Health Sciences and Technology (SAIHST), Sungkyunkwan University School of Medicine, Seoul 06351, South Korea; email: [email protected] ⁴Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115⁵Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115; email: [email protected] ⁶Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 11: 283 - 312

    • ...Here we describe various aspects of genomic instability as a cardinal feature of cancer that drives tumor evolution and facilitates other cancer hallmarks (5)....

  • Role of Intestinal HIF-2α in Health and Disease

    Sadeesh K. Ramakrishnan ¹ and Yatrik M. Shah ^{1,2 1}Department of Molecular & Integrative Physiology and²Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109; email: [email protected]

    Annual Review of Physiology Vol. 78: 301 - 325

    • ...two enabling factors are instrumental in acquiring and enhancing the hallmarks: (a) genome instability and mutation and (b) tumor-promoting inflammation (118)....

  • Introduction to the Theme "Cancer Pharmacology"

    Paul A. Insel, ¹ Susan G. Amara, ² Terrence F. Blaschke, ³ and Urs A. Meyer ^{4 1}Departments of Pharmacology and Medicine, University of California, San Diego, La Jolla, California 92093²National Institute of Mental Health, Bethesda, Maryland 20892³Departments of Medicine and Molecular Pharmacology, Stanford University School of Medicine, Stanford, California 94305⁴Division of Pharmacology and Neurobiology, University of Basel, Basel CH-4056, Switzerland

    Annual Review of Pharmacology and Toxicology Vol. 56: 19 - 22

    • ...and their sequential expression that ultimately contributes to the hallmark features of cancer (2) has led to the identification of what have been termed driver mutations in cancer cells....

  • Toward a Better Understanding of the Complexity of Cancer Drug Resistance

    Michael M. Gottesman, ¹ Orit Lavi, ¹ Matthew D. Hall, ¹ and Jean-Pierre Gillet ^{2 1}Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; email: [email protected], [email protected], [email protected]mail.nih.gov²Laboratory of Molecular Cancer Biology, Molecular Physiology Research Unit—URPhyM, Namur Research Institute for Life Sciences (NARILIS), Faculty of Medicine, University of Namur, B-5000 Namur, Belgium; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 85 - 102

    • ...we divide the cardinal features of drug resistance into specific biological mechanisms and those that facilitate biological processes (the underlying hallmarks of cancer that tend to favor the development of drug resistance; see 8)....

  • Modeling Signaling Networks to Advance New Cancer Therapies

    Julio Saez-Rodriguez, ^1,2, Aidan MacNamara, ^2, and Simon Cook ^{3, 1}Current address: Joint Research Center for Computational Biomedicine, RWTH Aachen University Hospital, D-52074 Aachen, Germany; email: [email protected] ²European Bioinformatics Institute, European Molecular Biology Laboratory, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SD, United Kingdom; email: [email protected] ³Signalling Laboratory, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, United Kingdom; email: [email protected]

    Annual Review of Biomedical Engineering Vol. 17: 143 - 163

    • ...So how does this deregulation occur? All cancers share a variety of unique properties or hallmarks that set them aside from normal cells (16), ...
    • ...driver mutation in the MAPK or PI3K pathways alone does not lead to full malignancy because deregulation of other cellular processes is necessary (16)....

  • Mechanotransduction's Impact on Animal Development, Evolution, and Tumorigenesis

    Maria-Elena Fernandez-Sanchez, ¹ Thibaut Brunet, ^1,2 Jens-Christian Röper, ¹ and Emmanuel Farge ^{1 1}Mechanics and Genetics of Embryonic and Tumor Development Team, CNRS UMR 168 Physicochimie Curie, Institut Curie Centre de Recherche, PSL Research University; Fondation Pierre-Gilles de Gennes; and INSERM, F-75005 Paris, France; email: [email protected] ²Evolution of the Nervous System in Bilateria Group, European Molecular Biology Laboratory, D-69117 Heidelberg, Germany

    Annual Review of Cell and Developmental Biology Vol. 31: 373 - 397

    • ...Our understanding of tumor progression has progressed considerably as a result of intensive biochemical and genetic studies of the pathways and master genes involved in the deregulation of tissue homeostasis (Hanahan & Weinberg 2011)....

  • Stress Signaling Between Organs in Metazoa

    Edward Owusu-Ansah ¹ and Norbert Perrimon ^{2,3 1}Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, NY 10032; email: [email protected] ²Department of Genetics and³Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115; email: [email protected]

    Annual Review of Cell and Developmental Biology Vol. 31: 497 - 522

    • ...One of the enabling characteristics that sustains the hallmarks of cancer is the elevation of proinflammatory cytokines that impact tumor prognosis and trigger organismal responses (Hanahan & Weinberg 2011)....

  • Unmasking the Lung Cancer Epigenome

    Steven A. BelinskyLung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108; email: [email protected]

    Annual Review of Physiology Vol. 77: 453 - 474

    • ...replicative immortality, angiogenesis, inflammation, altered metabolism, genomic stability, and metastasis signaling (10)....

  • Genetics and Epigenetics of Human Retinoblastoma

    Claudia A. Benavente ¹ and Michael A. Dyer ^{1,2 1}Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105; email: [email protected] ²Howard Hughes Medical Institute, Chevy Chase, Maryland 20815

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 547 - 562

    • ...acquisition of limitless replicative potential, sustained angiogenesis, local tissue invasion, and metastasis (4)....

  • Driver and Passenger Mutations in Cancer

    Julia R. Pon ¹ and Marco A. Marra ^{1,2 1}Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada V5Z 1L3; email: [email protected] ²Department of Medical Genetics, University of British Columbia, Vancouver, Canada V6T 1Z4; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 25 - 50

    • ...reprogramming energy metabolism and evading immune destruction can contribute indirectly to the likelihood that a cell will proliferate and are now considered hallmarks of cancer (85)....

  • DNA Replication Stress as a Hallmark of Cancer

    Morgane Macheret and Thanos D. HalazonetisDepartment of Molecular Biology, University of Geneva, 1205 Geneva, Switzerland; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 425 - 448

    • ...evasion of immune surveillance, deregulated cellular energetics, genomic instability, and tumor-promoting inflammation (2...
    • ...and genomic deletions (10 genes) to a recently described list of cancer hallmarks (3, 8, 11)....
    • ...would probably be assigned to the sustained proliferative signaling hallmark (3)....
    • ...top 10 genes focally amplified, and top 10 genes focally deleted) (3, 8, 11)....
    • ...is the identification of phenotypes and molecular changes that are shared by almost all cancers (2...

  • Impact of the Obesity Epidemic on Cancer

    Pamela J. Goodwin ¹ and Vuk Stambolic ^{2 1}Department of Medicine, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X4, Canada; email: [email protected] ²Princess Margaret Cancer Centre and Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2M9, Canada; email: [email protected]

    Annual Review of Medicine Vol. 66: 281 - 296

    • ...Inflammation has been recognized as one of the hallmarks of cancer (72)....

  • Synthetic Lethal Vulnerabilities of Cancer

    Ferran Fece de la Cruz, ^1, Bianca V. Gapp, ^1, and Sebastian M.B. Nijman ^{1 1}CeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, A1090 Vienna, Austria; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 55: 513 - 531

    • ...only a comparatively small number of targeted cancer treatments are currently available (1, 2)....
    • ...such as TP53, PTEN, KRAS, retinoblastoma 1 (RB1), and p16^INK4A (1, 2)....

  • Translating Genomics for Precision Cancer Medicine

    Sameek Roychowdhury ¹ and Arul M. Chinnaiyan ^{2 1}Department of Internal Medicine, Division of Medical Oncology, and Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210; email: [email protected] ²Michigan Center for Translational Pathology, Department of Pathology, Comprehensive Cancer Center, Howard Hughes Medical Institute, Department of Urology, and Center for Computational Medicine and Biology, University of Michigan Medical School, Ann Arbor, Michigan 48109; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 15: 395 - 415

    • ...where genetic alterations may contribute to the initiation and progression of disease (48)....

  • A New Toolbox for Assessing Single Cells

    Konstantinos Tsioris, ^1,2 Alexis J. Torres, ^1,2 Thomas B. Douce, ^1,2 and J. Christopher Love ^{1,2,3,4 1}Department of Chemical Engineering,²Koch Institute of Integrative Cancer Research,³Broad Institute of MIT and Harvard, and⁴Ragon Institute of MGH, MIT, and Harvard, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139-4307; email: [email protected], [email protected], [email protected], [email protected]

    Annual Review of Chemical and Biomolecular Engineering Vol. 5: 455 - 477

    • ...the tumor microenvironment has risen to prominence as a key factor in malignant progression (107)....

  • Activity-Based Profiling of Proteases

    Laura E. Sanman ¹ and Matthew Bogyo ^1,2,3 Departments of ¹Chemical and Systems Biology,²Microbiology and Immunology, and³Pathology, Stanford University School of Medicine, Stanford, California 94305-5324; email: [email protected]

    Annual Review of Biochemistry Vol. 83: 249 - 273

    • ...They are also useful biomarkers for cancer because increased protease activity is associated with many of the hallmark processes of cancer, including angiogenesis, tissue remodeling, and cell death (115)....

  • PTEN

    Carolyn A. Worby and Jack E. DixonDepartment of Pharmacology, University of California, San Diego, La Jolla, California 92093-0721; email: [email protected]

    Annual Review of Biochemistry Vol. 83: 641 - 669

    • ...Tumors depend on their microenvironment for growth factors, structural components, and nutrient supply (97, 98)....

  • Pathogenesis and Molecular Biology of a Transmissible Tumor in the Tasmanian Devil

    Hannah S. Bender, ^1,2 Jennifer A. Marshall Graves, ^1,3 and Janine E. Deakin ^{1,4, * 1}Research School of Biology, The Australian National University, Canberra, ACT 0200, Australia²School of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, WA 6150, Australia³La Trobe Institute of Molecular Sciences, La Trobe University, Melbourne, VIC 3086, Australia; email: [email protected] ⁴Institute of Applied Ecology, University of Canberra, Canberra, ACT 2601, Australia; email: [email protected]

    Annual Review of Animal Biosciences Vol. 2: 165 - 187

    • ...growth signal autonomy, resistance to suppressive signals, angiogenesis, and metastasis (67)....

  • Engineered Culture Models for Studies of Tumor-Microenvironment Interactions

    David W. Infanger, ¹ Maureen E. Lynch, ¹ and Claudia Fischbach ^{1,2 1}Department of Biomedical Engineering, Cornell University, Ithaca, New York 14853²Kavli Institute at Cornell for Nanoscale Science, Cornell University, Ithaca, New York 14853; email: [email protected]

    Annual Review of Biomedical Engineering Vol. 15: 29 - 53

    • ...necessarily excluding the participation of the immune response critical to cancer progression (11)....

  • Current Perspective on the Global and United States Cancer Burden Attributable to Lifestyle and Environmental Risk Factors

    David Schottenfeld, ^1,2,3 Jennifer L. Beebe-Dimmer, ^5,6 Patricia A. Buffler, ⁷ and Gilbert S. Omenn ^{1,3,4 1}School of Public Health,²Department of Epidemiology,³Medical School, Department of Internal Medicine,⁴Departments of Computational Medicine and Bioinformatics, Human Genetics, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected], [email protected] ⁵Karmanos Cancer Institute, Division of Population Studies and Disparities Research,⁶Department of Oncology, Wayne State University, Detroit, Michigan 48201; email: [email protected] ⁷School of Public Health, Department of Epidemiology, University of California, Berkeley, California 94720; email: [email protected]

    Annual Review of Public Health Vol. 34: 97 - 117

    • ...resulting in local invasion and distant dissemination of cancer cells (51)....

  • Aging, Cellular Senescence, and Cancer

    Judith CampisiBuck Institute for Research on Aging, Novato, California 94945; email: [email protected]Lawrence Berkeley National Laboratory, Berkeley, California 94720; email: [email protected]

    Annual Review of Physiology Vol. 75: 685 - 705

    • ...These phenotypes are, of course, hallmarks of lethal cancers (5)....

  • Chromosome Translocation, B Cell Lymphoma, and Activation-Induced Cytidine Deaminase

    Davide F. Robbiani ¹ and Michel C. Nussenzweig ^{1,2 1}Laboratory of Molecular Immunology and²Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065; email: [email protected], [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 8: 79 - 103

    • ...According to the multistep model of carcinogenesis, several genetic hits are required for full malignant transformation (21, 22)....

  • Cellular Heterogeneity and Molecular Evolution in Cancer

    Vanessa Almendro, ^1,2 Andriy Marusyk, ¹ and Kornelia Polyak ^{1 1}Department of Medical Oncology, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215; email: [email protected], [email protected], [email protected] ²Department of Medical Oncology, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, 08036 Barcelona, Spain

    Annual Review of Pathology: Mechanisms of Disease Vol. 8: 277 - 302

    • ...; increased genetic instability is considered one of the so-called hallmarks of cancer (25, 26)....

  • The PI3K, Metabolic, and Autophagy Networks: Interactive Partners in Cellular Health and Disease

    Naval P. Shanware, ¹ Kevin Bray, ¹ and Robert T. Abraham ^{2 1}Oncology Research Unit, Pfizer Worldwide Research and Development, Pearl River, New York 10965²Oncology Research Unit, Pfizer Worldwide Research and Development, San Diego, California 92121; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 53: 89 - 106

    • ...cancer cells upregulate the expression of glucose transporters and multiple glycolytic enzymes (20, 21)....

  • The Fluid Mechanics of Cancer and Its Therapy

    Petros Koumoutsakos, ¹ Igor Pivkin, ² and Florian Milde ^{1 1}Computational Science and Engineering Laboratory, ETH Zürich, CH-8092 Zürich, Switzerland; email: [email protected] ²Institute of Computational Science, Universitá della Svizzera Italiana, CH-6900 Lugano, Switzerland

    Annual Review of Fluid Mechanics Vol. 45: 325 - 355

    • ...Cancer is a complex phenomenon that can be characterized by a small set of hallmarks that point to a cascade of events from the molecular to the organismal level (Hanahan & Weinberg 2000, 2011)....
    • ...whose components (known as the hallmarks of cancer) have been brilliantly described in the authoritative articles of Hanahan & Weinberg (2000, 2011), ...
    • ...whereas two-way metastases have been observed between breast and liver cancer cells (Hanahan & Weinberg 2011)....

  • Mutations Arising During Repair of Chromosome Breaks

    Anna Malkova ¹ and James E. Haber ^{2 1}Department of Biology, School of Science, IUPUI, Indianapolis, Indiana 46202-5132; email: [email protected] ²Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Waltham, Massachusetts 02453; email: [email protected]

    Annual Review of Genetics Vol. 46: 455 - 473

    • ...It has been appreciated for some time that cancer cells suffer not only many chromosomal rearrangements but the accumulation of many mutations (34)....

  • Cell Polarity as a Regulator of Cancer Cell Behavior Plasticity

    Senthil K. Muthuswamy ^1,2 and Bin Xue ^{2 1}Ontario Cancer Institute, Campbell Family Institute for Breast Cancer Research, University of Toronto, Toronto M5G 2M9, Canada; email: [email protected] ²Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724

    Annual Review of Cell and Developmental Biology Vol. 28: 599 - 625

  • New Insights into the Troubles of Aneuploidy

    Jake J. Siegel and Angelika AmonDavid H. Koch Institute for Integrative Cancer Research and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected], [email protected]

    Annual Review of Cell and Developmental Biology Vol. 28: 189 - 214

    • ...the elevated proteotoxic stress and genomic instability observed in aneuploid cells are also key characteristics of cancer cells (reviewed in Hanahan & Weinberg 2011, Luo et al. 2009)....

  • Functional Genomic Studies: Insights into the Pathogenesis of Liver Cancer

    Ze-Guang Han ^{1,2 1}National Human Genome Center of Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China²Shanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center at Shanghai, Shanghai 201203, China; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 13: 171 - 205

    • ...enabling their outgrowth and eventual dominance in a local tissue environment (56)....
    • ...differentiation, death, and other homeostatic interactions with the tissue microenvironment (56)....
    • ...and activating the EMT as well as facilitating angiogenesis, invasion, and metastasis (37, 56, 120)....

  • What Is the Brain-Cancer Connection?

    Lei Cao and Matthew J. DuringCollege of Medicine, The Ohio State University, Columbus, Ohio 43210; email: [email protected], [email protected]

    Annual Review of Neuroscience Vol. 35: 331 - 345

    • ...Hanahan & Weinberg (2011) updated the concept of cancer hallmarks and summarized the development of mechanism-based targeted therapies to treat human cancers....
    • ...Thus the combination of mechanism-guided therapies cotargeting multiple hallmark capabilities is likely to be more effective and durable (Hanahan & Weinberg 2011)....

  • Cancer and Inflammation: An Old Intuition with Rapidly Evolving New Concepts

    Giorgio TrinchieriCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702-1201; email: [email protected]

    Annual Review of Immunology Vol. 30: 677 - 706

    • ...and tumorigenic mechanisms that depend on this interaction are now included as enabling characteristics or newly identified emerging hallmarks (2)....
    • ...A similar distinction was made by Hanahan & Weinberg (2) in their 2011 update of the "Hallmarks of Cancer" in which they described the avoidance of immune destruction as an emerging hallmark and defined tumor-promoting inflammation as an enabling characteristic....

  • Circulating Tumor Cells and Circulating Tumor DNA

    Catherine Alix-Panabières, ^1,2,3 Heidi Schwarzenbach, ⁴ and Klaus Pantel ^{4 1}University Medical Center, Saint-Eloi Hospital, Institute of Research in Biotherapy, Laboratory of Rare Human Circulating Cells, Montpellier, France;²University Medical Center, Laboratory of Cell and Hormonal Biology, Arnaud de Villeneuve Hospital, Montpellier, France;³University Institute of Clinical Research UM1 – EA2415 – Epidemiology, Biostatistics & Public Health; email: [email protected] ⁴Institute of Tumor Biology, University Medical Center, Hamburg-Eppendorf, 20246 Hamburg, Germany; email: [email protected]

    Annual Review of Medicine Vol. 63: 199 - 215

    • ...and the subsequent outgrowth of these cells in their new microenvironment (1, 2)....

  • Exploiting the Cancer Genome: Strategies for the Discovery and Clinical Development of Targeted Molecular Therapeutics

    Timothy A. Yap ^1,2 and Paul Workman ^{1 1}Cancer Research UK Cancer Therapeutics Unit, Division of Cancer Therapeutics, The Institute of Cancer Research, Haddow Laboratories, Sutton, Surrey SM2 5NG, United Kingdom; email: [email protected] ²Drug Development Unit, Division of Cancer Therapeutics and Division of Clinical Studies, The Institute of Cancer Research, Haddow Laboratories, Sutton; and Royal Marsden NHS Foundation Trust, Sutton, Surrey SM2 5PT, United Kingdom; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 52: 549 - 573

    • ...supporting the addition of stress management to the established hallmarks of cancer (72, 77)....

• 41.

  Hayek S , Gibson TM , Leisenring WM , Guida JL , Gramatges MM , et al. 2020. Prevalence and predictors of frailty in childhood cancer survivors and siblings: a report from the Childhood Cancer Survivor Study. J. Clin. Oncol. 38(3):232–47

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 42.

  More AR articles citing this reference

  • Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging

    Lei Zhang and Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email: [email protected]

    Annual Review of Genetics Vol. 52: 397 - 419

    • ...Most of the apparent stability of the DNA of the genome is rendered by a highly conserved system of genome maintenance mechanisms (60)....

  • Cell Cycle–Targeted Cancer Therapies

    Charles J. Sherr ^1,2 and Jiri Bartek ^{3,4 1}Howard Hughes Medical Institute, Chevy Chase, Maryland 20815²Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105; email: [email protected] ³Department of Biochemistry and Biophysics, Division of Translational Medicine and Chemical Biology, Science for Life Laboratory, Karolinska Institute, Stockholm S-171 21, Sweden⁴Danish Cancer Society Research Center, Copenhagen DK 2100, Denmark

    Annual Review of Cancer Biology Vol. 1: 41 - 57

    • ...Each of these checkpoint pathways involves the recruitment of protein complexes that sense and signal the presence of damaged DNA and engage effectors to repair different lesions (Goldstein & Kastan 2015, Hoeijmakers 2001, Jackson & Bartek 2009, O'Connor 2015)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...and transcription-coupled NER (TC-NER), which removes transcription-blocking lesions from actively transcribed DNA strands (49, 50)....
    • ...cells have evolved an intricate network of DNA repair systems, each with its own damage specificity (49)....

  • Genome Instability and Aging

    Jan Vijg ¹ and Yousin Suh ^{1,2 1}Department of Genetics, Albert Einstein College of Medicine, New York, NY 10461; email: [email protected], [email protected] ²Aging Research Institute, Guangdong Medical College, Dongguan 523808, Guangdong, China

    Annual Review of Physiology Vol. 75: 645 - 668

    • ...drastic responses to DNA damage are likely the exception; under normal circumstances DNA damage is recognized and repaired (right side of Figure 1). Figure 2 schematically depicts the major conserved DNA repair pathways with their DNA damage substrates (14). ...

  • Regulation of Homologous Recombination in Eukaryotes

    Wolf-Dietrich Heyer, ^1,2 Kirk T. Ehmsen, ¹ andJie Liu ^{1 1}Department of Microbiology, University of California, Davis, Davis, California 95616-8665; email: [email protected] ²Department of Molecular and Cellular Biology, University of California, Davis, Davis, California 95616-8665

    Annual Review of Genetics Vol. 44: 113 - 139

    • ...Defects in DNA repair proteins lead to various inherited human diseases sharing common features such as genome instability and cancer predisposition (71)....

  • Mutational Heterogeneity in Human Cancers: Origin and Consequences

    Jesse J. Salk, Edward J. Fox, and Lawrence A. LoebJoseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology, University of Washington, Seattle, Washington 98195; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 5: 51 - 75

    • ...mismatch repair, double-strand-break repair, and even direct reversal of adduct-mediated lesions (37)....

  • Structural and Functional Relationships of the XPF/MUS81 Family of Proteins

    Alberto Ciccia, ^1,3 Neil McDonald, ^1,2 and Stephen C. West ^{1 1}London Research Institute, Cancer Research UK, Clare Hall Laboratories, Hertfordshire EN6 3LD, United Kingdom; email: [email protected] ²School of Crystallography, Birkbeck College, London WC1E 7HX, United Kingdom³Present address: Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Biochemistry Vol. 77: 259 - 287

    • ...XP is a heterogeneous genetic disorder caused by mutations in one of eight genes (XPA, XPB, XPC, XPD, XPE, XPF, XPG, and XPV) (52)....
    • ...The GG-NER pathway has been reconstituted in vitro with purified yeast or human proteins, and the mechanism of repair is now well understood (52)....

  • DNA Double-Strand Break Repair: All's Well that Ends Well

    Claire Wyman and Roland KanaarDepartment of Cell Biology & Genetics and Department of Radiation Oncology, Erasmus MC, 3000 DR Rotterdam, The Netherlands; email: [email protected]

    Annual Review of Genetics Vol. 40: 363 - 383

    • ...such as those induced by exogenous DNA-damaging agents or endogenously produced reactive oxygen species, can promote genome rearrangements that initiate carcinogenesis or apoptosis (29)....

• 43.

  More AR articles citing this reference

  • Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions

    Laura Campello, Nivedita Singh, Jayshree Advani, Anupam K. Mondal, Ximena Corso-Díaz, and Anand SwaroopNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; email: [email protected]

    Annual Review of Vision Science Vol. 7: 633 - 664

    • ...Genomic and epigenomic alterations are widely observed during aging (Booth & Brunet 2016, Hoeijmakers 2009)....
    • ...The accumulation of DNA lesions with age has been widely recognized as a hallmark of aging in various organisms (Hoeijmakers 2009)....

  • Repair of DNA Breaks by Break-Induced Replication

    Z.W. Kockler, B. Osia, R. Lee, K. Musmaker, and A. MalkovaDepartment of Biology, University of Iowa, Iowa City, Iowa 52242, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 90: 165 - 191

    • ...potentially on the order of 10⁵ instances per cell per day (1)....

  • Checkpoint Responses to DNA Double-Strand Breaks

    David P. Waterman, ¹ James E. Haber, ^1, and Marcus B. Smolka ^{2, 1}Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA; email: [email protected] ²Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, New York 14853, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 89: 103 - 133

    • ...Human cells encounter up to 100,000 instances of DNA damage per day (1), ...

  • The BRCA Tumor Suppressor Network in Chromosome Damage Repair by Homologous Recombination

    Weixing Zhao, ^1,2, Claudia Wiese, ^3, Youngho Kwon, ^1,2 Robert Hromas, ⁴ and Patrick Sung ^{1,2 1}Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06520, USA²Department of Biochemistry and Structural Biology, University of Texas Health San Antonio, San Antonio, Texas 78229, USA; email: [email protected], [email protected] ³Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523, USA⁴Department of Medicine, University of Texas Health San Antonio, San Antonio, Texas 78229, USA

    Annual Review of Biochemistry Vol. 88: 221 - 245

    • ...and by reactive metabolites, such as aldehydes and free radicals, that damage DNA (1...
    • ...a defect in any of these detoxification mechanisms leads to genome destabilization and disease, cancer in particular (2, 4)....

  • Recent Advancements in DNA Damage–Transcription Crosstalk and High-Resolution Mapping of DNA Breaks

    Valerio Vitelli, ¹ Alessandro Galbiati, ¹ Fabio Iannelli, ¹ Fabio Pessina, ¹ Sheetal Sharma, ¹ and Fabrizio d'Adda di Fagagna ^{1,2 1}FIRC Institute of Molecular Oncology (IFOM), Milan 20139, Italy; email: [email protected] ²Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (CNR), Pavia 27100, Italy

    Annual Review of Genomics and Human Genetics Vol. 18: 87 - 113

    • ...Genomic instability in somatic cells is a well-known driver of malignant transformation of cells and fuels cancer progression (22, 56, 64)....

  • Gut Microbiota, Inflammation, and Colorectal Cancer

    Caitlin A. Brennan ¹ and Wendy S. Garrett ^{1,2,3,4 1}Departments of Immunology & Infectious Diseases and Genetics & Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115; email: [email protected], [email protected] ²Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115³Cancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142⁴Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Microbiology Vol. 70: 395 - 411

    • ...Aging and dietary patterns not only influence cancer susceptibility but also have profound effects on microbiota composition (17, 18, 21, 41, 47, 90)....

  • Mechanics and Single-Molecule Interrogation of DNA Recombination

    Jason C. Bell and Stephen C. KowalczykowskiDepartment of Microbiology and Molecular Genetics, and Department of Molecular and Cellular Biology, University of California, Davis, California 95616; email: [email protected]

    Annual Review of Biochemistry Vol. 85: 193 - 226

    • ...Inherited mutations in homologous recombination (HR) genes cause cancer predisposition and accelerated aging syndromes (3)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...which is associated with the severe, CS-like progeroid syndrome trichothiodystrophy (TTD) (53, 54)....
    • ...and very indirect consequences, and these consequences may be transmitted to daughter cells (54)....

  • Age-Related Macular Degeneration: Genetics and Biology Coming Together

    Lars G. Fritsche, ¹ Robert N. Fariss, ² Dwight Stambolian, ⁴ Gonçalo R. Abecasis, ¹ Christine A. Curcio, ⁵ and Anand Swaroop ^{3, 1}Center for Statistical Genetics, Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, Michigan 48109; email: [email protected], [email protected] ²Biological Imaging Core and³Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892; email: [email protected], [email protected] ⁴Departments of Ophthalmology and Genetics, University of Pennsylvania, Philadelphia, Pennsylvania 19104; email: [email protected] ⁵Department of Ophthalmology, University of Alabama at Birmingham, Birmingham, Alabama 35294; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 15: 151 - 171

    • ...aging is associated with increased DNA damage and deficiency of repair mechanisms (41)....

  • Tobacco Smoke–Induced Lung Fibrosis and Emphysema

    Danielle Morse ¹ and Ivan O. Rosas ^{1,2 1}Division of Pulmonary and Critical Care, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; email: [email protected] ²Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108

    Annual Review of Physiology Vol. 76: 493 - 513

    • ...compromised DNA damage repair results in accelerated aging, as occurs in progeroid syndromes (97)....

• 44.

  Hoshino S , Kobayashi M , Higami Y . 2018. Mechanisms of the anti-aging and prolongevity effects of caloric restriction: evidence from studies of genetically modified animals. Aging 10(9):2243–51

  • Crossref
  • Medline
  • Google Scholar

• 45.

  Hudson MM , Ness KK , Gurney JG , Mulrooney DA , Chemaitilly W , et al. 2013. Clinical ascertainment of health outcomes among adults treated for childhood cancer. J. Am. Med. Assoc. 309(22):2371–81

  • Crossref
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

• 46.

  More AR articles citing this reference

• 47.

  Jaarsma D , van der Pluijm I , van der Horst GTJ , Hoeijmakers JHJ . 2013. Cockayne syndrome pathogenesis: lessons from mouse models. Mech. Ageing Dev. 135(5–6):180–95

  • Crossref
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...TTD, and XFE premature aging phenotypes have been well described (55, 57...

• 48.

  Jönsson IK. 2007. Long-term experimental manipulation of moisture conditions and its impact on moss-living tardigrades. J. Limnol. 66(Suppl. 1):119–25

  • Crossref
  • Google Scholar

• 49.

  More AR articles citing this reference

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...Low-calorie states such as fasting and CR not only restrain tumor growth but also enhance the response to chemotherapy (9, 64)....
    • ...Activating mutations of the PI3K pathway decrease the sensitivity of cancer cells to CR, probably via modulation of downstream FOXO signaling (Figure 3a ) (64)....

  • Nutrient Sensing in Cancer

    Margaret E. Torrence and Brendan D. ManningDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts 02115, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 2: 251 - 269

    • ...with tumor cells that exhibit sustained activation of this pathway showing resistance to dietary restriction (Curry et al. 2013, Kalaany & Sabatini 2009)....

  • Metformin in Cancer Treatment and Prevention

    Daniel R. Morales ¹ and Andrew D. Morris ^{2 1}Population Health Sciences Division, Medical Research Institute, and²School of Medicine, University of Dundee, Dundee, United Kingdom; email: [email protected], [email protected]

    Annual Review of Medicine Vol. 66: 17 - 29

    • ...Reductions in insulin and IGF-1 induced by calorie restriction have been shown to reduce incidence of cancer in in vivo animal models (25)....

  • Regulation of Tissue Growth through Nutrient Sensing

    Ville Hietakangas ¹ and Stephen M. Cohen ^{1,2 1}Temasek Life Sciences Laboratory, Singapore 117604; email: [email protected] ²Department of Biological Sciences, National University of Singapore; email: [email protected]

    Annual Review of Genetics Vol. 43: 389 - 410

    • ...by loss of PTEN, renders the tumors insensitive to caloric restriction (64)....

• 50.

  More AR articles citing this reference

  • Novel Approaches for Omega-3 Fatty Acid Therapeutics: Chronic Versus Acute Administration to Protect Heart, Brain, and Spinal Cord

    Hylde Zirpoli, ¹ Chuchun L. Chang, ¹ Yvon A. Carpentier, ^2,3 Adina T. Michael-Titus, ⁴ Vadim S. Ten, ⁵ and Richard J. Deckelbaum ^{1,5 1}Institute of Human Nutrition, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA; email: [email protected] ²Clinical Nutrition Unit, Université Libre de Bruxelles, 1050 Brussels, Belgium³Nutrition Lipid Developments, SPRL, 1050 Brussels, Belgium⁴Center for Neuroscience, Surgery, and Trauma, Queen Mary University of London, London E1 4NS, United Kingdom⁵Department of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA

    Annual Review of Nutrition Vol. 40: 161 - 187

    • ...Ischemia/reperfusion leads to the activation of cell death programs, including apoptosis, autophagy, and necrosis (66)....

  • New Approaches to Target Inflammation in Heart Failure: Harnessing Insights from Studies of Immune Cell Diversity

    Aaron J. Rhee ¹ and Kory J. Lavine ^{1,2,3 1}Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA; email: [email protected] ²Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, USA³Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA

    Annual Review of Physiology Vol. 82: 1 - 20

    • ...and ferroptosis appear to stimulate robust inflammatory responses through the release of alarmins and danger-associated molecular patterns (DAMPs) (37)....

• 51.

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...clear dietary recommendations are sorely needed but do not currently exist for patients undergoing cancer treatment (96)....

  • Cell Biology of Canonical Wnt Signaling

    Lauren V. Albrecht, ^1,2 Nydia Tejeda-Muñoz, ¹ and Edward M. De Robertis ^{1 1}Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1662, USA; email: [email protected] ²Current affiliation: Department of Pharmaceutical Sciences, University of California, Irvine, California 92697, USA

    Annual Review of Cell and Developmental Biology Vol. 37: 369 - 389

    • ...and arginine and lysine levels have been linked to the progression of tumor cell proliferation (Kanarek et al. 2020)....

  • The Bidirectional Relationship Between Cancer Epigenetics and Metabolism

    Luke T. Izzo, Hayley C. Affronti, and Kathryn E. WellenDepartment of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 5: 235 - 257

    • ...The role of diet in tumorigenesis and in modifying therapeutic responses has also emerged as an important frontier in cancer biology (Bose et al. 2020, Kanarek et al. 2020, Tajan & Vousden 2020)....

  • Immunometabolism in the Tumor Microenvironment

    Dominic G. Roy, ¹ Irem Kaymak, ² Kelsey S. Williams, ² Eric H. Ma, ² and Russell G. Jones ^{2 1}Goodman Cancer Research Centre, Faculty of Medicine, McGill University, Montreal, Quebec H3A 1A3, Canada²Metabolic and Nutritional Programming, Center for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan 49503, USA; email: [email protected]

    Annual Review of Cancer Biology Vol. 5: 137 - 159

    • ...one of the rapidly expanding areas of cancer metabolism is the effect of diet on tumor growth (reviewed in detail in Kanarek et al. 2020)....

• 52.

  Kawai S , Vora S , Das S , Gachie E , Becker B , Neufeld AH . 2001. Modeling of risk factors for the degeneration of retinal ganglion cells following ischemia/reperfusion in rats: effects of age, caloric restriction, diabetes, pigmentation, and glaucoma. FASEB J. 15(7):1285–87

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 53.

  More AR articles citing this reference

  • Lessons from Worm Dendritic Patterning

    Sharon Inberg, ^1, Anna Meledin, ^1, Veronika Kravtsov, ¹ Yael Iosilevskii, ¹ Meital Oren-Suissa, ² and Benjamin Podbilewicz ^{1 1}Department of Biology, Technion Israel Institute of Technology, Haifa 3200003, Israel; email: [email protected] ²Department of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel

    Annual Review of Neuroscience Vol. 42: 365 - 383

    • ...and C. elegans is the insulin/insulin growth factor-1 (IGF-1) receptor DAF-2 and its downstream effector DAF-16 (a FOXO transcription factor) (Kenyon 2010, Kenyon et al. 1993)....
    • ...are considered to stay healthy for longer (Kenyon 2010, Kenyon et al. 1993), ...

  • β-Hydroxybutyrate: A Signaling Metabolite

    John C. Newman ^1,2,3 and Eric Verdin ^{1,2,3 1}Buck Institute for Research on Aging, Novato, California 94945; email: [email protected], [email protected] ²Gladstone Institutes, San Francisco, California 94158³Division of Geriatrics, University of California, San Francisco, California 94143

    Annual Review of Nutrition Vol. 37: 51 - 76

    • ...the mammalian ortholog of the stress-responsive transcriptional factor DAF16 that regulates life span in C. elegans (59)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...Suppression of insulin and IGF1 signaling are among the best-documented prolongevity pathways in model organisms ranging from worms and flies to mammals (119)....

  • The Roles of Cellular and Organismal Aging in the Development of Late-Onset Maladies

    Filipa Carvalhal Marques, ^1,2, Yuli Volovik, ^1, and Ehud Cohen ^{1 1}Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, Hebrew University School of Medicine, 91120 Jerusalem, Israel; email: [email protected] ²Centre of Ophthalmology and Vision Sciences, Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 1 - 23

    • ...reducing the activity of the insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) pathway (8), ...

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...and their health during aging improved, by quite simple environmental and genetic interventions (2)....
    • ...This evolutionary conservation is most firmly established for the effects of nutrition and of the molecular mechanisms involved in the sensing of nutrients (Figure 1) (2, 3). ...
    • ...and the initial mutations were in genes that were part of the insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) pathway (2, 22, 23, 24, 25)....
    • ...The insulin/IGF-1/TOR signaling network thus plays a conserved role in aging (Figure 1) (2, 47)....
    • ...and the SMK-1 and HCF-1 activators of FOXO (81, 82; reviewed in References 2...

  • Neurogenesis at the Brain–Cerebrospinal Fluid Interface

    Maria K. Lehtinen and Christopher A. WalshDivision of Genetics, Howard Hughes Medical Institute, and Manton Center for Orphan Disease Research, Children's Hospital Boston, Boston, Massachusetts 02115; e-mail: [email protected], [email protected]Departments of Pediatrics and Neurology, Harvard Medical School, and Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02142

    Annual Review of Cell and Developmental Biology Vol. 27: 653 - 679

    • ...IGF signaling in the CNS has been implicated in a remarkable diversity of processes, including longevity and aging (Kenyon 2010)...

  • HIV Infection, Inflammation, Immunosenescence, and Aging

    Steven G. DeeksDepartment of Medicine, San Francisco General Hospital, University of California San Francisco; email: [email protected]

    Annual Review of Medicine Vol. 62: 141 - 155

    • ...The FOXO transcription factors regulate a wide range of genes known to be involved in the stress response and are critically important in mediating the antiaging effects of caloric restriction and reduced insulin/IGF in worms (74)....
    • ...The apparent enrichment of certain genetic mutations within the insulin and IGF pathways among human centenarians strongly suggests that the ability of these crucial pathways to regulate longevity is conserved from worms to humans (74)....

• 54.

  More AR articles citing this reference

  • Revelations About Aging and Disease from Unconventional Vertebrate Model Organisms

    Yang Zhao, Andrei Seluanov, and Vera GorbunovaDepartment of Biology, University of Rochester, Rochester, New York 14627, USA; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 55: 135 - 159

    • ...Researchers have proposed that aging is a result of the accumulation of unrepaired cellular and molecular damage (87), ...

  • Brain Plasticity in Human Lifespan Development: The Exploration–Selection–Refinement Model

    Ulman Lindenberger, ^1,2 and Martin Lövdén ^{3 1}Center for Lifespan Psychology, Max Planck Institute for Human Development, 14195 Berlin, Germany; email: [email protected] ²Max Planck UCL Centre for Computational Psychiatry and Ageing Research, 14195 Berlin, Germany, and London WC1B 5EH, United Kingdom³Aging Research Center, Karolinska Institutet and Stockholm University, SE-171 77 Stockholm, Sweden; email: martin.[email protected]

    Annual Review of Developmental Psychology Vol. 1: 197 - 222

    • ...Maturation is under strong evolutionary control (Kirkwood 2005) and refers to the orderly and genetically orchestrated construction of neural structures from conception to adulthood that enable reproductive success (Elman et al. 1996)...
    • ...resulting in an accumulation of damage and the unwarranted continuation of biological programs that were vital in early development but become useless or harmful in the postreproductive period (Baltes 1997, Blagosklonny & Hall 2009, Kirkwood 2005)....

  • Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging

    Lei Zhang and Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email: [email protected]

    Annual Review of Genetics Vol. 52: 397 - 419

    • ...they gave rise to the idea that aging and its accompanying increase in disease incidence are caused by unrepaired somatic damage, including DNA damage (68)....

  • Senescence in COPD and Its Comorbidities

    Peter J. BarnesNational Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 79: 517 - 539

    • ...Aging is viewed as the progressive decline of homeostasis that occurs after the reproductive phase of life is complete, resulting in increased risk of disease or death (16)....

  • The Ins and Outs of Aging and Longevity

    Thomas A. RandoGlenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA 94305-5235; email: [email protected]

    Annual Review of Physiology Vol. 75: 617 - 619

    • ...in an attempt to unify extensive findings from diverse areas of biology (5)....

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...A major theory that integrates evolutionary (ultimate cause) and mechanistic (proximate cause) theories is that of disposable soma (61, 178)....
    • ...organisms will invest just sufficient resources in somatic maintenance to live long enough to reach the end of the reproductive period, resulting in a short-lived (or disposable) soma (61, 178)....

  • Somatic Mitochondrial DNA Mutations in Mammalian Aging

    Nils-Göran LarssonMax Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Biochemistry Vol. 79: 683 - 706

    • ...which is not caused by a genetic program, although genes certainly influence the aging process (2)....

  • Replicative Aging in Yeast: The Means to the End

    K.A. Steinkraus, ¹ M. Kaeberlein, ^1, and B.K. Kennedy ^{2, 1}Department of Pathology, University of Washington, Seattle, Washington 98195; email: [email protected] ²Department of Biochemistry, University of Washington, Seattle, Washington 98195; email: [email protected]

    Annual Review of Cell and Developmental Biology Vol. 24: 29 - 54

    • ...the inevitable consequence of an age-dependent decline in the forces of selection (Austad 2004, Kirkwood 2005)....

  • Toward a Control Theory Analysis of Aging

    Michael P. Murphy ¹ and Linda Partridge ^{2 1}Medical Research Council Dunn Human Nutrition Unit, Cambridge CB2 0XY, United Kingdom; email: [email protected] ²Centre for Research on Aging, University College London, Department of Biology, London WC1E 6BT, United Kingdom; email: [email protected]

    Annual Review of Biochemistry Vol. 77: 777 - 798

    • ...attempts to determine which particular types of aging-related damage are key to loss of function have been largely unsuccessful because the diversity of sources and types of damage is great and can vary with tissue, organism, and age (2, 8...

  • Kin Selection and the Evolutionary Theory of Aging

    Andrew F.G. BourkeSchool of Biological Sciences, University of East Anglia, Norwich, Norfolk NR4 7TJ, United Kingdom; email: [email protected]

    Annual Review of Ecology, Evolution, and Systematics Vol. 38: 103 - 128

    • ...aging is not a coordinated process under direct genetic control like development and hence is not programmed (e.g., Hayflick 2000, Kirkwood 2005, Kirkwood & Austad 2000, Partridge & Gems 2002a)....
    • ...Kirkwood 2005) hold this to be the case even in semelparous organisms in which death rapidly follows reproduction, ...

• 55.

  Klement RJ , Schäfer G , Sweeney RA . 2019. A ketogenic diet exerts beneficial effects on body composition of cancer patients during radiotherapy: an interim analysis of the KETOCOMP study. J. Tradit. Complement. Med. 10(3):180–87

  • Crossref
  • Medline
  • Google Scholar

• 56.

  Klement RJ , Sweeney RA. 2016. Impact of a ketogenic diet intervention during radiotherapy on body composition: I. Initial clinical experience with six prospectively studied patients. BMC Res. Notes 9:143

  • Crossref
  • Medline
  • Google Scholar

• 57.

  Kondo M , Shibata R , Miura R , Shimano M , Kondo K , et al. 2009. Caloric restriction stimulates revascularization in response to ischemia via adiponectin-mediated activation of endothelial nitric-oxide synthase. J. Biol. Chem. 284(3):1718–24

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 58.

  Kuraoka I , Kobertz WR , Ariza RR , Biggerstaff M , Essigmann JM , Wood RD . 2000. Repair of an interstrand DNA cross-link initiated by ERCC1-XPF repair/recombination nuclease. J. Biol. Chem. 275(34):26632–36

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Mechanisms of Vertebrate DNA Interstrand Cross-Link Repair

    Daniel R. Semlow ^1,2 and Johannes C. Walter ^{1,3 1}Department of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts 02115, USA; email: [email protected] ²Current affiliation: Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, USA³Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA

    Annual Review of Biochemistry Vol. 90: 107 - 135

    • ...While XPF has been proposed to incise both sides of an ICL (55...

  • How the Fanconi Anemia Pathway Guards the Genome

    George-Lucian Moldovan and Alan D. D'AndreaDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215; email: [email protected]

    Annual Review of Genetics Vol. 43: 223 - 249

    • ...given that cells deleted of these factors are exquisitely (the former) or moderately (the latter) sensitive to crosslinking agents (58, 70, 81, 102, 117)....

  • Structural and Functional Relationships of the XPF/MUS81 Family of Proteins

    Alberto Ciccia, ^1,3 Neil McDonald, ^1,2 and Stephen C. West ^{1 1}London Research Institute, Cancer Research UK, Clare Hall Laboratories, Hertfordshire EN6 3LD, United Kingdom; email: [email protected] ²School of Crystallography, Birkbeck College, London WC1E 7HX, United Kingdom³Present address: Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Biochemistry Vol. 77: 259 - 287

    • ...owing to the ability of XPF-ERCC1 to cleave branched DNA structures containing ICLs (149)....
    • ...and this cleavage reaction is catalyzed by XPF-ERCC1 (see Figure 10, step g) (149...

• 59.

  More AR articles citing this reference

• 60.

• 61.

  Lee C , Raffaghello L , Brandhorst S , Safdie FM , Bianchi G , et al. 2012. Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy. Sci. Transl. Med. 4(124):124ra27

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...Studies that have looked at the impact of fasting on the growth of implanted cancer cells in mice have found beneficial effects in some models (15, 23, 91, 96, 104, 145, 164)...
    • ...Studies that have looked at the impact of fasting on the growth of implanted cancer cells in mice have found beneficial effects in some models (15, 23, 91, 96, 104, 145, 164) but not in others (21, 36, 85, 91, 96, 134, 168), ...
    • ...and some studies have found beneficial effects on one cancer but not another (91, 96), ...

• 62.

  Lee C , Safdie FM , Raffaghello L , Wei M , Madia F , et al. 2010. Reduced levels of IGF-I mediate differential protection of normal and cancer cells in response to fasting and improve chemotherapeutic index. Cancer Res. 70(4):1564–72

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 63.

  More AR articles citing this reference

  • Pharmacogenomics in Pediatric Oncology: Mitigating Adverse Drug Reactions While Preserving Efficacy

    Abdelbaset A. Elzagallaai, ¹ Bruce C. Carleton, ^2,3,4 and Michael J. Rieder ^{1 1}Department of Pediatrics, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3M7, Canada; email: [email protected] ²Division of Translational Therapeutics, Department of Pediatrics, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada³Pharmaceutical Outcomes Programme, BC Children's Hospital, Vancouver, British Columbia V5Z 4H4, Canada⁴BC Children's Hospital Research Institute, Vancouver, British Columbia V5Z 4H4, Canada

    Annual Review of Pharmacology and Toxicology Vol. 61: 679 - 699

    • ...Doxorubicin is an effective antitumor agent but its tendency to cause cardiotoxicity was identified early on (68, 69)....

  • Common Cardiovascular Complications of Cancer Therapy: Epidemiology, Risk Prediction, and Prevention

    Vivek Narayan ^1,3 and Bonnie Ky ^{2,3,4 1}Division of Hematology/Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104; email: [email protected] ²Division of Cardiology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104; email: [email protected]uphs.upenn.edu³Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104⁴Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania 19104

    Annual Review of Medicine Vol. 69: 97 - 111

    • ...anthracyclines have been widely recognized to cause dose-dependent left ventricular dysfunction (LVD) that is both cumulative and irreversible (12, 13)....

• 64.

  Liao CY , Rikke BA , Johnson TE , Diaz V , Nelson JF . 2010. Genetic variation in the murine lifespan response to dietary restriction: from life extension to life shortening. Aging Cell 9(1):92–95

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Dietary Protein, Metabolism, and Aging

    George A. Soultoukis ¹ and Linda Partridge ^{1,2 1}Max Planck Institute for Biology of Ageing, Department of Biological Mechanisms of Ageing, Cologne 50931, Germany; email: [email protected], [email protected] ²Institute of Healthy Ageing and Department of Genetics, Evolution, and Environment, University College London, London WC1E 6BT, United Kingdom

    Annual Review of Biochemistry Vol. 85: 5 - 34

    • ...but the responses of mice of different strains to a single DR regime can be highly variable (135)...

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...found a huge variation in the response to CR, with CR being detrimental to some strains (86)....

• 65.

  More AR articles citing this reference

  • Ancient Plant Genomics in Archaeology, Herbaria, and the Environment

    Logan Kistler, ¹ Vanessa C. Bieker, ² Michael D. Martin, ² Mikkel Winther Pedersen, ³ Jazmín Ramos Madrigal, ⁴ and Nathan Wales ^{5 1}Department of Anthropology, National Museum of Natural History, Smithsonian Institution, Washington, DC 20560, USA; email: [email protected] ²Department of Natural History, NTNU University Museum, Norwegian University of Science and Technology, 7491 Trondheim, Norway; email: [email protected], [email protected] ³Lundbeck Foundation GeoGenetics Centre, GLOBE Institute, University of Copenhagen, 1350 Copenhagen, Denmark; email: [email protected] ⁴Natural History Museum of Denmark, University of Copenhagen, 1350 Copenhagen, Denmark; email: [email protected] ⁵Department of Archaeology, University of York, York YO1 7EP, United Kingdom; email: [email protected]

    Annual Review of Plant Biology Vol. 71: 605 - 629

    • ...Isolated DNA in solution is known to spontaneously break down at a predictable rate governed by temperature and the chemical environment (77)....
    • ...The number of DNA molecules at a given size decreases through exponential decay with a measurable half-life (77)....

  • Paleomicrobiology: Diagnosis and Evolution of Ancient Pathogens

    Kirsten I. Bos, ¹ Denise Kühnert, ² Alexander Herbig, ¹ Luis Roger Esquivel-Gomez, ² Aida Andrades Valtueña, ^1, Rodrigo Barquera, ^1, Karen Giffin, ^1, Aditya Kumar Lankapalli, ^1, Elizabeth A. Nelson, ^1, Susanna Sabin, ^1, Maria A. Spyrou, ^1, and Johannes Krause ^{1,3 1}Department of Archaeogenetics, Max Planck Institute for the Science of Human History, 07745 Jena, Germany; email: [email protected] ²Transmission, Infection, Diversification and Evolution Group, Max Planck Institute for the Science of Human History, 07745 Jena, Germany³Faculty of Biological Sciences, Friedrich Schiller University, 07737 Jena, Germany

    Annual Review of Microbiology Vol. 73: 639 - 666

    • ...the most common form of DNA damage in old molecules (100, 145)....

  • Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism

    William A. Beard, Julie K. Horton, Rajendra Prasad, and Samuel H. WilsonGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Science, National Institutes of Health, Research Triangle Park, North Carolina 27709-2233, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 88: 137 - 162

    • ...as the lesion disrupts many DNA and RNA transactions and leads to cytotoxic strand breaks, mutations, and other forms of genomic instability (16...

  • Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging

    Lei Zhang and Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email: [email protected]

    Annual Review of Genetics Vol. 52: 397 - 419

    • ...later it became clear that under physiological conditions DNA is highly vulnerable to damage varying from hydrolysis and alkylation to oxidation (78)....
    • ...often interconnected genome maintenance systems play a critical role in eliminating the many thousands of chemical lesions generated each day in a typical cell (78)....

  • Uses and Misuses of Environmental DNA in Biodiversity Science and Conservation

    Melania E. Cristescu ¹ and Paul D.N. Hebert ^{2 1}Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada; email: [email protected] ²Centre for Biodiversity Genomics and Department of Integrative Biology, University of Guelph, Ontario N1G 2W1, Canada

    Annual Review of Ecology, Evolution, and Systematics Vol. 49: 209 - 230

    • ...Although this relatively short persistence is ideal for studies of current biodiversity (Lindahl 1993), ...

  • Ancient Biomolecules and Evolutionary Inference

    Enrico Cappellini, ^1, Ana Prohaska, ^2, Fernando Racimo, ¹ Frido Welker, ^3,4 Mikkel Winther Pedersen, ² Morten E. Allentoft, ¹ Peter de Barros Damgaard, ¹ Petra Gutenbrunner, ⁵ Julie Dunne, ⁶ Simon Hammann, ^6,7 Mélanie Roffet-Salque, ⁶ Melissa Ilardo, ¹ J. Víctor Moreno-Mayar, ¹ Yucheng Wang, ¹ Martin Sikora, ¹ Lasse Vinner, ¹ Jürgen Cox, ⁵ Richard P. Evershed, ⁶ and Eske Willerslev ^{1,2,8 1}Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, 1350 Copenhagen, Denmark; email: [email protected], [email protected] ²Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, United Kingdom³Natural History Museum of Denmark, University of Copenhagen, 1350 Copenhagen, Denmark⁴Department of Human Evolution, Max Planck Institute for Evolutionary Anthropology, 04103 Leipzig, Germany⁵Computational Systems Biochemistry, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany⁶Organic Geochemistry Unit, School of Chemistry, University of Bristol, Bristol BS8 1TS, United Kingdom; email: [email protected] ⁷Department of Anthropology and Archaeology, University of Bristol, Bristol BS8 1UU, United Kingdom⁸Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, United Kingdom

    Annual Review of Biochemistry Vol. 87: 1029 - 1060

    • ...These factors facilitate destruction and/or inactivation of nucleases and reduce bacterial metabolic activity and hydrolytic attacks (50)....

  • Nuclear Genomic Instability and Aging

    Laura J. Niedernhofer, ¹ Aditi U. Gurkar, ^1,2 Yinsheng Wang, ³ Jan Vijg, ⁴ Jan H.J. Hoeijmakers, ⁵ and Paul D. Robbins ^{1 1}Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA; email: [email protected] ²Department of Medicine, Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA³Department of Chemistry, University of California, Riverside, California 92521, USA⁴Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, Bronx, New York 10461, USA⁵Department of Molecular Genetics, Erasmus University Medical Center, 3015 CE Rotterdam, The Netherlands

    Annual Review of Biochemistry Vol. 87: 295 - 322

    • ...the most abundant DNA lesions are unavoidable products of hydrolysis (deamination or depurination) (1)....

  • A Robust Framework for Microbial Archaeology

    Christina Warinner, ^1,2 Alexander Herbig, ¹ Allison Mann, ^1,2 James A. Fellows Yates, ¹ Clemens L. Weiß, ³ Hernán A. Burbano, ³ Ludovic Orlando, ^4,5 and Johannes Krause ^{1 1}Department of Archaeogenetics, Max Planck Institute for the Science of Human History, Jena 07745, Germany; email: [email protected] ²Department of Anthropology, University of Oklahoma, Norman, Oklahoma 73019³Research Group for Ancient Genomics and Evolution, Department of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen 72076, Germany⁴Centre for GeoGenetics, Natural History Museum of Denmark, 1350 Copenhagen K, Denmark⁵Laboratoire d'Anthropobiologie Moléculaire et d'Imagerie de Synthèse, CNRS UMR 5288, Université Toulouse III – Paul Sabatier, Toulouse 31000, France

    Annual Review of Genomics and Human Genetics Vol. 18: 321 - 356

    • ...aDNA is highly fragmented through a process that is driven by depurination followed by hydrolysis of the DNA backbone (105)....

  • Site-Specific Self-Catalyzed DNA Depurination: A Biological Mechanism That Leads to Mutations and Creates Sequence Diversity

    Jacques R. Fresco and Olga AmosovaDepartment of Molecular Biology, Princeton University, Princeton, New Jersey 08544; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 86: 461 - 484

    • ...Such AP sites can form spontaneously or can be produced by DNA glycosylase as an intermediate in repair of various DNA adducts (73, 74)....

  • Single-Molecule Analysis of Bacterial DNA Repair and Mutagenesis

    Stephan Uphoff and David J. SherrattDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom; email: [email protected], [email protected]

    Annual Review of Biophysics Vol. 46: 411 - 432

    • ...Genome integrity in all organisms is threatened by spontaneous decay of the DNA structure and endogenous DNA damage from reactive metabolites (83)....

  • Food Analysis Using Organelle DNA and the Effects of Processing on Assays

    Jane M. CaldwellTransAgra International Inc., Storm Lake, Iowa 50588; email: [email protected]

    Annual Review of Food Science and Technology Vol. 8: 57 - 74

    • ...The most labile linkage in the DNA structure is the N-glycosyl bond, which is susceptible to hydrolysis (Lindahl 1993)....
    • ...the mitochondria participate in oxidative phosphorylation to provide energy to the cell; thus, mtDNA should be more prone to oxidative damage (Lindahl 1993)....
    • ...helical strands are broken, causing an irreversible loss of secondary structure (Lindahl 1993)....

  • Eukaryotic DNA Polymerases in Homologous Recombination

    Mitch McVey, ¹ Varandt Y. Khodaverdian, ¹ Damon Meyer, ^2,4 Paula Gonçalves Cerqueira, ² and Wolf-Dietrich Heyer ^{2,3 1}Department of Biology, Tufts University, Medford, Massachusetts 02155; email: [email protected] ²Department of Microbiology and Molecular Genetics, University of California, Davis, California 95616; email: [email protected] ³Department of Molecular and Cellular Biology, University of California, Davis, California 95616⁴College of Health Sciences, California Northstate University, Rancho Cordova, California 95670

    Annual Review of Genetics Vol. 50: 393 - 421

    • ...HR involves the resection of DSBs to expose ssDNA. ssDNA is less chemically stable than double-stranded DNA (74), ...
    • ...One prominent feature of HR-associated mutagenesis is likely the result of the greater chemical instability of ssDNA (74)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...and advanced glycation end products from glycolysis, lipid peroxidation products, methyl donors, etc. (93, 94)....

  • Accessing the Inaccessible: The Organization, Transcription, Replication, and Repair of Heterochromatin in Plants

    Wei Feng ¹ and Scott D. Michaels ^{2, 1}Carnegie Institution for Science, Department of Plant Biology, Stanford, California 94305; email: [email protected] ²Department of Biology, Indiana University, Bloomington, Indiana 47405; email: [email protected]

    Annual Review of Genetics Vol. 49: 439 - 459

    • ...both of which can be caused by various external and internal sources, including irradiation and replication stress (89)....

  • Novel Functions of the Human Papillomavirus E6 Oncoproteins

    Nicholas A. Wallace and Denise A. GallowayDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109; email: [email protected]

    Annual Review of Virology Vol. 2: 403 - 423

    • ...each cell is estimated to repair 10,000 lesions per day (94)....

  • Determinants of Mutation Rate Variation in the Human Germline

    Laure Ségurel, ^1, Minyoung J. Wyman, ^2, and Molly Przeworski ^{3, 1}Laboratoire Éco-Anthropologie et Ethnobiologie, UMR 7206, Muséum National d'Histoire Naturelle–Centre National de la Recherche Scientifique–Université Paris 7 Diderot, Paris 75231, France; email: [email protected] ²Department of Biological Sciences, Columbia University, New York, NY 10027; email: [email protected] ³Department of Human Genetics and Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois 60637; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 15: 47 - 70

    • ...nonreplicatively) because of the instability of the structure of DNA (91) or are induced by endogenous or exogenous sources (i.e., ...

  • Biomolecular Archaeology

    Keri A. Brown and Terence A. BrownManchester Institute of Biotechnology, Faculty of Life Sciences, University of Manchester, Manchester M1 7DN, United Kingdom; email: [email protected], [email protected]

    Annual Review of Anthropology Vol. 42: 159 - 174

    • ...followed by a slower period of more gradual diagenesis within the archaeological specimen (Lindahl 1993)....
    • ...despite a clear realization that the kinetics of DNA decay provided little opportunity for survival of intact polynucleotides in specimens of more than ∼100,000 years in age (Lindahl 1993)....

  • Genome Instability and Aging

    Jan Vijg ¹ and Yousin Suh ^{1,2 1}Department of Genetics, Albert Einstein College of Medicine, New York, NY 10461; email: [email protected], [email protected] ²Aging Research Institute, Guangdong Medical College, Dongguan 523808, Guangdong, China

    Annual Review of Physiology Vol. 75: 645 - 668

    • ...a major lesion induced by oxygen free radicals, pairs with adenine to generate transversion mutations (16)....

  • 5-Methylcytosine DNA Demethylation: More Than Losing a Methyl Group

    Don-Marc Franchini, Kerstin-Maike Schmitz, and Svend K. Petersen-MahrtDNA Editing in Immunity and Epigenetics, IFOM-Fondazione Istituto FIRC di Oncologia Molecolare, 20139 Milano, Italy; email: [email protected], [email protected], [email protected]

    Annual Review of Genetics Vol. 46: 419 - 441

    • ...Mammalian genomes experience 20,000–30,000 DNA-damaging events a day (68), which are efficiently repaired via numerous DNA repair pathways....
    • ...including deamination of cytosine, is a major source of mutations in cancer (68)....

  • Environmental Stress and Lesion-Bypass DNA Polymerases

    Takehiko NohmiDivision of Genetics and Mutagenesis, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan, email: [email protected]

    Annual Review of Microbiology Vol. 60: 231 - 253

    • ...depurination, and oxidation at greatly increased rates at high temperatures (78)....
    • ...Hypoxanthine can pair with cytosine, thereby inducing AT-to-GC transitions if not repaired (78)....

  • Genetic Analyses from Ancient DNA

    Svante Pääbo, Hendrik Poinar, David Serre, Viviane Jaenicke-Després, Juliane Hebler, Nadin Rohland, Melanie Kuch, Johannes Krause, Linda Vigilant, and Michael HofreiterMax Planck Institute for Evolutionary Anthropology, D-04013 Leipzig, Germany; email: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Genetics Vol. 38: 645 - 679

    • ...the integrity of DNA molecules is continually maintained by enzymatic repair processes (85)....
    • ...The reduction in size is due to both enzymatic processes that occur shortly after death and nonenzymatic hydrolytic cleavage of phosphodiester bonds in the phosphate-sugar backbone (85, 131) that generate single-stranded nicks....
    • ...the chemical bonds of the deoxyribose residues are susceptible to oxidation resulting in fragmentation of the sugar ring (31, 85)....
    • ...the idea that DNA can survive for millions of years was questioned (85, 107)....

  • Flap Endonuclease 1: A Central Component of DNA Metabolism

    Yuan Liu Hui-I Kao and Robert A. BambaraDepartment of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642; email: [email protected] ,[email protected] ,[email protected]

    Annual Review of Biochemistry Vol. 73: 589 - 615

    • ...Cells can suffer extensive DNA damage from exposure to either endogenous reactive metabolites or exogenous DNA damaging agents that oxidize or alkylate DNA bases (82, 83)....

  • Covalent Trapping of Protein-DNA Complexes

    Gregory L. Verdine and Derek P.G. NormanDepartment of Chemistry and Chemical Biology, Harvard University, Cambridge, Massachusetts 02138; email: [email protected] ,[email protected]

    Annual Review of Biochemistry Vol. 72: 337 - 366

    • ...including electrophilic oxidants, ionizing radiation, ultraviolet light, methylating agents, and even water (13)....

  • Recombinational DNA Repair of Damaged Replication Forks in Escherichia coli: Questions

    Michael M. CoxDepartment of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706-1544; e-mail: [email protected]

    Annual Review of Genetics Vol. 35: 53 - 82

    • ...Estimates of the spontaneous frequency of events such as depurination and cytosine deamination are readily available (43, 74)....

  • Cellular Responses to DNA Damage

    Chris J Norbury and Ian D HicksonImperial Cancer Research Fund Laboratories, Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, OX3 9DS, United Kingdom; e-mail: [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 41: 367 - 401

    • ...The BER pathway has been reviewed in detail elsewhere (7, 8, 9, 10, 11, 12, 13, 14, 15, 16) and is depicted in Figure 1....
    • ...Base oxidation in cellular DNA can arise following exposure to ionizing radiation, radiomimetic chemicals, and intracellular reactive oxygen species (ROS) (7, 8, 9, 10, 11)....

  • Ancient DNA Studies in Physical Anthropology

    Dennis H. O'Rourke M. Geoffrey Hayes and Shawn W. CarlyleLaboratory of Biological Anthropology, University of Utah, Salt Lake City, Utah 84112-0060; e-mail: [email protected] [email protected] [email protected]

    Annual Review of Anthropology Vol. 29: 217 - 242

    • ...Nucleic acids of any antiquity are degraded and modified in various ways (Lindahl 1993, Höss et al 1996)....
    • ...Nucleic acids gradually degrade over time through processes such as hydrolysis and oxidation (reviewed in Lindahl 1993)....
    • ...most likely because of the stabilization of DNA binding to hydroxyapatite (Tuross 1993, 1994), which slows the hydrolytic depurination rate twofold (Lindahl 1993)....

  • Full of Sound and Fury: History of Ancient DNA

    Robert K. Wayne^*, Jennifer A. Leonard^*, and Alan Cooper^{+ *}Department of Organismic Biology, Ecology and Evolution, University of California, Los Angeles California 90095-1606; e-mail: [email protected] ;⁺Department of Biological Anthropology, University of Oxford, Oxford OX2 6QS, United Kingdom

    Annual Review of Ecology and Systematics Vol. 30: 457 - 477

    • ...the view now is that specimens much older than 100,000 years in age are unlikely to contain endogenous DNA that can be amplified (82, 84)....
    • ...Theoretical and empirical studies have demonstrated that DNA is best preserved in cold and dry environments protected from UV exposure and in remains less than 100,000 years old (82, 84, 101, 112)....
    • ...The absence of replication of million-year-old DNA studies and the theoretical and empirical research on DNA preservation all suggest that DNA is unlikely to be preserved much beyond 100,000 years (82, 112)....

  • DNA REPAIR MECHANISMS FOR THE RECOGNITION AND REMOVAL OF DAMAGED DNA BASES

    Clifford D. Mol, Sudip S. Parikh, Christopher D. Putnam, Terence P. Lo, and John A. TainerDepartment of Molecular Biology and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California 92037; e-mail: [email protected]

    Annual Review of Biophysics and Biomolecular Structure Vol. 28: 101 - 128

    • ...which must be recognized and removed by specific DNA repair enzymes (49)....

  • DNA DAMAGE AND REPAIR IN PLANTS

    Anne B. BrittSection of Plant Biology, University of California, Davis, California 95616

    Annual Review of Plant Physiology and Plant Molecular Biology Vol. 47: 75 - 100

    • ...from ancient sources) I direct the reader to a recent article (61)....

• 66.

  More AR articles citing this reference

  • The BRCA Tumor Suppressor Network in Chromosome Damage Repair by Homologous Recombination

    Weixing Zhao, ^1,2, Claudia Wiese, ^3, Youngho Kwon, ^1,2 Robert Hromas, ⁴ and Patrick Sung ^{1,2 1}Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06520, USA²Department of Biochemistry and Structural Biology, University of Texas Health San Antonio, San Antonio, Texas 78229, USA; email: [email protected], [email protected] ³Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523, USA⁴Department of Medicine, University of Texas Health San Antonio, San Antonio, Texas 78229, USA

    Annual Review of Biochemistry Vol. 88: 221 - 245

    • ...and by reactive metabolites, such as aldehydes and free radicals, that damage DNA (1...

  • Aging in a Dish: iPSC-Derived and Directly Induced Neurons for Studying Brain Aging and Age-Related Neurodegenerative Diseases

    Jerome Mertens, ^1,2 Dylan Reid, ¹ Shong Lau, ¹ Yongsung Kim, ¹ and Fred H. Gage ^{1 1}Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA; email: [email protected] ²Department of Genomics, Stem Cell Biology and Regenerative Medicine, Institute of Molecular Biology, and Center for Molecular Biosciences Innsbruck, University of Innsbruck, A-6020 Innsbruck, Austria

    Annual Review of Genetics Vol. 52: 271 - 293

    • ...according to calculations, repair over 100,000 DNA lesions per cell every day (75)....

  • Recent Advancements in DNA Damage–Transcription Crosstalk and High-Resolution Mapping of DNA Breaks

    Valerio Vitelli, ¹ Alessandro Galbiati, ¹ Fabio Iannelli, ¹ Fabio Pessina, ¹ Sheetal Sharma, ¹ and Fabrizio d'Adda di Fagagna ^{1,2 1}FIRC Institute of Molecular Oncology (IFOM), Milan 20139, Italy; email: [email protected] ²Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (CNR), Pavia 27100, Italy

    Annual Review of Genomics and Human Genetics Vol. 18: 87 - 113

    • ...Because DNA lesions occur frequently—it has been estimated that human cells are exposed to thousands of lesions per day (82)—cells need a way to detect, ...

  • Clusters of Multiple Mutations: Incidence and Molecular Mechanisms

    Kin Chan and Dmitry A. GordeninMechanisms of Genome Dynamics Group, National Institute of Environmental Health Sciences, Department of Health and Human Services, National Institutes of Health, Durham, North Carolina 27709; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 49: 243 - 267

    • ...which for the human genome would result in 10⁵–10⁶ lesions genome wide (44, 69)....

  • Repair and Genetic Consequences of Endogenous DNA Base Damage in Mammalian Cells

    Deborah E. Barnes and Tomas LindahlCancer Research UK, London Research Institute, Clare Hall Laboratories, South Mimms, Hertfordshire EN6 3LD, United Kingdom; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 38: 445 - 476

    • ...The total load of AP sites in a mammalian cell from these sources is over 10,000 per day and is a challenge to the cellular base excision-repair system (85)....

• 67.

  More AR articles citing this reference

  • Revelations About Aging and Disease from Unconventional Vertebrate Model Organisms

    Yang Zhao, Andrei Seluanov, and Vera GorbunovaDepartment of Biology, University of Rochester, Rochester, New York 14627, USA; email: [email protected], [email protected]

    Annual Review of Genetics Vol. 55: 135 - 159

    • ...Aging is a persistent functional decline in fitness that occurs in most organisms over time (100, 140)....
    • ...These changes are closely correlated with aging and age-associated diseases and thus are referred to as the hallmarks of aging (100)....

  • Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions

    Laura Campello, Nivedita Singh, Jayshree Advani, Anupam K. Mondal, Ximena Corso-Díaz, and Anand SwaroopNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; email: [email protected]

    Annual Review of Vision Science Vol. 7: 633 - 664

    • ...This general decline of functional capabilities through an organismal life is fairly conserved among species (Lopez-Otin et al. 2013)....
    • ...stem cell exhaustion, and altered intracellular communication (Lopez-Otin et al. 2013)....
    • ...The key components involved in sensing nutrient abundance or scarcity during aging include insulin and IGF signaling; mammalian target of rapamycin (mTOR); adenosine monophosphate-activated protein kinase (AMPK); and sirtuins (Lopez-Otin et al. 2013), ...
    • ...AMPK and sirtuins play protective roles in aging (Lopez-Otin et al. 2013)....

  • Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span

    Paul D. Robbins, ¹ Diana Jurk, ² Sundeep Khosla, ² James L. Kirkland, ² Nathan K. LeBrasseur, ² Jordan D. Miller, ² João F. Passos, ² Robert J. Pignolo, ² Tamar Tchkonia, ² and Laura J. Niedernhofer ^{1 1}Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA; email: [email protected] ²Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA

    Annual Review of Pharmacology and Toxicology Vol. 61: 779 - 803

    • ...Old age is the greatest risk factor for the chronic diseases responsible for the majority of morbidity, mortality, and health-care costs worldwide (1, 2)....
    • ...There is a tremendous potential health and economic benefit to targeting fundamental aging mechanisms as opposed to treating each disease separately (2)....

  • Aging, Life History, and Human Evolution

    Richard G. BribiescasDepartment of Anthropology, Yale University, New Haven, Connecticut 06520, USA; email: [email protected]

    Annual Review of Anthropology Vol. 49: 101 - 121

    • ...other aspects of physiology such as immune and neurological function along with genetic and epigenetic challenges often reveal differential somatic changes with aging (López-Otín et al. 2013, Sadighi Akha 2018, Stegeman & Weake 2017)....

  • Calorie Restriction and Aging in Humans

    Emily W. Flanagan, ¹ Jasper Most, ² Jacob T. Mey, ¹ and Leanne M. Redman ^{1 1}Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808, USA; email: [email protected] ²Nutrition and Movement Sciences, Maastricht University, 6229 ER Maastricht, The Netherlands

    Annual Review of Nutrition Vol. 40: 105 - 133

    • ...and organ-level changes that are affected by these stressors and cause a decline in physiological function have been described as overlapping sets of 5–10 processes (72)....

  • Lighting Up Live-Cell and In Vivo Central Carbon Metabolism with Genetically Encoded Fluorescent Sensors

    Zhuo Zhang, ^1,2 Xiawei Cheng, ^1,2 Yuzheng Zhao, ^1,2 and Yi Yang ^{1,3 1}Optogenetics and Synthetic Biology Interdisciplinary Research Center, State Key Laboratory of Bioreactor Engineering, Shanghai Collaborative Innovation Center for Biomanufacturing Technology, Research Unit of Chinese Academy of Medical Sciences, East China University of Science and Technology, Shanghai 200237, China; email: [email protected], [email protected] ²Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China³CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

    Annual Review of Analytical Chemistry Vol. 13: 293 - 314

    • ...central carbon metabolism is weaved into a large number of physiologic or pathological processes of cells and organisms, ranging from embryonic development to aging (1, 2), ...

  • Mitochondria-Associated Proteostasis

    Linhao Ruan, ^1,2,3 Yuhao Wang, ^1,2,3 Xi Zhang, ^1,3 Alexis Tomaszewski, ^1,2,3 Joshua T. McNamara, ^1,2,3 and Rong Li ^{1,3 1}Center for Cell Dynamics, Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA; email: [email protected], [email protected], [email protected], [email protected], [email protected], [email protected] ²Biochemistry, Cellular and Molecular Biology (BCMB) Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA³Department of Chemical and Biomolecular Engineering, Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland 21218, USA

    Annual Review of Biophysics Vol. 49: 41 - 67

    • ..., which also contributes to fitness decline during organismal aging (97, 156)....

  • Psychosocial Stressors and Telomere Length: A Current Review of the Science

    Kelly E. Rentscher, ¹ Judith E. Carroll, ¹ and Colter Mitchell ^{2 1}Cousins Center for Psychoneuroimmunology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, California 90095, USA; email: [email protected], [email protected] ²Institute for Social Research, University of Michigan, Ann Arbor, Michigan 48106, USA; email: [email protected]

    Annual Review of Public Health Vol. 41: 223 - 245

    • ...as telomeres that reach a critically short length can initiate a replicative senescence response (8, 70)....
    • ...and TL attrition is activation of cellular senescence, a hallmark of biological aging (70)....
    • ...Beyond TL, other hallmarks of biological aging have been proposed (70), ...
    • ...the imperative to conduct convincing scientific inquiry to delineate how psychosocial factors "get under the skin" to influence aging and health requires that future investigations apply a multimodal assessment that captures dynamic cellular aging by tracking multiple hallmarks of aging (e.g., mitochondrial function, cellular senescence, the epigenetic clock) (56, 70)....

  • Neuronal Mechanisms that Drive Organismal Aging Through the Lens of Perception

    Christi M. Gendron, ¹ Tuhin S. Chakraborty, ¹ Brian Y. Chung, ¹ Zachary M. Harvanek, ¹ Kristina J. Holme, ¹ Jacob C. Johnson, ¹ Yang Lyu, ¹ Allyson S. Munneke, ² and Scott D. Pletcher ^{1,2 1}Department of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan 48109, USA; email: [email protected] ²Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109, USA

    Annual Review of Physiology Vol. 82: 227 - 249

    • ...the unfolded protein response, genomic instabilities, epigenetic drift, mitochondrial dysfunction, and cellular senescence (5)....
    • ...While extended discussions on the theories of aging in light of each of these pathways are beyond the scope of this review and are examined in detail elsewhere (5), ...

  • The Microbiome and Aging

    Bianca Bana ¹ and Filipe Cabreiro ^{2,3 1}Institute of Structural and Molecular Biology, University College London and Birkbeck, University of London, London WC1E 6BT, United Kingdom²MRC London Institute of Medical Sciences, London W12 0NN, United Kingdom; email: [email protected] ³Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, United Kingdom

    Annual Review of Genetics Vol. 53: 239 - 261

    • ...In an attempt to better characterize aging and determine its underlying mechanisms, López-Otín et al. (93) described nine hallmarks of aging, ...
    • ...The result is stem cell exhaustion and altered intercellular communication, which are ultimately responsible for organismal aging (93)....
    • ...Aging has physiological effects on both the host (93) and the microbiome (12)...
    • ...aging has a deleterious effect on pluripotent stem cells, hindering their renewal and differentiation abilities (93)....
    • ...Caloric restriction (CR) is a well-known intervention that promotes longevity and improves health across species (93)....
    • ...specifically through reduced ATP production and progressive decline in respiratory chain efficacy (93)....
    • ...cause oxidative damage that accumulates and leads to organismal aging (93)....
    • ...Longevity correlates with good proteasomal function, as observed in healthy centenarians (93)....
    • ...Several studies showed that extending telomeres increased longevity, whereas shortening telomeres decreased it (93)....
    • ...Epigenetic alterations influence organisms throughout their lifetime, through DNA methylation, histone modifications, or chromatin remodeling (93)....
    • ...senescence might deplete stem or progenitor cell reserves, creating an imbalance that favors damage and impairs function (93)....
    • ...Although there is currently no direct experimental evidence that shows altered DNA methylation patterns can extend life span (93), ...

  • NAD+ Metabolism in Aging and Cancer

    Tyler G. Demarest, ^1,2 Mansi Babbar, ¹ Mustafa N. Okur, ¹ Xiuli Dan, ¹ Deborah L. Croteau, ¹ Nima B. Fakouri, ¹ Mark P. Mattson, ² and Vilhelm A. Bohr ^{1 1}Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA; email: [email protected] ²Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA

    Annual Review of Cancer Biology Vol. 3: 105 - 130

    • ...Hallmarks of aging (Lopez-Otin et al. 2013) and cancer have recently been proposed (Hanahan & Weinberg 2011)...
    • ...Senescent cells are also a hallmark of aging (Lopez-Otin et al. 2013)....

  • Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging

    Lei Zhang and Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email: [email protected]

    Annual Review of Genetics Vol. 52: 397 - 419

    • ...generally considered a hallmark of disease, such as cancer (98), and aging (82)....

  • Aging in a Dish: iPSC-Derived and Directly Induced Neurons for Studying Brain Aging and Age-Related Neurodegenerative Diseases

    Jerome Mertens, ^1,2 Dylan Reid, ¹ Shong Lau, ¹ Yongsung Kim, ¹ and Fred H. Gage ^{1 1}Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA; email: [email protected] ²Department of Genomics, Stem Cell Biology and Regenerative Medicine, Institute of Molecular Biology, and Center for Molecular Biosciences Innsbruck, University of Innsbruck, A-6020 Innsbruck, Austria

    Annual Review of Genetics Vol. 52: 271 - 293

    • ...Although many different research approaches are being pursued to better understand the process of aging (81), ...
    • ...the contributions of numerous molecular mechanisms and pathways that define the etiology of the aging process have been elucidated (81)....

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...The accumulation of mutations in adult stem cells that occurs during aging carries the dual risk: compromised regeneration and enhanced oncogenic transformation (77)....
    • ...The lifespan effects of CR can be attributed at least in part to improved function of stem cells, central actors in maintaining tissue integrity (77)....

  • Aging in the Cardiovascular System: Lessons from Hutchinson-Gilford Progeria Syndrome

    Magda R. Hamczyk, ^1,2, Lara del Campo, ^1,2, and Vicente Andrés ^{1,2 1}Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain; email: [email protected] ²CIBER de Enfermedades Cardiovasculares (CIBER-CV), 28029 Madrid, Spain

    Annual Review of Physiology Vol. 80: 27 - 48

    • ...Animal and human studies have identified four main causes of accumulated damage that are proposed to drive mammalian aging: genomic instability, telomere attrition, epigenetic alterations, and loss of proteostasis (6)....
    • ...all the hallmarks of normal aging proposed by López-Otín et al. (6) have been described in animal models of progeria, ...
    • ...both of which are thought to contribute to normal aging (6), ...
    • ...most of the processes affected in HGPS are implicated in normal aging (6)....
    • ...leading to integrative hallmarks (stem cell exhaustion and altered intercellular communication) (6)....

  • Senescence in COPD and Its Comorbidities

    Peter J. BarnesNational Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 79: 517 - 539

    • ...loss of proteostasis, mitochondrial dysfunction, deregulated nutrient sensing, and stem cell exhaustion (23)....
    • ...as it clears tissues from damaged and potentially oncogenic cells (23)....
    • ...A defective ability to repair tissue is associated with depletion of stem cells (23)....

  • Dietary Protein, Metabolism, and Aging

    George A. Soultoukis ¹ and Linda Partridge ^{1,2 1}Max Planck Institute for Biology of Ageing, Department of Biological Mechanisms of Ageing, Cologne 50931, Germany; email: [email protected], [email protected] ²Institute of Healthy Ageing and Department of Genetics, Evolution, and Environment, University College London, London WC1E 6BT, United Kingdom

    Annual Review of Biochemistry Vol. 85: 5 - 34

    • ...and genome stability and the promotion of proteostasis and energy homeostasis (5, 16)....
    • ...mTOR activity in mouse hypothalamic neurons increases, silencing anorexic neurons and contributing to age-related obesity (16)....
    • ...Activation of FOXO transcription factors mediates the life-extending effect of IIS downregulation across species (5, 16)....

  • Structure and Function of the Mitochondrial Ribosome

    Basil J. Greber ^1, * and Nenad Ban ^{1 1}Department of Biology, Institute of Molecular Biology and Biophysics, ETH Zurich, CH-8093 Zurich, Switzerland; email: [email protected]*Present address: California Institute for Quantitative Biosciences (QB3), University of California, Berkeley, California 94720-3220

    Annual Review of Biochemistry Vol. 85: 103 - 132

    • ...they play an important part in diverse cellular processes, such as apoptosis (10) and aging (11)....

  • Signaling Networks Determining Life Span

    Celine E. Riera, ^1,2,3 Carsten Merkwirth, ^1,2,3 C. Daniel De Magalhaes Filho, ^2,4 and Andrew Dillin ^{1,2,3 1}Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; email: [email protected] ²Howard Hughes Medical Institute, Chevy Chase, Maryland 20815³Glenn Center for Research on Aging, University of California, Berkeley, California 94720⁴The Salk Institute for Biological Studies, La Jolla, California 92037

    Annual Review of Biochemistry Vol. 85: 35 - 64

    • ...Efforts in geroscience research have proven that aging is more than just a passive process and can be regulated in well-defined settings and isolated genetic backgrounds using model organisms (2)....
    • ...The research of epigenetics is gaining increasing attention within the aging field and contributes significantly to our understanding of how environmental cues impinge on the regulation of the natural aging process (2, 134)....

  • DNA Damage and Repair in Vascular Disease

    Anna Uryga, ¹ Kelly Gray, ² and Martin Bennett ^{1, 1}Division of Cardiovascular Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom; email: [email protected], [email protected] ²Cardiovascular Safety, AstraZeneca, Cambridge CB4 0FZ, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 78: 45 - 66

    • ...Adapted from Reference 141....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...loss of proteostasis, cellular senescence, and adult stem cell exhaustion (92)....

  • The Mechanobiology of Aging

    Jude M. Phillip, ^1,2, Ivie Aifuwa, ^1,2, Jeremy Walston, ³ and Denis Wirtz ^{1,2,4 1}Department of Chemical and Biomolecular Engineering and²Johns Hopkins Physical Sciences–Oncology Center, Institute for Nanobiotechnology, Johns Hopkins University, Baltimore, Maryland, 21218; email: [email protected] ³Department of Medicine, Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224⁴Departments of Oncology and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231

    Annual Review of Biomedical Engineering Vol. 17: 113 - 141

    • ...These changes include the increased incidences of cardiovascular disease and cancer (43), ...
    • ...as well as errors in heterochromatin, and epigenetic errors and defects (43) (Figure 2)....
    • ...specific changes occur that lead to diminished integrity in the mitochondrial structure–function relationship (43, 131)....
    • ...The popular free-radical theory of aging proposes that this cumulative damage to biological macromolecules caused by ROS leads to irreversible cellular damage and overall functional decline (43, 134, 135)....
    • ...] and turnover (due to reduced biogenesis, inefficient mitochondrial degradation, or both; and mitophagy) (43, 134, 150) (Figure 4)....
    • ...or a combination of these, have recently sparked a reevaluation mitochondrial free-radical theory (43)....
    • ...a novel framework postulated by Lopez-Otin et al. (43) may help explain the confounding evidence regarding the roles of ROS....
    • ...This increased level of ROS facilitates the perpetual cell-associated damage (43)...
    • ...when ROS regulation becomes progressively more inefficient in dictating cellular responses to stress, it leads to impaired bioenergetics and cell death (43)....
    • ...and (g) defective mitochondrial turnover and quality control by mitophagy (43)....
    • ...through endurance training or exercise); early diagnosis of age-related phenotypes (e.g., prefrail or frail phenotypes) (157); and therapeutic interventions (43, 134)....

• 68.

  More AR articles citing this reference

  • The Microbiome and Aging

    Bianca Bana ¹ and Filipe Cabreiro ^{2,3 1}Institute of Structural and Molecular Biology, University College London and Birkbeck, University of London, London WC1E 6BT, United Kingdom²MRC London Institute of Medical Sciences, London W12 0NN, United Kingdom; email: [email protected] ³Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, United Kingdom

    Annual Review of Genetics Vol. 53: 239 - 261

    • ...These hallmarks have provided a general framework not only for investigating mechanisms underlying the aging process but also for finding interventions and strategies targeting them to increase longevity and improve health (94) (Figure 1)....

  • Chromatin and Metabolism

    Tamaki Suganuma and Jerry L. WorkmanStowers Institute for Medical Research, Kansas City, Missouri 64110, USA; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 87: 27 - 49

    • ...as seen in studies of aging, which propose that calorie restriction is beneficial for longevity (3), ...
    • ...Seven SIRTs (1–7) have been found in mammalian cells....

• 69.

  More AR articles citing this reference

  • Metabolic Gatekeepers of Pathological B Cell Activation

    Teresa Sadras, ¹ Lai N. Chan, ¹ Gang Xiao, ² and Markus Müschen ^{1 1}Center of Molecular and Cellular Oncology, Yale Cancer Center, and Department of Immunobiology, Yale University, New Haven, Connecticut 06520, USA; email: [email protected] ²Current affiliation: Department of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China

    Annual Review of Pathology: Mechanisms of Disease Vol. 16: 323 - 349

    • ...indicating that malignant B cells may be more sensitive than other lineages to limiting energy supply (146)....

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...Leptin receptor expression has been associated with improved outcome in leukemia (82, 96)....
    • ...Studies that have looked at the impact of fasting on the growth of implanted cancer cells in mice have found beneficial effects in some models (15, 23, 91, 96, 104, 145, 164)...
    • ...Studies that have looked at the impact of fasting on the growth of implanted cancer cells in mice have found beneficial effects in some models (15, 23, 91, 96, 104, 145, 164) but not in others (21, 36, 85, 91, 96, 134, 168), ...
    • ...and some studies have found beneficial effects on one cancer but not another (91, 96), ...
    • ...Lu et al. (96) elegantly showed that leukemia cells in obese mice were resistant to leptin but, ...

• 70.

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...A dramatic example in humans is the observation that cancer survivors treated with genotoxic chemotherapy show multiple symptoms of premature aging (114)....

• 71.

  Madeo F , Carmona-Gutierrez D , Hofer SJ , Kroemer G . 2019. Caloric restriction mimetics against age-associated disease: targets, mechanisms, and therapeutic potential. Cell Metab. 29(3):592–610

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Nutritional Aspects of Spermidine

    Frank Madeo, ^1,2,3 Sebastian J. Hofer, ¹ Tobias Pendl, ¹ Maria A. Bauer, ¹ Tobias Eisenberg, ^1,2,3,4 Didac Carmona-Gutierrez, ¹ and Guido Kroemer ^{5,6,7,8,9 1}Institute of Molecular Biosciences, NAWI Graz, University of Graz, 8010 Graz, Austria; email: [email protected] ²BioTechMed-Graz, 8010 Graz, Austria³Field of Excellence BioHealth, University of Graz, 8010 Graz, Austria⁴Central Lab Graz Cell Informatics and Analyses (GRACIA), NAWI Graz, University of Graz, 8010 Graz, Austria⁵Equipe Labellisée par la Ligue Contre le Cancer, Université de Paris, Sorbonne Université, INSERM U1138, Centre de Recherche des Cordeliers, 75006 Paris, France; email: [email protected] ⁶Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, F-94805 Villejuif, France⁷Pôle de Biologie, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, F-75015 Paris, France⁸Suzhou Institute for Systems Medicine, Chinese Academy of Medical Sciences, Jiangsu 215163, Suzhou, China⁹Department of Women's and Children's Health, Karolinska Institute, Karolinska University, S-17177 Solna, Sweden

    Annual Review of Nutrition Vol. 40: 135 - 159

    • ...Importantly, external administration of spermidine has general antiaging effects (32, 34, 82, 83, 145, 178), as it confers a variety of positive effects on different organs, ...

  • Contributions of Aging to Cerebral Small Vessel Disease

    T. Michael De Silva ¹ and Frank M. Faraci ^{2 1}Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne Campus, Bundoora, Victoria 3086, Australia; email: [email protected] ²Departments of Internal Medicine, Neuroscience, and Pharmacology, Francois M. Abboud Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA; email: [email protected]

    Annual Review of Physiology Vol. 82: 275 - 295

    • ...is known to improve life span (or health span) in multiple organisms (126)....
    • ...interest in identifying and testing effects of potential caloric restriction mimetics has become a priority (126), ...
    • ...the plant-derived polyphenol resveratrol is accepted as a caloric restriction mimetic (126)....

• 72.

• 73.

  Malietzis G , Currie AC , Athanasiou T , Johns N , Anyamene N , et al. 2016. Influence of body composition profile on outcomes following colorectal cancer surgery. Br. J. Surg. 103(5):572–80

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • The Obesity Paradox in Cancer: How Important Is Muscle?

    Elizabeth M. Cespedes Feliciano, Candyce H. Kroenke, and Bette J. CaanDivision of Research, Kaiser Permanente, Oakland, California 94612, USA; email: [email protected], [email protected], [email protected]

    Annual Review of Nutrition Vol. 38: 357 - 379

    • ...or both (45, 49, 54, 58, 75, 80, 98, 106, 108, 125, 131, 136, 149, 151, 171, 174); 15 on colon or rectal cancer, or both (10, 11, 16, 66, 81, 82, 85, 93, 94, 96, 109, 113, 126, 130, 152)...

• 74.

  More AR articles citing this reference

  • Nucleotide Excision Repair and Transcriptional Regulation: TFIIH and Beyond

    Emmanuel Compe and Jean-Marc EglyInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/Université de Strasbourg, 67404 Illkirch Cedex, Commune Urbaine Strasbourg, France; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 85: 265 - 290

    • ...Following dual incision-excision and DNA into chromatin (118)....

  • DNA Damage and Repair in Vascular Disease

    Anna Uryga, ¹ Kelly Gray, ² and Martin Bennett ^{1, 1}Division of Cardiovascular Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom; email: [email protected], [email protected] ²Cardiovascular Safety, AstraZeneca, Cambridge CB4 0FZ, United Kingdom; email: [email protected]

    Annual Review of Physiology Vol. 78: 45 - 66

    • ...Two major pathways are employed by NER to repair these lesions: global genome NER (GG-NER) and transcription-coupled NER (TC-NER) (97, 98)....
    • ...The complexes are then detected by a set of shared components involved in unwinding, dual incision, and gap filling (98)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...and transcription-coupled NER (TC-NER), which removes transcription-blocking lesions from actively transcribed DNA strands (49, 50)....

• 75.

  Martin-McGill KJ , Marson AG , Tudur Smith C , Young B , Mills SJ , et al. 2020. Ketogenic diets as an adjuvant therapy for glioblastoma (KEATING): a randomized, mixed methods, feasibility study. J. Neuro-Oncol. 143:213–227

  • Crossref
  • Google Scholar

• 76.

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...experience delayed onset of age-related conditions, and generally live longer compared with controls (126)....

  • Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions

    Laura Campello, Nivedita Singh, Jayshree Advani, Anupam K. Mondal, Ximena Corso-Díaz, and Anand SwaroopNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; email: [email protected]

    Annual Review of Vision Science Vol. 7: 633 - 664

    • ...CR during aging is reportedly beneficial in vertebrate models and humans (Mattison et al. 2017)....

  • Calorie Restriction and Aging in Humans

    Emily W. Flanagan, ¹ Jasper Most, ² Jacob T. Mey, ¹ and Leanne M. Redman ^{1 1}Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808, USA; email: [email protected] ²Nutrition and Movement Sciences, Maastricht University, 6229 ER Maastricht, The Netherlands

    Annual Review of Nutrition Vol. 40: 105 - 133

    • ...these differences have been attributed to discrepancies in age of CR onset and animal husbandry practices (i.e., feeding protocols, treatment of age-related diseases) (81)....
    • ...ad libitum–fed animals had double the rate and more severe cases of age-associated diseases, including diabetes, cancer, cardiovascular disease, and osteoporosis (81)....

  • Using Macaques to Address Critical Questions in Zika Virus Research

    Dawn M. Dudley, ¹ Matthew T. Aliota, ² Emma L. Mohr, ³ Christina M. Newman, ¹ Thaddeus G. Golos, ^4,5 Thomas C. Friedrich, ^4,6 and David H. O'Connor ^{1,4 1}Department of Pathology and Laboratory Medicine, University of Wisconsin–Madison, Madison, Wisconsin 53711, USA; email: [email protected], [email protected], [email protected] ²Department of Veterinary and Biomedical Sciences, University of Minnesota, Twin Cities, Saint Paul, Minnesota 55108, USA; email: [email protected] ³Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin–Madison, Madison, Wisconsin 53792, USA; email: [email protected] ⁴Wisconsin National Primate Research Center, University of Wisconsin–Madison, Madison, Wisconsin 53715, USA; email: [email protected], [email protected] ⁵Departments of Comparative Biosciences and Obstetrics and Gynecology, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA⁶Department of Pathobiological Sciences, University of Wisconsin–Madison, Madison, Wisconsin 53706, USA

    Annual Review of Virology Vol. 6: 481 - 500

    • ...that increase life expectancy and decrease the incidence of age-related diseases (cancer, cardiovascular disease, and diabetes) (144)....

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...Another study in CR macaques failed to demonstrate an improvement in survival, but CR monkeys had improved metabolic profiles (84, 85)....

  • Nutrition and Inflammation: Are Centenarians Similar to Individuals on Calorie-Restricted Diets?

    Claudio Franceschi, ¹ Rita Ostan, ² and Aurelia Santoro ^{2 1}IRCCS Institute of Neurological Sciences of Bologna, 40139 Bologna, Italy; email: [email protected] ²Department of Experimental, Diagnostic, and Specialty Medicine (DIMES) and Interdepartmental Centre "L. Galvani" (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; email: [email protected], [email protected]

    Annual Review of Nutrition Vol. 38: 329 - 356

    • ...CR is the most thoroughly studied nutritional intervention considered to modulate aging and to increase health span and life span in a variety of animal models, from the unicellular yeast to primates (78)....
    • ...but what about primates? Two independent longitudinal studies of CR on nonhuman primates (monkeys) were conducted at the US National Institute on Aging in 1987 and at the University of Wisconsin in 1989 (78)....
    • ...with this difference likely being a consequence of the different age of onset of the two diet regimens (78)....

• 77.

  Mattison JA , Roth GS , Beasley TM , Tilmont EM , Handy AM , et al. 2012. Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study. Nature 489(7415):318–21

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Nutritional Regulation of Intestinal Stem Cells

    Salvador Alonso ^1,2,3 and Ömer H. Yilmaz ^{2,4 1}Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; email: [email protected] ²Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA; email: [email protected] ³Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA⁴Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

    Annual Review of Nutrition Vol. 38: 273 - 301

    • ...Another study in CR macaques failed to demonstrate an improvement in survival, but CR monkeys had improved metabolic profiles (84, 85)....

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...and the NIA NHP CR studies have highlighted the subtle differences in response to CR (137, 138)....

  • The Roles of Cellular and Organismal Aging in the Development of Late-Onset Maladies

    Filipa Carvalhal Marques, ^1,2, Yuli Volovik, ^1, and Ehud Cohen ^{1 1}Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, Hebrew University School of Medicine, 91120 Jerusalem, Israel; email: [email protected] ²Centre of Ophthalmology and Vision Sciences, Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 1 - 23

    • ...two independent research groups (12, 13) addressed the question of whether the DR-associated longevity and prolonged health span phenotypes are conserved in primates....
    • ...the other research team found that DR had no significant effect on life span but efficiently reduced morbidity (13)....

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...as well as in rhesus monkeys (5, 6, 7) and in a number of nonmodel organisms....
    • ...such as the major advances achieved in developing DR mimetic drugs, with the discovery that DR slows aging in primates (5, 6, 7)...

• 78.

  McCay CM , Crowell MF , Maynard LA . 1935. The effect of retarded growth upon the length of life span and upon the ultimate body size. J. Nutr. 10(1):63–79

  • Crossref
  • Google Scholar

  More AR articles citing this reference

  • Hormesis Mediates Acquired Resilience: Using Plant-Derived Chemicals to Enhance Health

    Edward J. CalabreseDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, Massachusetts 01003, USA; email: [email protected]

    Annual Review of Food Science and Technology Vol. 12: 355 - 381

    • ...The major initiating development was the publication by McCay et al. (1935) showing that restriction of food intake significantly extended the life span of rats as compared to controls fed ad libitum....

  • Neuronal Mechanisms that Drive Organismal Aging Through the Lens of Perception

    Christi M. Gendron, ¹ Tuhin S. Chakraborty, ¹ Brian Y. Chung, ¹ Zachary M. Harvanek, ¹ Kristina J. Holme, ¹ Jacob C. Johnson, ¹ Yang Lyu, ¹ Allyson S. Munneke, ² and Scott D. Pletcher ^{1,2 1}Department of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan 48109, USA; email: [email protected] ²Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109, USA

    Annual Review of Physiology Vol. 82: 227 - 249

    • ...Early work by Pearl's and McCay's groups (1, 2) showed that systematic experimental manipulation can alter life span in different species, ...
    • ...McKay and colleagues (1) reported that feeding rats a calorically restricted diet also significantly extended life span....

  • Dietary Protein, Metabolism, and Aging

    George A. Soultoukis ¹ and Linda Partridge ^{1,2 1}Max Planck Institute for Biology of Ageing, Department of Biological Mechanisms of Ageing, Cologne 50931, Germany; email: [email protected], [email protected] ²Institute of Healthy Ageing and Department of Genetics, Evolution, and Environment, University College London, London WC1E 6BT, United Kingdom

    Annual Review of Biochemistry Vol. 85: 5 - 34

    • ...and this notion was quickly adopted as an explanation of the life span response to DR (32)....

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...Caloric (83) and methionine (84) restriction remain the only non-genetic, non-pharmacological interventions to increase life span in mice....

  • Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts

    David Gems ¹ and Linda Partridge ^{2 1}Institute of Healthy Ageing and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom²Max Planck Institute for Biology of Ageing, Cologne D-50931, Germany; email: [email protected]

    Annual Review of Physiology Vol. 75: 621 - 644

    • ...dietary restriction (DR) was discovered to extend life span of rats subjected to reduced food intake that fell short of malnutrition (4)....

  • The Ins and Outs of Aging and Longevity

    Thomas A. RandoGlenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA 94305-5235; email: [email protected]

    Annual Review of Physiology Vol. 75: 617 - 619

    • ...recognized as an effective intervention since the 1930s, can also markedly increase life span (15, 16)....

  • After 65 Years, Research Is Still Fun

    William HanselLiberty Hyde Bailey Emeritus Professor, Cornell University, Ithaca, New York 14853Gordon Cain Professor Emeritus, Louisiana State University, Baton Rouge, Louisiana 70803Professor, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana 70808; email: [email protected]

    

    Annual Review of Animal Biosciences Vol. 1: 1 - 20

    • ...a major effort was made at Cornell in the early post–World War II period to extend the results of McCay's studies (1, 2) on the effects of growth retardation on life span in rats to domestic animals....

  • Nicotinic Acid, Nicotinamide, and Nicotinamide Riboside: A Molecular Evaluation of NAD+ Precursor Vitamins in Human Nutrition

    Katrina L. Bogan and Charles BrennerDepartments of Genetics and Biochemistry and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire 03756; email: [email protected]

    Annual Review of Nutrition Vol. 28: 115 - 130

    • ...CR is defined as a 20% reduction versus ad libitum feeding without compromising adequate nutrition (56)....

  • Aging and Survival: The Genetics of Life Span Extension by Dietary Restriction

    William Mair and Andrew DillinThe Salk Institute for Biological Studies, La Jolla, California 92037; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 77: 727 - 754

  • Conserved and Tissue-Specific Genic and Physiologic Responses to Caloric Restriction and Altered IGFI Signaling in Mitotic and Postmitotic Tissues

    Stephen R. Spindler ¹ and Joseph M. Dhahbi ^{2 1}Department of Biochemistry, University of California, Riverside, California 92521; email: [email protected] ²Children's Hospital Oakland Research Institute, Oakland, California 94609; email: [email protected]

    Annual Review of Nutrition Vol. 27: 193 - 217

    • ...Many of the physiological effects of CR were described 65 years ago (85, 86), ...

  • Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans

    Stephen D. Hursting,^1,2,4 Jackie A. Lavigne,^1,2 David Berrigan,^1,2,3 Susan N. Perkins,^1,2 and J. Carl Barrett^{1 1}Laboratory of Biosystems and Cancer, Center for Cancer Research; National Cancer Institute, Bethesda, Maryland 20892; e-mail: [email protected] ²Cancer Prevention Fellowship Program, Division of Cancer Prevention; National Cancer Institute, Bethesda, Maryland 20892; ³Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland 20892;

    Annual Review of Medicine Vol. 54: 131 - 152

    • ...when McCay et al. showed that a reduced food intake increased lifespan in rodents (4)....

• 79.

  McCormack L , Petrowsky H , Jochum W , Furrer K , Clavien PA . 2007. Hepatic steatosis is a risk factor for postoperative complications after major hepatectomy: a matched case-control study. Ann. Surg. 245(6):923–30

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 80.

  Menezes-Filho SL , Amigo I , Prado FM , Ferreira NC , Koike MK , et al. 2017. Caloric restriction protects livers from ischemia/reperfusion damage by preventing Ca²⁺-induced mitochondrial permeability transition. Free Radic. Biol. Med. 110:219–27

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 81.

  Milanese C , Bombardieri CR , Sepe S , Barnhoorn S , Payán-Goméz C , et al. 2019. DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering. Nat. Commun. 10:4887

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 82.

  Mitchell JR , Verweij M , Brand K , van de Ven M , Goemaere N , et al. 2010. Short-term dietary restriction and fasting precondition against ischemia reperfusion injury in mice. Aging Cell 9(1):40–53

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 83.

  Morselli E , Maiuri MC , Markaki M , Megalou E , Pasparaki A , et al. 2010. Caloric restriction and resveratrol promote longevity through the Sirtuin-1-dependent induction of autophagy. Cell Death Dis. 1:e10

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 84.

  More AR articles citing this reference

  • Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism

    William A. Beard, Julie K. Horton, Rajendra Prasad, and Samuel H. WilsonGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Science, National Institutes of Health, Research Triangle Park, North Carolina 27709-2233, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 88: 137 - 162

    • ...and it accumulates at surprisingly high steady-state levels (50,000–200,000 AP-sites per mammalian cell) in several mammalian tissues (14, 15)....

  • Determinants of Mutation Rate Variation in the Human Germline

    Laure Ségurel, ^1, Minyoung J. Wyman, ^2, and Molly Przeworski ^{3, 1}Laboratoire Éco-Anthropologie et Ethnobiologie, UMR 7206, Muséum National d'Histoire Naturelle–Centre National de la Recherche Scientifique–Université Paris 7 Diderot, Paris 75231, France; email: [email protected] ²Department of Biological Sciences, Columbia University, New York, NY 10027; email: [email protected] ³Department of Human Genetics and Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois 60637; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 15: 47 - 70

    • ...which are created by endogenous lesions (113) and are constantly being repaired in a manner dependent on the source of the DNA damage....

  • Flap Endonuclease 1

    Lata Balakrishnan ¹ and Robert A. Bambara ^{2 1}Department of Biochemistry and Biophysics and²Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 82: 119 - 138

    • ...By-products of metabolism in the form of reactive oxygen species modify mammalian DNA structure at a very high rate, producing 1,000 to 100,000 lesions per cell per day (51, 52, 53)....

• 85.

  More AR articles citing this reference

  • Checkpoint Responses to DNA Double-Strand Breaks

    David P. Waterman, ¹ James E. Haber, ^1, and Marcus B. Smolka ^{2, 1}Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA; email: [email protected] ²Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, New York 14853, USA; email: [email protected]

    Annual Review of Biochemistry Vol. 89: 103 - 133

    • ...Mutations in DDC genes such as ATM and TP53 are a central factor in contributing to genomic instability seen in tumors because they allow for the accumulation of more mutations over many cell generations (220, 221)....

  • Cancer Treatment in the Genomic Era

    Gary J. Doherty, ¹ Michele Petruzzelli, ^1,2, Emma Beddowes, ^1,3, Saif S. Ahmad, ^1,2,3, Carlos Caldas, ^1,3 and Richard J. Gilbertson ^{1,3 1}Department of Oncology, Addenbrooke's Hospital, Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge CB2 0QQ, United Kingdom; email: [email protected], [email protected] ²Medical Research Council (MRC) Cancer Unit, University of Cambridge, Cambridge CB2 0XZ, United Kingdom³Cancer Research United Kingdom Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, United Kingdom

    Annual Review of Biochemistry Vol. 88: 247 - 280

    • ...Large aberrant genomic amplifications and deletions can be caused by DNA replication stress, via the slowing or collapsing of replication forks (121)....

  • Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging

    Lei Zhang and Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email: [email protected]

    Annual Review of Genetics Vol. 52: 397 - 419

    • ...DNA mutations represent the phenomenon of genome instability, generally considered a hallmark of disease, such as cancer (98), ...

  • Mechanisms and Consequences of Cancer Genome Instability: Lessons from Genome Sequencing Studies

    June-Koo Lee, ¹ Yoon-La Choi, ^2,3 Mijung Kwon, ^4,5 and Peter J. Park ^{6 1}Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, South Korea; email: [email protected] ²Department of Pathology and Translational Genomics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, South Korea³Department of Health Sciences and Technology, Samsung Advanced Institute of Health Sciences and Technology (SAIHST), Sungkyunkwan University School of Medicine, Seoul 06351, South Korea; email: [email protected] ⁴Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115⁵Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115; email: [email protected] ⁶Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 11: 283 - 312

    • ... and what the underlying biological mechanisms are for this instability (4)....
    • ... KRAS and CCND1) or inactivation of tumor suppressor genes (e.g., RB1 and APC) (4)....

  • Genetics and Epigenetics of Human Retinoblastoma

    Claudia A. Benavente ¹ and Michael A. Dyer ^{1,2 1}Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105; email: [email protected] ²Howard Hughes Medical Institute, Chevy Chase, Maryland 20815

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 547 - 562

    • ...and CIN is an important hallmark of many of the most aggressive forms of sporadic human cancers (10)....

  • DNA Replication Stress as a Hallmark of Cancer

    Morgane Macheret and Thanos D. HalazonetisDepartment of Molecular Biology, University of Geneva, 1205 Geneva, Switzerland; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 10: 425 - 448

    • ...We have argued in the past that these two hallmarks are in fact two sides of the same coin (26)....
    • ...It appears that almost all cancers have genomic instability (5, 26, 34–36), defined as a higher rate of acquisition of genomic changes per cell division compared to normal cells....
    • ...but such mutations are not common in sporadic human cancers (26)....

  • Cellular Heterogeneity and Molecular Evolution in Cancer

    Vanessa Almendro, ^1,2 Andriy Marusyk, ¹ and Kornelia Polyak ^{1 1}Department of Medical Oncology, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215; email: [email protected], [email protected], [email protected] ²Department of Medical Oncology, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, 08036 Barcelona, Spain

    Annual Review of Pathology: Mechanisms of Disease Vol. 8: 277 - 302

    • ...; increased genetic instability is considered one of the so-called hallmarks of cancer (25, 26)....

  • The Fluid Mechanics of Cancer and Its Therapy

    Petros Koumoutsakos, ¹ Igor Pivkin, ² and Florian Milde ^{1 1}Computational Science and Engineering Laboratory, ETH Zürich, CH-8092 Zürich, Switzerland; email: [email protected] ²Institute of Computational Science, Universitá della Svizzera Italiana, CH-6900 Lugano, Switzerland

    Annual Review of Fluid Mechanics Vol. 45: 325 - 355

    • ...the rate of mutations increases as the genomic maintenance machinery breaks down (Negrini et al. 2010, Salk et al. 2010)....

  • The Causes and Consequences of Polyploidy in Normal Development and Cancer

    Teresa Davoli and Titia de LangeLaboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10065; email: [email protected]

    Annual Review of Cell and Developmental Biology Vol. 27: 585 - 610

    • ...which has been proposed to occur in many early neoplastic lesions (see for a review Negrini et al. 2010)....

• 86.

  Ness K , Howell C , Bjornard K . 2017. Frailty and quality of life in adult survivors of childhood cancer. Expert Rev. Qual. Life Cancer Care 2(2):79–85

  • Crossref
  • Medline
  • Google Scholar

• 87.

  Ness K , Kirkland JL , Gramatges MM , Wang Z , Kundu M , et al. 2018. Premature physiologic aging as a paradigm for understanding increased risk of adverse health across the lifespan of survivors of childhood cancer. J. Clin. Oncol. 36(21):2206–15

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 88.

• 89.

  Niedernhofer LJ , Garinis GA , Raams A , Lalai AS , Robinson AR , et al. 2006. A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis. Nature 444(7122):1038–43

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Nuclear Genomic Instability and Aging

    Laura J. Niedernhofer, ¹ Aditi U. Gurkar, ^1,2 Yinsheng Wang, ³ Jan Vijg, ⁴ Jan H.J. Hoeijmakers, ⁵ and Paul D. Robbins ^{1 1}Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA; email: [email protected] ²Department of Medicine, Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA³Department of Chemistry, University of California, Riverside, California 92521, USA⁴Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, Bronx, New York 10461, USA⁵Department of Molecular Genetics, Erasmus University Medical Center, 3015 CE Rotterdam, The Netherlands

    Annual Review of Biochemistry Vol. 87: 295 - 322

    • ...cardiovascular, hepatobiliary, urogenital, hematopoietic, and central and peripheral nervous systems (3)....
    • ...we know that reduced expression of the repair endonuclease ERCC1-XPF causes accelerated aging (3), ...
    • ...in murine models of genome instability disorders with accelerated aging, serum IGF-1 is low, yet cellular senescence is increased (3)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...Yet another severe DNA repair disorder is associated with mutations in the NER endonuclease complex XPF-ERCC1, named the XpF-Ercc1 (XFE) progeroid syndrome (55)....
    • ...TTD, and XFE premature aging phenotypes have been well described (55, 57...
    • ... Ercc1 knockout mice display numerous age-related pathologies and have a very short life span (a few weeks) (55)....
    • ...Hoeijmakers, unpublished results) (55, 61, 63–86)....
    • ...Hoeijmakers, unpublished results) (55, 87–91)....
    • ...have been shown to induce distinct gene expression changes that are highly similar to naturally aged organs (55, 60, 104)....
    • ...Hoeijmakers, unpublished results) (55, 85, 87, 104, 106)....

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...transcriptional profiling in the liver of ERCC1-deficient mice at postnatal day 15 shows attenuation of the IGF-1 axis (75)....

  • Genome Instability and Aging

    Jan Vijg ¹ and Yousin Suh ^{1,2 1}Department of Genetics, Albert Einstein College of Medicine, New York, NY 10461; email: [email protected], [email protected] ²Aging Research Institute, Guangdong Medical College, Dongguan 523808, Guangdong, China

    Annual Review of Physiology Vol. 75: 645 - 668

    • ...with progressive liver and kidney dysfunction, cachexia, hypertension, neuronal degeneration, and skin atrophy (101)....

  • Structural and Functional Relationships of the XPF/MUS81 Family of Proteins

    Alberto Ciccia, ^1,3 Neil McDonald, ^1,2 and Stephen C. West ^{1 1}London Research Institute, Cancer Research UK, Clare Hall Laboratories, Hertfordshire EN6 3LD, United Kingdom; email: [email protected] ²School of Crystallography, Birkbeck College, London WC1E 7HX, United Kingdom³Present address: Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Biochemistry Vol. 77: 259 - 287

    • ...known as XFE, is caused by a mutation within XPF (73)....
    • ...cerebral atrophy, visual and hearing loss, anemia, and liver dysfunction (73, 74)....
    • ...displayed a decrease in the levels of insulin-like growth factor 1 (IGF-1) (73)....
    • ...it is thought that the persistent accumulation of DNA damage could induce accelerated aging (73)....

  • The Aging Brain

    Bruce A. Yankner, Tao Lu, and Patrick LoerchDepartment of Pathology, Harvard Medical School, Boston, Massachusetts 02115; email: [email protected]

    Annual Review of Pathology: Mechanisms of Disease Vol. 3: 41 - 66

    • ...suggesting that this type of DNA damage may contribute to the aging process (51)....

• 90.

  Niedernhofer LJ , Gurkar AU , Wang Y , Vijg J , Hoeijmakers JHJ , Robbins PD . 2018. Nuclear genomic instability and aging. Annu. Rev. Biochem. 87:295–322

  • Link
  • Web of Science ®
  • Google Scholar

• 91.

  Niedernhofer LJ , Odijk H , Budzowska M , van Drunen E , Maas A , et al. 2004. The structure-specific endonuclease Ercc1-Xpf is required to resolve DNA interstrand cross-link-induced double-strand breaks. Mol. Cell. Biol. 24(13):5776–87

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • How the Fanconi Anemia Pathway Guards the Genome

    George-Lucian Moldovan and Alan D. D'AndreaDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215; email: [email protected]

    Annual Review of Genetics Vol. 43: 223 - 249

    • ...Once the same strand is cleaved on the other side of the lesion (102), ...
    • ...given that cells deleted of these factors are exquisitely (the former) or moderately (the latter) sensitive to crosslinking agents (58, 70, 81, 102, 117)....

  • Structural and Functional Relationships of the XPF/MUS81 Family of Proteins

    Alberto Ciccia, ^1,3 Neil McDonald, ^1,2 and Stephen C. West ^{1 1}London Research Institute, Cancer Research UK, Clare Hall Laboratories, Hertfordshire EN6 3LD, United Kingdom; email: [email protected] ²School of Crystallography, Birkbeck College, London WC1E 7HX, United Kingdom³Present address: Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Biochemistry Vol. 77: 259 - 287

    • ...it now appears that ICL-induced DSBs are generated in the absence of XPF or ERCC1 (145, 150)....
    • ...cell lines defective for XPF or ERCC1 are hypersensitive to cross-linking agents and defective in the repair of ICL-induced DSBs (146, 150, 152)....

• 92.

  Osborne TB , Mendel LB , Ferry EL . 1917. The effect of retardation of growth upon the breeding period and duration of life of rats. Science 45(1160):294–95

  • Crossref
  • Medline
  • Google Scholar

• 93.

  Pang B , Qiao X , Janssen L , Velds A , Groothuis T , et al. 2013. Drug-induced histone eviction from open chromatin contributes to the chemotherapeutic effects of doxorubicin. Nat. Commun. 4:1908

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 94.

  Pifferi F , Terrien J , Marchal J , Dal-Pan A , Djelti F , et al. 2018. Caloric restriction increases lifespan but affects brain integrity in grey mouse lemur primates. Commun. Biol. 1:30

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 95.

  Prado CMM , Baracos VE , McCargar LJ , Reiman T , Mourtzakis M , et al. 2009. Sarcopenia as a determinant of chemotherapy toxicity and time to tumor progression in metastatic breast cancer patients receiving capecitabine treatment. Clin. Cancer Res. 15(8):2920–26

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span

    Paul D. Robbins, ¹ Diana Jurk, ² Sundeep Khosla, ² James L. Kirkland, ² Nathan K. LeBrasseur, ² Jordan D. Miller, ² João F. Passos, ² Robert J. Pignolo, ² Tamar Tchkonia, ² and Laura J. Niedernhofer ^{1 1}Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA; email: [email protected] ²Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA

    Annual Review of Pharmacology and Toxicology Vol. 61: 779 - 803

    • ...Older persons with low muscle mass experience higher rates of surgical complications and infections (48), delayed recovery (49), chemotherapy toxicity (50), ...

  • Muscle Wasting in Cancer Cachexia: Clinical Implications, Diagnosis, and Emerging Treatment Strategies

    Shontelle Dodson, ¹ Vickie E. Baracos, ² Aminah Jatoi, ³ William J. Evans, ⁴ David Cella, ⁵ James T. Dalton, ¹ and Mitchell S. Steiner ^{1 1}GTx, Inc., Memphis, Tennessee 38103-2802;²Department of Oncology, University of Alberta Cross Cancer Institute, Edmonton, Alberta, Canada;³Department of Oncology, Mayo Clinic, Rochester, Minnesota 55905;⁴Muscle Metabolism Discovery Performance Unit, GlaxoSmithKline, Research Triangle Park, North Carolina 27709;⁵Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, Illinois 60611; email: [email protected]

    Annual Review of Medicine Vol. 62: 265 - 279

    • ...has also been cited as a predictor of poor treatment outcomes, increased toxicity in patients receiving chemotherapy, and mortality (2, 11, 12)....
    • ...respectively; p = 0.03) and a significantly shorter time to tumor progression (101.4 versus 173.3 days; p = 0.05) (11)....

• 96.

  Raffaghello L , Lee C , Safdie FM , Wei M , Madia F , et al. 2008. Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy. PNAS 105(24):8215–20

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...Studies that have looked at the impact of fasting on the growth of implanted cancer cells in mice have found beneficial effects in some models (15, 23, 91, 96, 104, 145, 164) but not in others (21, 36, 85, 91, 96, 134, 168), ...
    • ...Fasting has been shown to protect mice from toxicity induced by etoposide (134), ...
    • ...A primary hypothesis on how fasting, and potentially caloric restriction, works is termed differential stress (134)....

• 97.

  Reeves JG , Suriawinata AA , Ng DP , Holubar SD , Mills JB , Barth RJ . 2013. Short-term preoperative diet modification reduces steatosis and blood loss in patients undergoing liver resection. Surgery 154(5):1031–37

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 98.

• 99.

• 100.

  Safdie FM , Dorff T , Quinn D , Fontana L , Wei M , et al. 2009. Fasting and cancer treatment in humans: a case series report. Aging 1(12):988–1007

  • Crossref
  • Medline
  • Google Scholar

  More AR articles citing this reference

  • The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

    Steven D. MittelmanDivision of Pediatric Endocrinology, University of California, Los Angeles (UCLA), Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA; email: [email protected]

    Annual Review of Nutrition Vol. 40: 273 - 297

    • ...A case series by Safdie et al. (144) demonstrated that complete fasting, ...

• 101.

  Schuitema I , Deprez S , Van Hecke W , Daams M , Uyttebroeck A , et al. 2013. Accelerated aging, decreased white matter integrity, and associated neuropsychological dysfunction 25 years after pediatric lymphoid malignancies. J. Clin. Oncol. 31(27):3378–88

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

• 102.

  Schumacher B , Van Der Pluijm I , Moorhouse MJ , Kosteas T , Robinson AR , et al. 2008. Delayed and accelerated aging share common longevity assurance mechanisms. PLOS Genet. 4(8):e1000161

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], j.ho[email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...Hoeijmakers, unpublished results) (55, 87–91)....
    • ...Hoeijmakers, unpublished results) (55, 85, 87, 104, 106)....
    • ...which is a hallmark of many progeroid syndromes and corresponding mouse models (87)....

• 103.

  Shinmura K , Tamaki K , Bolli R . 2005. Short-term caloric restriction improves ischemic tolerance independent of opening of ATP-sensitive K⁺ channels in both young and aged hearts. J. Mol. Cell. Cardiol. 39(2):285–96

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 104.

• 105.

  Smitherman AB , Anderson C , Lund JL , Bensen JT , Rosenstein DL , Nichols HB . 2018. Frailty and comorbidities among survivors of adolescent and young adult cancer: a cross-sectional examination of a hospital-based survivorship cohort. J. Adolesc. Young Adult Oncol. 7(3):374–83

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 106.

• 107.

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...is the only robust universal intervention with widespread documented longevity- and health-promoting effects in numerous species (117)....

  • Metabolic and Neuropsychiatric Effects of Calorie Restriction and Sirtuins

    Sergiy Libert and Leonard GuarenteGlenn Laboratory for the Science of Aging, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected]

    Annual Review of Physiology Vol. 75: 669 - 684

    • ...Decreases in the circulating levels of this hormone not only may negatively impact quality of life due to decreased sex drive (110) but also may result in more severe problems such as loss of muscle mass and loss of bone density....

• 108.

  Swenberg JA , Lu K , Moeller BC , Gao L , Upton PB , et al. 2011. Endogenous versus exogenous DNA adducts: their role in carcinogenesis, epidemiology, and risk assessment. Toxicol. Sci. 120(Suppl. 1):S130–45

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Nucleotide Excision Repair and Transcriptional Regulation: TFIIH and Beyond

    Emmanuel Compe and Jean-Marc EglyInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/Université de Strasbourg, 67404 Illkirch Cedex, Commune Urbaine Strasbourg, France; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 85: 265 - 290

    • ...Damage loads may amount to 10⁴–10⁵ DNA lesions per mammalian cell per day (90)....

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...and advanced glycation end products from glycolysis, lipid peroxidation products, methyl donors, etc. (93, 94)....

• 109.

  Tan-Shalaby JL , Carrick J , Edinger K , Genovese D , Liman AD , et al. 2016. Modified Atkins diet in advanced malignancies: final results of a safety and feasibility trial within the Veterans Affairs Pittsburgh Healthcare System. Nutr. Metab. 13:52

  • Crossref
  • Web of Science ®
  • Google Scholar

• 110.

  More AR articles citing this reference

  • Preventing and Treating Anthracycline Cardiotoxicity: New Insights

    Konrad Teodor Sawicki, ¹ Valentina Sala, ² Lorenzo Prever, ² Emilio Hirsch, ² Hossein Ardehali, ¹ and Alessandra Ghigo ^{2 1}Division of Cardiology, Feinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA; email: [email protected] ²Department of Molecular Biotechnology and Health Sciences, University of Torino, 10126 Torino, Italy; email: [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 61: 309 - 332

    • ...Anthracyclines exert cytotoxic effects by intercalating DNA through complexes with DNA topoisomerases to promote DNA cleavage (89)....

• 111.

  More AR articles citing this reference

• 112.

  Van Der Pluijm I , Garinis GA , Brandt RMC , Gorgels TGMF , Wijnhoven SW , et al. 2006. Impaired genome maintenance suppresses the growth hormone–insulin-like growth factor 1 axis in mice with cockayne syndrome. PLOS Biol. 5(1):e2

  • Crossref
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...TTD, and XFE premature aging phenotypes have been well described (55, 57...
    • ...have been shown to induce distinct gene expression changes that are highly similar to naturally aged organs (55, 60, 104)....

  • Animal Models of Aging Research: Implications for Human Aging and Age-Related Diseases

    Sarah J. Mitchell, ^1, Morten Scheibye-Knudsen, ^2, Dan L. Longo, ³ and Rafael de Cabo ^{1 1}Translational Gerontology Branch,²Laboratory of Molecular Gerontology, and³Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; email: [email protected]; [email protected]; [email protected]; [email protected]

    Annual Review of Animal Biosciences Vol. 3: 283 - 303

    • ...the same transcriptional changes are observed in Xpa ^−/−/Csa ^−/− double-knockout mice (76)....

• 113.

  Van Nieuwenhove Y , Dambrauskas Z , Campillo-Soto A , Van Dielen F , Wiezer R , et al. 2011. Preoperative very low-calorie diet and operative outcome after laparoscopic gastric bypass: a randomized multicenter study. Arch. Surg. 146(11):1300–5

  • Crossref
  • Medline
  • Google Scholar

• 114.

• 115.

  Vauthey JN , Pawlik TM , Ribero D , Wu TT , Zorzi D , et al. 2006. Chemotherapy regimen predicts steatohepatitis and an increase in 90-day mortality after surgery for hepatic colorectal metastases. J. Clin. Oncol. 24(13):2065–72

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Resection of Liver Metastases in Colorectal Cancer in the Era of Expanding Systemic Therapy

    Robert P. Jones ^1,2 and Graeme J. Poston ^{1 1}North Western Hepatobiliary Unit, Aintree University Hospital, Liverpool L9 7AL, United Kingdom; email: [email protected] ²School of Cancer Studies, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, United Kingdom; email: gra[email protected]

    Annual Review of Medicine Vol. 68: 183 - 196

    • ...which is known to be associated with increased 90-day postoperative mortality (57)....

• 116.

  Vermeij WP , Dollé MET , Reiling E , Jaarsma D , Payan-Gomez C , et al. 2016a. Restricted diet delays accelerated ageing and genomic stress in DNA-repair-deficient mice. Nature 537(7620):427–31

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Aging in a Dish: iPSC-Derived and Directly Induced Neurons for Studying Brain Aging and Age-Related Neurodegenerative Diseases

    Jerome Mertens, ^1,2 Dylan Reid, ¹ Shong Lau, ¹ Yongsung Kim, ¹ and Fred H. Gage ^{1 1}Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA; email: [email protected] ²Department of Genomics, Stem Cell Biology and Regenerative Medicine, Institute of Molecular Biology, and Center for Molecular Biosciences Innsbruck, University of Innsbruck, A-6020 Innsbruck, Austria

    Annual Review of Genetics Vol. 52: 271 - 293

    • ...resulting in decreased transcriptional output and a shift in cellular metabolism to maintain cell viability (55, 141)....
    • ...leading to decreased function of these cells but greater longevity (141)....

• 117.

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...and the deficient repair process determines which organs and tissue are affected most (62)....
    • ...some DNA lesions are difficult to repair, which leads to persistent DDR signaling (62)....

• 118.

  Vermeij WP , Hoeijmakers JHJ , Pothof J . 2016b. Genome integrity in aging: human syndromes, mouse models, and therapeutic options. Annu. Rev. Pharmacol. Toxicol. 56:427–45

  • Link
  • Web of Science ®
  • Google Scholar

• 119.

  Vermeulen W , Rademakers S , Jaspers NGJ , Appeldoorn E , Raams A , et al. 2001. A temperature-sensitive disorder in basal transcription and DNA repair in humans. Nat. Genet. 27(3):299–303

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • DISEASE GENE DISCOVERY THROUGH INTEGRATIVE GENOMICS

    Cosmas Giallourakis, ^1,2 Charlotte Henson, ¹ Michael Reich, ¹ Xiaohui Xie, and ¹ Vamsi K. Mootha ^{1,3,4 1}Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02139;²Gastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts 02114;³Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02446;⁴Center for Human Genetics Research, Massachusetts General Hospital, Boston, Massachusetts 02114; email: [email protected]

    Annual Review of Genomics and Human Genetics Vol. 6: 381 - 406

    • ...had been identified in three families in whom the TFIIH complex exhibited biochemical instability; however, none of the previously known components were mutated (112)....

• 120.

  Verweij M , Van Ginhoven TM , Mitchell JR , Sluiter W , Van Den Engel S , et al. 2011. Preoperative fasting protects mice against hepatic ischemia/reperfusion injury: mechanisms and effects on liver regeneration. Liver Transplant. 17(6):695–704

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 121.

• 122.

  Wan R , Ahmet I , Brown M , Cheng A , Kamimura N , et al. 2010. Cardioprotective effect of intermittent fasting is associated with an elevation of adiponectin levels in rats. J. Nutr. Biochem. 21(5):413–17

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 123.

  Weeda G , Donker I , De Wit J , Morreau H , Janssens R , et al. 1997. Disruption of mouse ERCC1 results in a novel repair syndrome with growth failure, nuclear abnormalities and senescence. Curr. Biol. 7(6):427–39

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Genome Integrity in Aging: Human Syndromes, Mouse Models, and Therapeutic Options

    Wilbert P. Vermeij, Jan H.J. Hoeijmakers, and Joris PothofDepartment of Genetics, Erasmus University Medical Center, Postbus 2040, 3000 CA, Rotterdam, The Netherlands; email: [email protected], [email protected], [email protected]

    Annual Review of Pharmacology and Toxicology Vol. 56: 427 - 445

    • ...Hoeijmakers, unpublished results) (55, 61, 63–86)....

  • Structural and Functional Relationships of the XPF/MUS81 Family of Proteins

    Alberto Ciccia, ^1,3 Neil McDonald, ^1,2 and Stephen C. West ^{1 1}London Research Institute, Cancer Research UK, Clare Hall Laboratories, Hertfordshire EN6 3LD, United Kingdom; email: [email protected] ²School of Crystallography, Birkbeck College, London WC1E 7HX, United Kingdom³Present address: Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115

    Annual Review of Biochemistry Vol. 77: 259 - 287

    • ...reduction of the number of hematopoietic progenitors, neuronal degeneration, and skin atrophy (71, 72)....

  • DNA Repair Defects in Stem Cell Function and Aging

    Youngji Park ¹ and Stanton L. Gerson ^{2 1,2} Division of Hematology and Oncology, ² Comprehensive Cancer Center and Center for Stem Cell Regenerative Medicine, ^1,2 University Hospitals of Cleveland and Case Western Reserve University, Cleveland, Ohio 44106-4937; email: [email protected], [email protected]

    Annual Review of Medicine Vol. 56: 495 - 508

    • ...They have growth failure, nuclear abnormalities, and senescence, which mimic premature aging (72, 73), ...

• 124.

  Wei M , Brandhorst S , Shelehchi M , Mirzaei H , Cheng CW , et al. 2017. Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease. Sci. Transl. Med. 9(377):eaai8700

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Designing Relevant Preclinical Rodent Models for Studying Links Between Nutrition, Obesity, Metabolism, and Cancer

    Elaine M. Glenny, ¹ Michael F. Coleman, ¹ Erin D. Giles, ² Elizabeth A. Wellberg, ³ and Stephen D. Hursting ^{1,4,5 1}Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; email: [email protected] ²Department of Nutrition, Texas A&M University, College Station, Texas 77843, USA³Department of Pathology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA⁴Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA⁵Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina 28081, USA

    Annual Review of Nutrition Vol. 41: 253 - 282

    • ...People adhering to a FMD reduce caloric intake into a range of 300–1,000 calories per day by consuming foods and beverages that are low in carbohydrates and proteins but high in unsaturated fats (205)....

• 125.

  More AR articles citing this reference

  • Conserved and Tissue-Specific Genic and Physiologic Responses to Caloric Restriction and Altered IGFI Signaling in Mitotic and Postmitotic Tissues

    Stephen R. Spindler ¹ and Joseph M. Dhahbi ^{2 1}Department of Biochemistry, University of California, Riverside, California 92521; email: [email protected] ²Children's Hospital Oakland Research Institute, Oakland, California 94609; email: [email protected]

    Annual Review of Nutrition Vol. 27: 193 - 217

    • ...the sum of these effects appears to produce higher rates of protein turnover and smaller visceral organ sizes (132)....
    • ...prostate, and skeletal muscle of rats by 25% to 50% (132)....

  • ENERGY INTAKE, MEAL FREQUENCY, AND HEALTH: A Neurobiological Perspective

    Mark P. MattsonLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; email: [email protected]

    Annual Review of Nutrition Vol. 25: 237 - 260

    • ...The ability of caloric restriction (CR) during adult life to lengthen life span has been observed consistently in many different species of mammals (134)....
    • ...Both the amount of the energy restriction and the duration of restriction period influence the extent to which life span is increased (134)....
    • ...Both mean and maximum life spans are increased by EODF in different species and in most (but not all) strains of rodents (134)....
    • ...CR reduces body weight and retards body weight gain in adults of all species of organisms (134)....
    • ...reduced-meal-frequency diets has been collected from studies of rodents, monkeys, and humans (56, 82, 134)....
    • ...and 134 are review articles that include references to the relevant primary studies....
    • ...One mechanism involves the production and removal of free radicals, and the second involves stress resistance (84, 93, 134)....

• 126.

  Weindruch R , Walford RL , Fligiel S , Guthrie D . 1986. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. J. Nutr. 116(4):641–54

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

  More AR articles citing this reference

  • Hormesis Mediates Acquired Resilience: Using Plant-Derived Chemicals to Enhance Health

    Edward J. CalabreseDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, Massachusetts 01003, USA; email: [email protected]

    Annual Review of Food Science and Technology Vol. 12: 355 - 381

    • ...employing a wide range of mouse and rat genotypes (Weindruch et al. 1986, Weindruch & Walford 1982)....
    • ...and significant findings of caloric-restriction research generated profound interest in the 1980s (Masoro 2010, McDonald & Ramsey 2010, Weindruch et al. 1986, Weindruch & Walford 1982)....

  • Metabolic and Neuropsychiatric Effects of Calorie Restriction and Sirtuins

    Sergiy Libert and Leonard GuarenteGlenn Laboratory for the Science of Aging, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; email: [email protected]

    Annual Review of Physiology Vol. 75: 669 - 684

    • ...CR lowers body temperature in mice (26), rats, rhesus monkeys (27), and humans (28)...

  • Aging and Survival: The Genetics of Life Span Extension by Dietary Restriction

    William Mair and Andrew DillinThe Salk Institute for Biological Studies, La Jolla, California 92037; email: [email protected], [email protected]

    Annual Review of Biochemistry Vol. 77: 727 - 754

    • ...progressive reduction in food intake also results in incremental increases in life span extension (24), ...

  • Insulin-Like Signaling, Nutrient Homeostasis, and Life Span

    Akiko Taguchi and Morris F. WhiteHoward Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Karp Family Research Laboratories, Boston, Massachusetts 02115; email: [email protected]

    Annual Review of Physiology Vol. 70: 191 - 212

    • ...calorie restriction with adequate nutrition reliably increases animal longevity (4, 8, 9); second, ...

  • Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans

    Stephen D. Hursting,^1,2,4 Jackie A. Lavigne,^1,2 David Berrigan,^1,2,3 Susan N. Perkins,^1,2 and J. Carl Barrett^{1 1}Laboratory of Biosystems and Cancer, Center for Cancer Research; National Cancer Institute, Bethesda, Maryland 20892; e-mail: [email protected] ²Cancer Prevention Fellowship Program, Division of Cancer Prevention; National Cancer Institute, Bethesda, Maryland 20892; ³Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland 20892;

    Annual Review of Medicine Vol. 54: 131 - 152

    • ...The other studies used C3B10RF1 mice (120); Sprague-Dawley rats (121); Fischer 344 rats (122)...

• 127.

  Yip C , Dinkel C , Mahajan A , Siddique M , Cook GJR , Goh V . 2015. Imaging body composition in cancer patients: visceral obesity, sarcopenia and sarcopenic obesity may impact on clinical outcome. Insights Imaging 6(4):489–97

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

• 128.

  Zahra A , Fath MA , Opat E , Mapuskar KA , Bhatia SK , et al. 2017. Consuming a ketogenic diet while receiving radiation and chemotherapy for locally advanced lung cancer and pancreatic cancer: the University of Iowa Experience of Two phase 1 clinical trials. Radiat. Res. 187(6):743–54

  • Crossref
  • Medline
  • Web of Science ®
  • Google Scholar

University of Chicago Brain Tumors Overcoming Plant Based Diet

Source: https://www.annualreviews.org/doi/10.1146/annurev-cancerbio-060820-090737

Share :