Regular use of aspirin reduces the risk of a colorectal neoplasm, but the mechanism by which aspirin affects carcinogenesis in the colon is not well understood.
Dr Andrew T. Chan and colleagues from Boston estimated cyclooxygenase-2 (COX-2) expression by immunohistochemical assay of sections from paraffin-embedded colorectal-cancer specimens from two large cohorts of participants, who provided data on aspirin use from a questionnaire every 2 years.
They applied Cox regression to a competing-risks analysis to compare the effects of aspirin use on the relative risk of colorectal cancer in relation to the expression of COX-2 in the tumor.
|67% of tumors had moderate or strong COX-2 expression.|
| The New England Journal of Medicine |
During 2,446,431 person-years of follow-up of 82,911 women and 47,363 men, the team found 636 incident colorectal cancers that were accessible for determination of COX-2 expression.
Of the tumors, 423 (67%) had moderate or strong COX-2 expression.
The effect of aspirin use differed significantly in relation to COX-2 expression (P for heterogeneity=0.02).
Regular aspirin use conferred a significant reduction in the risk of colorectal cancers that overexpressed COX-2 (multivariate relative risk, 0.64; 95% confidence interval [CI], 0.52 to 0.78), whereas regular aspirin use had no influence on tumors with weak or absent expression of COX-2 (multivariate relative risk, 0.96; 95% CI, 0.73 to 1.26).
The age-standardized incidence rate for cancers that overexpressed COX-2 was 37 per 100,000 person-years among regular aspirin users, as compared with 56 per 100,000 person-years among those who did not use aspirin regularly.
In contrast, the rate for cancers with weak or absent COX-2 expression was 27 per 100,000 person-years among regular aspirin users, as compared with 28 per 100,000 person-years among nonregular aspirin users.
Dr Chan concluded that, "Regular use of aspirin appears to reduce the risk of colorectal cancers that overexpress COX-2 but not the risk of colorectal cancers with weak or absent expression of COX-2.