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Role of Diet Modulation and AMPK in Ovarian Cancer Progression and Outcome

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Final rept. 30 Sep 2011-29 Sep 2014

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Ovarian cancer is the leading cause of death from gynecologic malignancies in the United States. Given the ambiguity concerning the etiology, difficulties in early detection, absence of any markers, low survival rates and the overall obscurity related with ovarian cancer, more research is needed to identify factors and approaches that could improve ovarian cancer disease initiation, progression and disease free survival. One of these factors which have been largely unexplored is the influence of diet and the metabolic state of the patients. Unfortunately, the role of dietary factors in ovarian cancer prognosis is largely unknown. Particularly, no attention has been given to the metabolic state of a cancer cell and how this state can be modulated by calorie restriction. To determine the effect of diet on ovarian cancer, C57B6 mice were subjected to three types of diet regular diet RD, high-energy diet HED and calorie-restricted diet CRD.. Post 30 days of diet, 5x106 ID8 mouse ovarian cancer cells were injected in the intra-peritoneal cavity and mice were sacrificed after 60 days, followed by tumor burden evaluation and physiological parameters. A set of mice were treated with metformin Compared to RD and CRD, HED fed mice showed the most extensive tumor nodule formation and the highest tumor score diaphragm, peritoneum, bowel, liver, kidney, spleen with higher levels of insulin and leptin in both ascites and serum compared to RD and CRD. The cytokines, MCP-1, VEGF and IL-6, were also higher in the serum and ascites of HED mice. On the other hand, CRD fed mice exhibited a notably reduced tumor burden at every examined site compared to RD and HED mice. This was associated with a significant reduction in levels of insulin, IGF-1, leptin, MCP-1, VEGF and IL-6 both in serum and ascites, compared to RD or HED fed mice.

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  • Medicine and Medical Research

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