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Folate deficiency has been implicated in the development of several cancers, including cancer of the colorectum, breast, ovary, pancreas, brain, lung and cervix. Generally, data from the majority of human studies suggest that people who habitually consume the highest level of folate, or with the highest blood folate concentrations, have a significantly reduced risk of developing colon polyps or cancer. However, an entirely protective role for folate against carcinogenesis has been questioned, and recent data indicate that an excessive intake of synthetic folic acid (from high\u2010dose supplements or fortified foods) may increase human cancers by accelerating growth of precancerous lesions. Nonetheless, on balance, evidence from the majority of human studies indicates that dietary folate is genoprotective against colon cancer. Suboptimal folate status in humans is widespread. Folate maintains genomic stability by regulating DNA biosynthesis, repair and methylation. Folate deficiency induces and accelerates carcinogenesis by perturbing each of these processes. This review presents recent evidence describing how these mechanisms act, and interact, to modify colon cancer risk.<\/jats:p>","DOI":"10.1007\/s10545-010-9128-0","type":"journal-article","created":{"date-parts":[[2010,6,10]],"date-time":"2010-06-10T03:14:27Z","timestamp":1276139667000},"page":"101-109","source":"Crossref","is-referenced-by-count":219,"title":["Folate and cancer: how DNA damage, repair and methylation impact on colon carcinogenesis"],"prefix":"10.1002","volume":"34","author":[{"given":"Susan J.","family":"Duthie","sequence":"first","affiliation":[{"name":"Nutrition and Epigenetics Group, Division of Vascular Health, Rowett Institute of Nutrition and Health University of Aberdeen Greenburn Road, Bucksburn Aberdeen AB21 9SB 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