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• W2169131719 abstract "Future OncologyVol. 10, No. 16 EditorialFree AccessWhat benefits could caloric restriction bring to cancer patients?Tu D Dan, Christopher M Wright & Nicole L SimoneTu D Dan Department of Radiation Oncology, Kimmel Cancer Center, Jefferson Medical College, Thomas Jefferson University, 1020 Walnut Street, Philadelphia, PA 19107, USASearch for more papers by this author, Christopher M Wright Department of Radiation Oncology, Kimmel Cancer Center, Jefferson Medical College, Thomas Jefferson University, 1020 Walnut Street, Philadelphia, PA 19107, USASearch for more papers by this author & Nicole L Simone*Author for correspondence: E-mail Address: nicole.simone@jefferson.edu Department of Radiation Oncology, Kimmel Cancer Center, Jefferson Medical College, Thomas Jefferson University, 1020 Walnut Street, Philadelphia, PA 19107, USASearch for more papers by this authorPublished Online:22 Dec 2014https://doi.org/10.2217/fon.14.241AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInRedditEmail Keywords: caloric restrictioncancer dietcancer obesitydiet radiationdietary restrictionCaloric restriction (CR) – reducing food intake by approximately 30% – is thought to lessen age-related changes, decrease oxidative stress and extend lifespan in mammals [1]. Since the seminal findings of McCay and colleagues, there has been a growing interest in applying CR as an adjunct in a variety of conditions, including longevity, cardiovascular disease, chronic inflammatory conditions and more recently, cancer [2,3]. As global rates of obesity have continued to soar, there is increasing evidence suggesting a link between dysregulated metabolic pathways and carcinogenesis. In a recent landmark study, a direct linear effect of weight on cancer development was observed in several common malignancies [4]. Furthermore, there is compelling evidence that not only is obesity implicated in cancer development, but it may also be a key driver of cancer progression and recurrence.Due to the number of overlapping pathways involved in metabolism and cancer, utilization of CR may have a number of benefits in the cancer patient. At the molecular level, CR is thought to exert its effects by targeting growth factor regulated proliferation pathways, including insulin-dependent pathways that are dysfunctional in both obesity and cancer development [5]. In this paper, we will discuss the clinical applications of CR and the settings it may be most beneficial to the cancer patient, including its utilization in prevention, as a complement to existing therapies, and in survivorship.PreventionSince Moreschi initially demonstrated the antitumorigenic properties of CR in rodents over a century ago, the link between diet and carcinogenesis has been explored [6]. Reduced caloric intake in experimental animal models has been repeatedly shown to be one of the most effective ways of decreasing spontaneous mammary tumors. A 14-study meta-analysis of the effect of CR on the spontaneous formation of mammary tumors in mice revealed that CR decreased tumor incidence by more than half [7]. Similarly, a growing body of evidence seems to demonstrate this effect in humans. A retrospective cohort study of over 7000 women with history of anorexia nervosa and low BMI demonstrated a comparable 50% reduction in the incidence of breast cancer, suggesting severe CR in humans may confer protection from invasive breast cancer [8]. Correspondingly, excess caloric intake has been directly associated with an increase in the incidence of cancer in a number of studies. In one of the largest population-based studies covering almost 1/10th of the UK population, a linear link between BMI and cancer incidence was found. In this study, a 5 kg/m2 increase in BMI was linearly correlated with increasing incidence of cancers of the uterus, gallbladder, kidney, cervix, thyroid and bone marrow.The molecular underpinnings regarding the role of CR in cancer prevention remain under investigation. It is thought that CR may confer an advantageous molecular phenotype that inhibits carcinogenesis. Through alteration of driver hormone and growth factors, CR leads to an increase in apoptosis and a decrease in cellular proliferation and angiogenesis [9]. In particular, IGF-1 pathways have been found to be significantly downregulated in calorically restricted mice. Downstream targets of the IGF-1 receptor such as PI3K and Ras G-protein are thought to be reduced in response to CR, leading to an increase in cell-cycle arrest and apoptosis [10]. Additionally, CR is associated with a significant anti-inflammatory response and may inhibit neoplastic progression and malignant conversion by blunting chronic inflammatory states [11]. In human studies, the combination of exercise and implementation of CR led to a reduction in various inflammatory biomarkers, including high-sensitivity C-reactive protein, IL-6 and serum amyloid A [12].TreatmentMore recently, CR is being increasingly utilized as a novel complement to standard cancer therapies and as an aid to help reduce treatment-related morbidity. A growing body of evidence has begun to demonstrate the benefits of using concurrent diet modification to enhance cancer treatment. Previous data from our laboratory have demonstrated that in a murine model, CR combined with radiation therapy (RT) aids in tumor regression and delays metastases [13]. Similar to use of metformin, CR is thought to increase the therapeutic ratio by targeting key molecular pathways altered in cancer progression such as IGF1-R, mTOR and AMP-K, therefore rendering cells more susceptible to cytotoxic treatment [14]. CR is an attractive complement to standard therapies due to its nonoverlapping side-effect profile with traditional cytotoxics. In addition, CR may even be useful in mitigating treatment-related chemotherapy toxicity by inducing a differential stress resistance response in normal tissues but preserving cytotoxicity in cancer cells [15].Currently, there are a number of clinical trials investigating the use of CR in conjunction with standard treatments. One particular trial, the CAREFOR study, is currently underway at Thomas Jefferson University investigating the use of CR in patients with stage 0–I breast cancer during surgery and radiation therapy (identifier: NCT01819233) [16]. This pilot trial aims to measure diet adherence over the course of radiation treatment, subsequent weight change, tumor recurrence and metastasis and progression-free survival. Other trials are currently exploring the application of CR in several other disease sites, including head and neck, brain, colorectal and prostate cancers [16].SurvivorshipCR has a number of applications in the survivorship setting. Perhaps its greatest applicability is its role in normalizing BMI and ameliorating metabolic syndromes following treatment. It is well documented that post-treatment weight gain is a negative prognostic factor in a number of cancers. The greatest amount of research in this area has come from the breast cancer literature, where a post-treatment increase in BMI of as little 0.5 kg/m2 has been associated with an increase of breast cancer-related mortality [17]. Similarly, in other hormone-sensitive cancers such as prostate cancer, there is growing evidence that there may be a direct link between increasing BMI and biochemical disease recurrence [18].Mechanisms underlying the role of weight gain in cancer recurrence are likely multifactorial. CR may target multiple pathways related to both metabolic disturbances and cancer recurrence. In breast cancer, CR can potentially decrease circulating hormones that could be drivers of cancer recurrence, such as circulating reproductive steroid hormones [19]. In prostate cancer, it is hypothesized that hyperinsulinemia may be a candidate mediator driving increased biochemical failure [18]. In addition, a number of studies have implicated chronic inflammation as a risk factor for not only cancer development, but also disease recurrence. In women with breast cancer, elevated levels of biomarkers of inflammation following treatment are associated with reduced survival [20]. Similar to the prevention setting, CR may play a role in preventing recurrences by altering the pro-inflammatory milieu, particularly in those involving adipokine pathways [21].Additionally, CR may also be indirectly beneficial by alleviating post-treatment morbidity and minimizing late effects of treatments. One of the most common complications from breast cancer treatment is lymphedema. Development of lymphedema is strongly associated with weight and BMI. Normalizing body mass through CR may not only decrease incidence of lymphedema in breast cancer patients, but also in other cancers where lymph node dissections routinely are performed, such as head and neck and gynecologic cancers.ConclusionCR is an attractive complement to standard approaches in cancer prevention, treatment and survivorship. On the basis of its effects on metabolism alone, CR may be a useful tool in the armamentarium against cancer. Although preclinical research regarding its usefulness in cancer treatment has been known for decades, only in recent years has data emerged in the clinical setting of cancer patients. Currently, there are over 500 studies looking at the impact of diet and cancer registered on ClinicalTrials.gov. As data in this field continue to develop, a greater understanding of the mechanisms of CR will become available and its role in cancer treatment better defined. At the current time, there appears to be ample evidence that the potential benefits of supplementing CR with standard therapies may be well worth its low toxicity profile and may reap benefits across multiple health domains in the cancer patient.Financial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.No writing assistance was utilized in the production of this manuscript.References1 Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. Science 273(5271), 59–63 (1996).Crossref, Medline, CAS, Google Scholar2 McCay CM, Crowell MF, Maynard LA. The effect of retarded growth upon the length of life span and upon the ultimate body size one figure. J. Nutr. 10(1), 63–79 (1935).Crossref, CAS, Google Scholar3 Hursting SD, Smith SM, Lashinger LM, Harvey AE, Perkins SN. Calories and carcinogenesis: lessons learned from 30 years of calorie restriction research. Carcinogenesis 31(1), 83–89 (2010).Crossref, Medline, CAS, Google Scholar4 Bhaskaran K, Douglas I, Forbes H, dos-Santos-Silva I, Leon DA, Smeeth L. Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults. Lancet 384(9945), 755–765 (2014).Crossref, Medline, Google Scholar5 Renehan AG, Frystyk J, Flyvbjerg A. Obesity and cancer risk: the role of the insulin–IGF axis. Trends Endocrinol. Metab. 17(8), 328–336 (2006).Crossref, Medline, CAS, Google Scholar6 Moreschi C. Beziehungen zwischen ernahrung und tumorwachstum. Z. Immunitatsforsch 2, 651–75 (1909).Google Scholar7 Dirx MJM, Zeegers MPA, Dagnelie PC, van den Bogaard T, van den Brandt PA. Energy restriction and the risk of spontaneous mammary tumors in mice: a meta-analysis. Int. J. Cancer 106(5), 766–770 (2003).Crossref, Medline, CAS, Google Scholar8 Michels KB, Ekbom A. CAloric restriction and incidence of breast cancer. JAMA 291(10), 1226–1230 (2004).Crossref, Medline, CAS, Google Scholar9 Ruggeri BA, Klurfeld DM, Kritchevsky D, Furlanetto RW. Caloric restriction and 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth in rats: alterations in circulating insulin, insulin-like growth factors I and II, and epidermal growth factor. Cancer Res. 49(15), 4130–4134 (1989).Medline, CAS, Google Scholar10 Xie L, Jiang Y, Ouyang P et al. Effects of dietary calorie restriction or exercise on the PI3K and Ras signaling pathways in the skin of mice. J. Biol. Chem. 282(38), 28025–28035 (2007).Crossref, Medline, CAS, Google Scholar11 Coussens LM, Werb Z. Inflammation and cancer. Nature 420(6917), 860–867 (2002).Crossref, Medline, CAS, Google Scholar12 Imayama I, Ulrich CM, Alfano CM et al. Effects of a caloric restriction weight loss diet and exercise on inflammatory biomarkers in overweight/obese postmenopausal women: a randomized controlled trial. Cancer Res. 72(9), 2314–2326 (2012).Crossref, Medline, CAS, Google Scholar13 Saleh AD, Simone BA, Palazzo J et al. Caloric restriction augments radiation efficacy in breast cancer. Cell Cycle 12(12), 1955–1963 (2013).Crossref, Medline, CAS, Google Scholar14 Zakikhani M, Dowling R, Fantus IG, Sonenberg N, Pollak M. Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells. Cancer Res. 66(21), 10269–10273 (2006).Crossref, Medline, CAS, Google Scholar15 Raffaghello L, Safdie F, Bianchi G, Dorff T, Fontana L, Longo VD. Fasting and differential chemotherapy protection in patients. Cell Cycle 9(22), 4474–4476 (2010).Crossref, Medline, CAS, Google Scholar16 Thomas Jefferson University; Ladies of Port Richmond. Caloric Restriction in Treating Patients With Stage 0-I Breast Cancer Undergoing Surgery and Radiation Therapy (CAREFOR). In: ClinicalTrials.gov [Internet]. Bethesda (MD): National Library of Medicine (US). http://clinicaltrials.gov/show/NCT01819233.Google Scholar17 Kroenke CH, Chen WY, Rosner B, Holmes MD. Weight, weight gain, and survival after breast cancer diagnosis. J. Clin. Oncol. 23(7), 1370–1378 (2005).Crossref, Medline, Google Scholar18 Ma J, Li H, Giovannucci E et al. Prediagnostic body-mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis. Lancet Oncol. 9(11), 1039–1047 (2008).Crossref, Medline, CAS, Google Scholar19 Rock CL, Flatt SW, Laughlin GA et al. Reproductive steroid hormones and recurrence-free survival in women with a history of breast cancer. Cancer Epidemiol. Biomarkers Prev. 17(3), 614–620 (2008).Crossref, Medline, CAS, Google Scholar20 Pierce BL, Ballard-Barbash R, Bernstein L et al. Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients. J. Clin. Oncol. 27(21), 3437–3444 (2009).Crossref, Medline, CAS, Google Scholar21 Grossmann ME, Ray A, Nkhata KJ et al. Obesity and breast cancer: status of leptin and adiponectin in pathological processes. Cancer Metastasis Rev. 29(4), 641–653 (2010).Crossref, Medline, CAS, Google ScholarFiguresReferencesRelatedDetailsCited ByDietary patterns and the neoplastic‐prone tissue landscape of old age24 October 2020 | Aging and Cancer, Vol. 1, No. 1-4Dietary and pharmacological modification of the insulin/IGF-1 system: exploiting the full repertoire against cancer15 February 2016 | Oncogenesis, Vol. 5, No. 2 Vol. 10, No. 16 eToC Sign up Follow us on social media for the latest updates Metrics History Published online 22 December 2014 Published in print December 2014 Information© Future Medicine LtdKeywordscaloric restrictioncancer dietcancer obesitydiet radiationdietary restrictionFinancial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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