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Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. Berquin IM, Min Y, Wu R, Wu J, Perry D, Cline JM, Thomas MJ, Thornburg T, Kulik G, Smith A, Edwards IJ, D'Agostino R, Zhang H, Wu H, Kang JX, Chen YQ. J Clin Invest. 2007 Jul;117(7):1866-75. PMID: 17607361 Our data suggest that modulation of prostate cancer development by polyunsaturated fatty acids is mediated in part through Bad-dependent apoptosis. This study highlights the importance of gene-diet interactions in prostate cancer.

Beta glucan is a scientifically proven biological defense modifier (BDM) that nutritionally potentiates and modulates the immune response. As a supplement, after swallowing orally, Beta glucan is ingested primarily through macrophage and dendritic immune cells, to nutritionally and safely yield, through immune response potentiation and modulation, in many instances various therapeutic healing effects generated by the immune cells.  For many years Glucans have been investigated (History) for these immune enhancing properties, particularly their ability to activate macrophage immune cells and NK-Cells, plus in turn, the T-Cells, and B-Cells including selected cytokines and complement. 

Schroeder CP, Yang P, Newman RA, Lotan R. Eicosanoid metabolism in squamous cell carcinoma cell lines derived from primary and metastatic head and neck cancer and its modulation by celecoxib. Cancer Biol Ther. 2004 Sep;3(9):847-52. Epub 2004 Sep 18. P

Wang M. Extending the good diet, good health paradigm: modulation of breast cancer resistance protein (BCRP) by flavonoids. Toxicol Sci. 2007 Apr;96(2):203-5. PMID: 17407835 [PubMed - in process]

Ginger inhibits cell growth and modulates angiogenic factors in ovarian cancer cells. Rhode J, Fogoros S, Zick S, Wahl H, Griffith KA, Huang J, Liu JR. BMC Complement Altern Med. 2007 Dec 20;7:44. PMID: 18096028 doi:10.1186/1472-6882-7-44

Prostate tumor growth and recurrence can be modulated by the omega-6:omega-3 ratio in diet: athymic mouse xenograft model simulating radical prostatectomy. Kelavkar UP, Hutzley J, Dhir R, Kim P, Allen KG, McHugh K. Neoplasia. 2006 Feb;8(2):112-24. PMID: 16611404

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Michelakis ED, Webster L, Mackey JR. Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review. PMID: 18766181 doi:10.1038/sj.bjc.6604554 The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res

Israeli 'cancer shift' over heart disease mortality may be led by greater risk in women with high intake of n-6 fatty acids. Shapira N. Eur J Cancer Prev. 2007 Oct;16(5):486-94. PMID: 17923822 doi: 10.1097/CEJ.0b013e3280145b6d Population studies of Israeli Jews, Arabs, and women support the association of high n-6 polyunsaturated fatty acid intake with increased cancer risk and higher female sensitivity. Research findings suggest that gender and sex hormones may influence n-6 polyunsaturated fatty acid metabolism and carcinogenesis. This appears to be the first time gender has been proposed to modulate national cancer epidemiology, suggesting implications for differential nutritional prevention, warranting further research.