Pogribny Igor P, Beland Frederick A
Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Cancer Lett. 2013 Jun 28;334(1):39-45. doi: 10.1016/j.canlet.2012.09.010. Epub 2012 Sep 23.
Carcinogenesis, a complex multifactorial process of the transformation of normal cells into malignant cells, is characterized by many biologically significant and interdependent alterations triggered by the mutational and/or non-mutational (i.e., epigenetic) events. One of these events, specific to all types of cancer, is alterations in DNA methylation. This review summarizes the current knowledge of the role of DNA methylation changes induced by various genotoxic chemicals (carcinogenic agents that interact with DNA) and non-genotoxic carcinogens (chemicals causing tumor by mechanisms other than directly damaging DNA) in the lung, colorectal, liver, and hematologic carcinogenesis. It also emphasizes the potential role for epigenetic changes to serve as markers for carcinogen exposure and carcinogen risk assessment.
癌症发生是一个将正常细胞转变为恶性细胞的复杂多因素过程,其特征是由突变和/或非突变(即表观遗传)事件引发的许多具有生物学意义且相互依存的改变。所有类型癌症共有的其中一个事件是DNA甲基化改变。本综述总结了目前关于各种遗传毒性化学物质(与DNA相互作用的致癌剂)和非遗传毒性致癌物(通过直接损伤DNA以外的机制导致肿瘤的化学物质)诱导的DNA甲基化变化在肺癌、结直肠癌、肝癌和血液系统癌症发生中所起作用的认识。它还强调了表观遗传变化作为致癌物暴露和致癌物风险评估标志物的潜在作用。