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There is increasing evidence to suggest thatO  6-alkyl guanine DNA-alkyltransferase (MGMT) activity provides protection against alkylating agent induced formation of GC→AT transition mutations in the K-rasoncogene of colorectal tumours. As this mutagenic event occurs during the growth of adenomas, both biomarkers of exposure (N7-methylguanine levels in DNA) and susceptibility (MGMT activity) were measured in biopsy samples obtained from normal and adenomatous tissue from 34 patients with large adenomas (&gt;10 mm in size). There was no correlation between MGMT activity in the adenoma and in matched normal tissue. However, MGMT activity was significantly lower in adenoma tissue than in adjacent normal mucosa (5.18 versus 7.05 fmol/µg DNA,P= 0.01), particularly in men and those whose age was greater than the median. Upon stratification by K-rasmutational status, MGMT activity was lower in adenomas bearing a K-rasGC→AT transition mutation (mean 4.21 fmol/µg DNA) than in adjacent normal tissue (mean 7.7 fmol/µg DNA;P&lt; 0.004). In contrast, there was no significant difference in MGMT activity in adenomas lacking a K-rasGC→AT transition mutation and adjacent normal mucosa. N7-methylguanine levels however did not vary with age, gender, K-rasmutational status or MGMT activity. These results are consistent with the acquisition of K-rasGC→AT transition mutations in adenomas with low MGMT activity as a result of unavoidable exposure to methylating agents.

carcinogenesis

Reduced MGMT activity in human colorectal adenomas is associated with K-              ras               GC→AT transition mutations in a population exposed to methylating agents