Folate status and colorectal cancer risk: A 2016 update

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• 作者：Joel B. Mason^a ; ^c ; ^{joel.mason@tufts.edu} ; San Yuan Tang^b ; ^c
• 关键词：CRC ; colorectal cancer ; DFE ; dietary folate equivalent ; MTHFR ; methylenetetrahydrofolate reductase ; RCTs ; randomized clinical trials
• 刊名：Molecular Aspects of Medicine
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：53
• 期：Complete
• 页码：73-79
• 全文大小：308 K
• 卷排序：53

文摘

The consensus of epidemiologic evidence indicates that an abundant intake of foodstuffs rich in folate conveys protection against the development of colorectal cancer, and perhaps some other common cancers as well. Pre-clinical models substantiate that the relationship is a genuinely causal one. Pre-clinical models have also lent mechanistic insights into the biochemical and molecular pathways by which adequate folate exposure conveys these protective effects, and human studies are beginning to confirm the relevance of this mechanistic understanding to human cancer biology. Enhancement of genetic stability appears to be a major mechanism by which folate sufficiency protects against carcinogenesis. To date, the Wnt signaling cascade has been the pathway most examined in this regard. The relationship between folate exposure and colorectal cancer risk is a complex one, in part because a number of extrinsic and intrinsic factors act as effect modifiers. This review discusses how the intake of the other three B-vitamins integral to the 1-carbon pathway acts as one such effect modifier. In addition, two concepts that remain matters of considerable debate are whether parental intake of folate impacts on subsequent cancer risk in the offspring, and whether excessive intakes of folate may have a paradoxical cancer-promoting effect: observations underlying these two concepts are presented as well.