Journal
CANCER PREVENTION RESEARCH
Volume 3, Issue 12, Pages 1505-1508Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1940-6207.CAPR-10-0298
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Funding
- NCI NIH HHS [R01 CA 114467, R01 CA 120523, R01 CA105437, R01 CA105437-04, R01 CA112516-05S1, R01 CA120523-04, R01 CA 112516, R01 CA112516, R01 CA114467, R01 CA114467-05, R01 CA120523] Funding Source: Medline
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Cancer is the consequence of genetic and epigenetic alterations. Genetic mutations likely result in part from exposure to environmental carcinogens, giving rise to a large field of cancer-prevention study of these carcinogens and ways to develop strategies to avoid them. Our understanding of regulatory epigenetic mechanisms associated with DNA methylation, histone modifications, and microRNA production is increasing rapidly. The involvement of these processes in carcinogenesis raises the possibility that environmental exposures may promote or prevent cancer through affecting the epigenome. Modifying the epigenome to prevent cancer is particularly intriguing because epigenetic alterations are potentially reversible, unlike gene mutations, and because certain dietary factors, such as the B-vitamin folate, may affect genes' DNA methylation status (as reported by Wallace et al., beginning on page 1552 in this issue of the journal). Rapidly improving techniques for assessing epigenetic alterations promise to yield important insights for cancer prevention. Cancer Prev Res; 3(12); 1505-8. (C) 2010 AACR.
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