By S. Srivastava
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Extra info for Pancreatic Cancer - Molecular Mechanism and Targets
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1999. Chemopreventive effects of tea extracts and various components on human pancreatic and prostate tumor cells in vitro. Nutr Cancer 35(1):80-86. [74] Lyn-Cook BD, Sttoman HL, YanY, Blann EB, and Hammons GJ. 1999. The effects of phytoestrogens on human pancreatic tumor cells in vitro. Cancer Letters 142:111119. [75] Lowenfels A, and Maisonneuve P. 2004. Epidemiology and prevention of pancreatic cancer. Clinical Oncology 34(5):238-244. [76] Jones S, Zhang X, Parsons DW, Lin J CH, et al. 2008.
41] Kondo E, Furukawa T, Yoshinaga K, Kijima H, et al. 2000. Not hMSH2 but hMLH1 is frequently silenced by hypermethylation in endometrial cancer but rarely silenced in pancreatic cancer with microsatellite instability. Int J. Oncol. 13(3):535-541. [42] Esteller M, Corn PG, Baylin SB, and Herman JG. 2001. A gene hypermethylation profile of human cancer. Cancer Research 61:3225-3228. [43] House MG, Herman JG, GuoMZ, Hooker CM, et al. 2003. Aberrant hypermethylation of tumor suppressor genes in pancreatic endocrine neoplasms.
Bioactive Components of Food that Influence Histone Modification in Pancreatic Cancer In addition to bioactive nutrients modulating histone modifications, studies have also shown that caloric restriction, another unexplored area of research on epigenetics, reduces the expression of inflammatory genes such as NF-κB, AP1, COX-2, and iNOS (119). NF-κB is known to be activated by histone aceylation. Activation of NF-κB occurs through p300 HAT acetylation of the p50 subunit of NF-κB. This increases NF-κB binding and transactivation.