A population-based, case-control study demonstrated that HMG CoA reductase inhibitors (statins) are associated with a 46% reduction in the risk of colorectal cancer after adjustment for other known risk factors. This paper was presented in the Plenary session of the 40th annual meeting of the American Society of Clinical Oncology held in New Orleans LA, June 5-8, 2004.

HMG CoA reductase, an enzyme in the liver that is involved in making cholesterol, is known to be overexpressed in colorectal cancer cell lines. HMG CoA reductase inhibitors (statins) are reportedly associated with a reduced risk of colorectal cancer (CRC) in a randomized clinical trial of patients with myocardial infarction.

This recent study, called The Molecular Epidemiology of Colorectal Cancer Study (MECC) evaluated 1766 patients with colorectal cancer diagnosed in northern Israel between 1998 and 2002. Subjects participated in an interview which assessed personal and family history of cancer, screening practices, other medical conditions, medication use, physical activity, and nutritional data including a food frequency questionnaire.

Use of statins was measured by self report. Those with a minimum duration of use of five years were defined as “users”, and accounted for 328 (9.19%) of the 3571 cases evaluated in this study. The most commonly used statins were prevastatin (44% of users) and simvastatin (54% of users).

Results showed a significant protective effect among statin users, with an unadjusted odds ratio of 0.54 (p=0.0002). This association remained unchanged (OR 0.54, p=0.0001) when adjusted for potential confounders (age, hypercholesterolemia, ethnicity, physical activity, diet, aspirin or NSAID use). There was no evidence of synergy between statin and NSAID use (p=0.54). The reduction of cancer risk was significant for both colon and rectal cancer patients (OR 0.53 and 0.38, respectively).

Reference: Poynter JN, Rennert G, Bonner JD, Rennert HS, et al. HMG CoA reductase inhibitors and the risk of colorectal cancer. Proceedings from the 40th annual meeting of the American Society of Clinical Oncology, New Orleans LA, June 5-8, 2004; Abstract #1.