Carcinogenesis, Vol. 24, No. 3, 565-571,
March 2003
© 2003 Oxford University Press
CARCINOGENESIS |
Cigarette smoking and genetic alterations in sporadic colon carcinomas
Division of Human Nutrition and Epidemiology, Wageningen University, PO Box 8129, 6700 EV Wageningen and
1 Department of Pathology, UMC St Radboud, Nijmegen, The Netherlands
Cigarette smoking has been inconsistently associated with colon cancer risk. To evaluate the hypothesis that smoking is primarily linked to a specific colon tumor subgroup(s), we assessed associations between smoking and the occurrence of mutations in the APC, K-ras and p53 genes, p53 overexpression, and microsatellite instability (MSI) in a Dutch population-based case–control study on sporadic colon carcinomas. The study population consisted of 176 cases and 249 controls. Smoking status (never, ever), number of cigarettes smoked per day (never, <15, 
15), total years of smoking (never, 
30, >30), and years since first started smoking (never, 35, >35) were all evaluated. Cigarette smoking status was significantly differently related to p53 overexpression-positive (p53pos) tumors compared with p53 overexpression-negative (p53neg) tumors (p53pos versus p53neg, OR 0.4, 95% CI 0.2–0.9), as well as to tumors with transversion mutations in APC, K-ras or p53 (transv+) compared with tumors without transversion mutations in one of these genes (transv–) (transv+ versus transv–, OR 2.5, 95% CI 1.0–5.9). Positive associations were observed with p53neg tumors and transv+ tumors when compared with the population-based controls (ever versus transv–, OR 1.5, 95% CI 0.9–2.8 and OR 2.2, 95% CI 0.9–5.6, respectively), inverse associations with p53pos tumors and transv– tumors (ever versus never, OR 0.5, 95% CI 0.3–1.0 and OR 0.8, 95% CI 0.5–1.3, respectively). Similar patterns of association were observed for the other smoking variables evaluated. In addition, although statistically non-significant, smoking was more notably positively associated with tumors that exhibit K-ras mutations, especially K-ras transversion mutations, than with tumors without K-ras mutations. An inverse relationship between smoking and the occurrence of APC mutations was suggested, whereas no clear associations were observed with MSI. Our data suggest that smoking-related colon cancers develop through a p53neg pathway and that smoking particularly results in colon carcinomas with transversion mutations.
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