Low folate intake may increase risk for colorectal cancer by inducing DNA hypomethylation.
In this study, researchers assessed the influence of folate status, DNA methylation, and polymorphisms of methylenetetrahydrofolate reductase, methionine synthase, and cystathionine-beta-synthase on risk of colorectal neoplasia.
The team's findings are published in the May issue of Gastroenterology.
The team included 35 patients with adenoma, 28 patients with cancer, and 76 controls in this case control study.
|Cancer patients had 26% lower folate status.|
They obtained blood samples for determination of blood folates, vitamin B12, homocysteine, DNA methylation, and genotypes.
In addition, they collected tissue biopsy samples at colonoscopy, for determination of DNA methylation in colonic mucosa.
The researchers assessed folate status by constructing a score from estimates of dietary intake and serum and erythrocyte folate.
The team determined that cancer patients had 26% lower folate status, as well as a 21% lower serum vitamin B12 concentration, when compared with the controls.
Furthermore, [3H] methyl incorporation into colonic DNA was 26% higher in patients with adenoma and 30% higher in patients with cancer, when compared with controls.
The team found that high folate status was associated with decreased risk for cancer.
In addition, colonic and leukocyte DNA hypomethylation were associated with increased risk for adenoma, and a non-significantly increased risk for cancer.
Dr Maria Pufulete's team concluded, "Low folate status and DNA hypomethylation are associated with colorectal neoplasia".