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Aspirin use after diagnosis of colon cancer reduces mortality

Clinical Question:
Does aspirin use after the diagnosis and treatment of nonmetastatic colon cancer reduce mortality?

Bottom Line:
Regular aspirin use after the diagnosis and treatment of nonmetastatic colon cancer reduces cancer-specific and all-cause mortality. The benefit is strongest in patients with primary tumors that overexpress cyclooxygenase 2 (COX-2). This study found no benefit in reduced mortality among patients regularly using aspirin before the diagnosis of colorectal cancer. (LOE = 2b)

Reference:
Chan AT, Ogino S, Fuchs CS. Aspirin use and survival after diagnosis of colorectal cancer. JAMA 2009;302(6):649-659.  [PMID:19671906]

Study Design:
Cohort (prospective)

Setting:
Population-based

Synopsis:
Although regular aspirin use reduces the risk of developing colon cancer, it remains uncertain if aspirin use also reduces mortality in patients with established colon cancer. These investigators analyzed data from 2 large nationwide prospective cohort studies -- the Nurses' Health Study and the Health Professionals Follow-up Study -- to study the effect of aspirin use on patients with nonmetastatic colorectal cancer (stages I, II, and III). Study participants received a questionnaire at baseline and every 2 years thereafter inquiring about regular aspirin use. Individuals masked to drug exposure data reviewed all medical records for cancer diagnosis and cause of death. Follow-up occurred for more than 92% of patients for a median time of 11.8 years. Regular use of aspirin after diagnosis significantly reduced the risk of colorectal cancer-specific mortality (hazard ratio [HR] = 0.71; 95% CI, 0.53-0.95) and all-cause mortality (HR = 0.79; 0.65-0.97). The benefit of aspirin remained significant for stage I, stage II, and stage III disease. However, aspirin use before cancer diagnosis was not significantly associated with reduced cancer-specific mortality or all-cause mortality. The benefit of aspirin use after cancer diagnosis was strongest in patients whose primary tumors overexpressed COX-2.

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