© 2005 by BMJ Publishing Group Ltd & British Society of Gastroenterology
COMMENTARY
Colorectal cancer
Reversal of DNA hypomethylation by folic acid supplements: possible role in colorectal cancer prevention
Correspondence to:
Correspondence to:
Professor J C Mathers
Human Nutrition Research Centre, School of Clinical Medical Sciences, University of Newcastle, Newcastle upon Tyne, NE1 7RU, UK; john.mathers@ncl.ac.uk
Low folate intake may predispose to a greater risk of colorectal cancer
Keywords: folic acid; DNA methylation; colorectal adenoma; colorectal cancer; biomarker; folic acid
| The first 150 words of the full text of this article appear below. |
The deranged gene expression that is causal for colorectal cancer (CRC) development results from unrepaired genomic damage which accumulates in successive generations of mucosal cells and which provides the neoplasm with a growth and/or survival advantage. Such damage includes disabling mutations in tumour suppressor (TS) genes and facilitates inappropriate expression of oncogenes. Approximately 25 years ago, evidence began to appear that changes in methylation status of DNA might be responsible for changes in gene expression. The potential importance of aberrant DNA methylation in tumorigenesis was signalled when, on 6 January 1983, Nature carried an article by Feinberg and Vogelstein1 reporting the first evidence of hypomethylation of some genes in tumours compared with "normal" tissue from the same individuals. That same year, Gama-Sosa and colleagues2 used high performance liquid chromatography to demonstrate that metastatic tumours had a significantly lower content of 5-methylcytosine than did benign neoplasms or normal tissues.
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