Abstract

Folate is required for DNA synthesis, repair and methylation, and low folate status has been implicated in carcinogenesis possibly as a result of higher rate of genetic damage. To investigate the relationship between DNA damage and folate status in breast cancer and benign breast disease control patients. Fasting blood samples from 52 histologically confirmed untreated breast cancer patients (mean age: 57 years) and 30 benign breast disease control patients (mean age: 51 years) were obtained. Mononuclear cells were isolated for genetic damage analysis using basic alkaline comet assay (which detects DNA single-strand breaks) and modified comet assay (using endonuclease III and formamidopyrimidine glycosylase (FPG) to recognize oxidatively damaged pyrimidines and purines, respectively). Results are expressed as tail moment. Results were log transformed to normalize the data and presented as geometric mean (95 per cent confidence interval). DNA damage was found to be significantly higher in mononuclear cells of breast cancer patients compared to benign breast disease control patients. Breast cancer patients tended to have lower red cell folate and higher plasma homocysteine concentrations, but these differences were not significant. A mechanistic role for low folate status in the aetiology of breast cancer is under further investigation.

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