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An 18 year old Subway employee died protecting his mom during

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Calorie restriction and cancer prevention: a mechanistic perspective

11th Monday, 2013  |   Others  |  no comments

Source: Hursting SD, Dunlap SM, Ford NA, et al. Cancer & Metabolism. 2013, No.1:10 doi:10.1186/2049-3002-1-10 <http://www.cancerandmetabolism.com/content/pdf/2049-3002-1-10.pdf>   Calorie restriction (CR) is one of the most potent broadly acting dietary interventions for inducing weight loss and for inhibiting cancer in experimental models. Translation of the mechanistic lessons learned from research on CR to cancer prevention strategies in human beings is important given the high prevalence of excess energy intake, obesity, and metabolic syndrome in many parts of the world and the established links between obesity-associated metabolic perturbations and increased risk or progression of many types of cancer. This review synthesizes findings on the biological mechanisms underlying many of the anticancer effects of CR, with emphasis on the impact of CR on growth factor signaling pathways, inflammation, cellular and systemic energy homeostasis pathways, vascular perturbations, and the tumor microenvironment. These CR-responsive pathways and processes represent targets for translating CR research into effective cancer prevention strategies in human beings. Calorie restriction (CR), a dietary regimen in which subjects (typically test animals) receive a reduced energy diet (typically, a 20 to 40% reduction in total energy intake relative to an unrestricted comparison group), is one of the most potent and broadly acting dietary interventions for preventing or reversing weight gain and inhibiting cancer in experimental tumor models [1]. Recent reports of decreased risk of diabetes, neurological degeneration, and cancer in response to CR in rhesus monkeys [2,3], and observations that CR decreases inflammatory and endocrine markers associated with increased breast cancer risk in women [4,5], suggest that the beneficial effects of CR on metabolism and chronic disease risk observed in rodent models may extend to human beings.   The peptide hormone insulin is produced by beta cells in the pancreas and released in response to hyperglycemia, which is associated with insulin resistance, aberrant glucose metabolism, chronic inflammation, and the production of other metabolic hormones, such as IGF-1, leptin, and adiponectin [6]. Clinical and epidemiologic evidence suggests that elevated levels of circulating insulin or the cleavage product of proinsulin (C-peptide) are associated with increased risk or progression of cancers of the breast (pre- and postmenopausal), endometrium, colon, kidney, and pancreas [6,7]. High circulating levels of insulin also upregulate hepatic synthesis of IGF-1 critical to growth and development of many tissues, particularly during the prenatal period [6,8]. In the circulation, IGF-1 is typically bound to IGF-binding proteins (IGFBPs) that regulate the amount of free IGF-1 bioavailable to elicit growth or survival signaling [6,8]. An elevated level of circulating IGF-1 is an established risk factor for many cancer types [6-10].   A connection between chronic inflammation and cancer development was observed 150 years ago when Rudolph Virchow noted an abundance of leukocytes in neoplastic tissue [11]. Inflammation is now considered a hallmark of cancer, and evidence is accumulating that chronic, ‘smoldering’ inflammation is associated with increased cancer risk [12-14]. Indeed, several tissue-specific inflammatory lesions are established neoplastic precursors for invasive cancer, including inflammatory bowel disease for colon cancer, pancreatitis for pancreatic cancer, dermatitis for certain forms of skin cancer, and gastritis for gastric cancer [15,16]. Tumor and pre-neoplastic microenvironments are composed of mixtures of cell types including epithelial cells, fibroblasts, mast cells, and cells of the innate and adaptive immune system [17]. As discussed previously, macrophages, which are activated in the obese state, infiltrate tumors and amplify the inflammatory tumor microenvironment, often through NF-? B-dependent production of cytokines and angiogenic factors [17]. COX-2 is another important cancer-related inflammatory mediator that is up-regulated in most tumors and catalyzes the synthesis of the potent inflammatory lipid metabolite, prostaglandin E2. COX-2 expression, an indicator of poor prognosis in many cancer types, is increased in response to obesity [18].   References: 1. Hursting SD, Smith SM, Lashinger LM, et al. Calories and carcinogenesis: lessons learned from 30 years of calorie restriction research. Carcinogenesis. 2010, 31:83–89. 2. Colman RJ, Anderson RM, Johnson SC, et al. Caloric restriction delays disease onset and mortality in rhesus monkeys. Science. 2009, 325:201–204. 3. Mattison JA, Roth GS, Beasley TM, et al. Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study. Nature. 2012, 489:318–321. 4. Harvie M, Howell A. Energy restriction and the prevention of breast cancer. Proc Nutr Soc. 2012, 71:263–275. 5. Imayama I, Ulrich CM, Alfanao CM, et al. Effects of a caloric restriction weight loss diet and exercise on inflammatory biomarkers in overweight/obese postmenopausal women: a randomizedcontrolled trial. Cancer Res. 2012, 72 :2314–2326. 6. Pollak M. The insulin and insulin-like growth factor receptor family in neoplasia: an update. Nat Rev Cancer. 2012, 12 :159–169. 7. Hursting SD, Berger NA. Energy balance, host-related factors, and cancer progression. J Clin Onco. 2010, 28 :4058–4065. 8. Gallagher EJ, Fierz Y, Ferguson RD, LeRoith D. The pathway from diabetes and obesity to cancer, on the route to targeted therapy. Endocr Pract. 2010, 16:864–873. 9. Renehan AG, Zwahlen M, Minder C, et al. Insulin-like growth factor (IGF)-1, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis. Lance. 2004, 363:1346–1353. 10. Price AJ, Allen NE, Appleby PN, et al. Insulin-like growth factor-1 concentration and risk of prostate cancer: results from the European Prospective Investigation into Cancer and Nutrition. Cancer Epidemiol Biom Pre. 2012, 21 :1531–1541. 11. Virchow R: Die krankhaften Geschwülste. In Aetologie der neoplastischen Geschwülste/Pathogenie der neoplastischen Geschwülste. Berlin, Germany: Verlag von August Hirchwald; 1863:58. 12. Aggarwal BB, Gehlot P. Inflammation and cancer: how friendly is the relationship for patients? Curr Opin Pharmaco. 2009, 9 :351–369. 13. Ono M. Molecular links between tumor angiogenesis and inflammation: inflammatory stimuli of macrophages and cancer cells as targets for therapeutic strategy. Cancer Sci 2008, 99 :1501–1506. 14. Del Prete A, Allavena P, Santoro G, et al. Molecular pathways in cancer-related inflammation. Biochem Med 2011, 21:264–275. 15. Foltz CJ, Fox JG, Cahill R, et al. Spontaneous inflammatory bowel disease in multiple mutant mouse lines: association with colonization by Helicobacter hepaticus. Helicobacter. 1998, 3:69–78. 16. Coussens LM, Werb Z. Inflammation and cancer. Nature 2002, 420:860–867. 17. Allavena P, Sica A, Garlanda C, Mantovani A. The Yin-Yang of tumor-associated macrophages in neoplastic progression and immune surveillance. Immunol Rev. 2008, 222:155–161. 18. Koki A, Khan NK, Woerner BM, et al. Cyclooxygenase-2 in human pathological disease. Adv Exp Med Biol. 2002, 507 :177–184.

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Copper Depletion Therapy Keeps High-Risk Triple-Negative Breast Cancer at Bay

8th Friday, 2013  |   Breast Cancer  |  no comments

New Weill Cornell Study Shows Anti-Copper Drug Might Prevent the Spread of Cancer to Organs


  An anti-copper drug compound that disables the ability of bone marrow cells from setting up a “home” in organs to receive and nurture migrating cancer tumor cells has shown surprising benefit in one of the most difficult-to-treat forms of cancer — high-risk triple-negative breast cancer. The median survival for metastatic triple-negative breast cancer patients is historically nine months. However, results of a new phase II clinical trial conducted by researchers at Weill Cornell Medical College and reported in the Annals of Oncology shows if patients at high-risk of relapse with no current visible breast cancer are copper depleted, it results in a prolonged period of time with no cancer recurrence. In fact, only two of 11 study participants with a history of advanced triple-negative breast cancer relapsed within 10 months after using the anti-copper drug, tetrathiomolybdate (TM). “These study findings are very promising and potentially a very exciting advance in our efforts to help women who are at the highest risk of recurrence,” says the study’s senior investigator, Dr. Linda Vahdat, director of the Breast Cancer Research Program, chief of the Solid Tumor Service and professor of medicine at Weill Cornell Medical College. Dr. Vahdat says four of the study participants with a history of metastatic triple-negative breast cancer have had long-term benefit remaining disease free for between three and five and a half years. “The anti-copper compound appears to be keeping tumors that want to spread in a dormant state,” reports Dr. Vahdat, who is also medical oncologist at the Iris Cantor Women’s Health Center at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. “We believe one of the important ways it works is by affecting the tumor microenvironment, specifically the bone marrow-derived cells that are critical for metastasis progression.” In addition, study participants with other forms of high-risk for relapse breast cancers — either stage 3 or stage 4 — without evidence of disease after treatment have also fared well. The progression-free survival rate among these 29 patients in the study has been 85 percent, to date. “As good as these interim findings look to us, we cannot talk about significant benefit until we compare TM treatment to other therapies,” she says. Dr. Vahdat expects to launch a phase III randomized clinical trial in the near future. This research is a report of the first 40 patients. The clinical trial, which began in 2007, has been expanded many times and now includes 60 patients, more than half of who have triple-negative breast cancer.   Deplete Copper to Prevent Cancer Spread New discoveries in the science of metastasis and examination of the body’s utilization of copper to promote cancer spread led to this clinical trial. Investigators at Weill Cornell, including some of this study’s co-authors, have contributed to the recent understanding of the role bone marrow cells play in promoting metastasis. They previously found that a collection of bone marrow-derived cells, which include VEGFR1+ hematopoietic progenitor cells (HPCs), prepare a site in distant organs to accept cancer cells. HPCs also recruit endothelial progenitor cells (EPCs), among others, to activate an “angiogenic switch” that establish blood vessels at the site to feed newly migrated cancer cells. Breast cancer research studies conducted at Weill Cornell have also found that immediately prior to cancer relapse, levels of EPCs and HPCs rise significantly further, suggesting that the EPC target of the copper depletion approach is one that makes sense. “Breast tumors want to move to specific organs, and these EPCs and HPCs cells leave a ‘popcorn trail’ for cancer cells to follow, as well as provide the building blocks for blood vessels to greet them as they arrive,” Dr. Vahdat says. Copper is critical to mobilizing these cells. Copper is essential to the metastatic process. It is a key component of enzymes that help turn on angiogenesis in the tumor microenvironment, and it also appears to play a role in directing cancer cell migration and invasion, according to researchers. TM is a copper chelation compound used to treat Wilson’s disease, a hereditary copper metabolism disorder, and has been studied in phase I and phase II clinical trials for a number of disorders. Animal studies have demonstrated that depleting copper decreases proliferation of EPCs, as well as blood vessel formation and tumor growth. Dr. Vahdat’s study is the first human clinical trial to utilize a copper depletion strategy to modulate EPCs in breast cancer patients with an extraordinarily high risk of relapse from hidden residual disease. Most of the studies in other solid tumors with visible advanced disease have been disappointing, say researchers. Despite improvements in breast cancer therapy, there is significant risk of relapse in a high-risk subset of patients. The risk of relapse in stage 3 patients is 50-75 percent over five years, and patients with stage 4 breast cancer always recur. Triple-negative breast cancer patients have a poorer prognosis even when diagnosed in early disease stages. “These triple-negative patients represent a substantial proportion of metastatic breast cancer patients,” says Dr. Vahdat. “These are the patients that need the most attention, which is why we have focused most of the resources of our Metastases Research Program on this problem.” In the study, researchers found that 75 percent of patients achieved the copper depletion target using TM after one month of therapy, and that copper depletion was most efficient (91 percent) in patients with triple-negative tumors, compared to other tumor types (41 percent). In copper-depleted patients only, there was a significant reduction in EPCs, and the 10-month relapse-free survival was 85 percent. In addition, TM was found to be safe and well-tolerated in patients. The study shows copper depletion appears to inhibit the production, release, and mobilization of EPCs from the bone marrow, leading to a suppressed angiogenic switch and tumor dormancy. “There are a lot of cancer experts at Weill Cornell working very hard to understand this precise mechanism, define the clinical benefit in this ongoing copper depletion drug clinical trial, and determine its future study,” says Dr. Vahdat. “Keeping cancer dormant is what we all want for our patients — especially triple-negative breast cancer patients at highest risk of recurrence.” Study co-authors include Dr. Sarika Jain, Maureen M. Ward, Naomi Kornhauser, Dr. Ellen Chuang, Dr. Tessa Cigler, Dr. Anne Moore, Diana Donovan, Christina Lam, Marta V. Cobham, Sarah Schneider, Sandra M. Dr. Hurtado Rúa, Celine Mathijsen Greenwood, Dr. Richard Zelkowitz, Dr. J. David Warren, Dr. Maureen E. Lane, Dr. Vivek Mittal and Dr. Shahin Rafii from Weill Cornell; Dr. Jules Cohen from Stony Brook University Cancer Center, Stony Brook, N.Y.; and Steven Benkert from NewYork-Presbyterian Hospital. The study was funded by the grants from the Anne Moore Breast Cancer Research Fund, Stephen and Madeline Anbinder Foundation, Rozaliya Kosmandel Research Fund, Susan G Komen for the Cure, New York Community Trust, Cancer Research and Treatment Fund, Manhasset Women’s Coalition Against Breast Cancer and Berman Fund. Source: http://weill.cornell.edu/news/releases/wcmc/wcmc_2013/02_13_13.shtml