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Editorial
June 6, 2007

Folate and Cancer—Timing Is Everything

Author Affiliations
 

Author Affiliations: Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Wash.

JAMA. 2007;297(21):2408-2409. doi:10.1001/jama.297.21.2408

A large number of epidemiological studies have shown that a higher intake of folate, as well as higher intakes of vegetables and fruit, is associated with a decreased risk of colorectal polyps and cancer.1 These results have been corroborated by animal experiments,2 and biological mechanisms underlying these associations have been proposed3: folate functions as a source of carbon moieties in the synthesis of nucleotides that are essential for DNA replication and repair. Folate deficiency leads to mutations and chromosomal damage—effects that are also central to the efficacy of antifolate chemotherapeutic agents (eg, methotrexate). In addition, folate status is important for the provision of S-adenosylmethionine, the universal methyl donor, involved in normal and pathological methylation of DNA. Disturbances in DNA methylation are relevant in carcinogenesis4; however, the role of folate in these epigenetic changes is not yet understood.

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