Although statins are widely prescribed for lowering cholesterol and have a strong safety record, their link to prostate cancer risk has remained inconclusive. Some earlier studies hinted at a protective effect, while others showed no meaningful association. To understand these mixed findings, the research team focused on pharmacogenomics—the study of how genetic differences affect a person's response to drugs.
The study retrospectively analyzed clinical and genetic data from 3,481 men who underwent prostate biopsies between 1996 and 2014 at the University Health Network in Toronto. Among them, 1,104 patients (32%) had documented statin use for at least three months before biopsy. These individuals tended to be older, have a higher body mass index (BMI), and present with more aggressive tumor characteristics.
Prostate cancer was diagnosed in 2,061 participants (59%), and nearly half of these cases (45%) were classified as high-grade (Grade Group ≥2). Using a case-control design and adjusting for clinical factors such as age, BMI, PSA levels, prostate volume, and medication history, researchers found no statistically significant link between statin use and a reduced risk of either overall or high-grade prostate cancer.
To delve deeper, the team conducted a genome-wide association study (GWAS) and used a custom single-nucleotide polymorphism (SNP) array targeting 54 genetic variants linked to statin metabolism.
The key findings were as follows:
- Most of the analyzed SNPs showed no association with prostate cancer risk.
- Two genetic variants—rs10276036 in the ABCB1 gene and rs17222723 in the ABCC2 gene—indicated a potential interaction between statin use and prostate cancer risk.
- Statin users carrying the GG genotype of rs10276036 had a lower risk of developing prostate cancer, with a hazard ratio of 0.71.
- Despite this observation, the association did not reach genome-wide significance.
The study concludes that statins alone do not reduce the risk of prostate cancer, even in high-grade forms. However, genetic differences may influence how individuals respond to statins, pointing toward the need for more personalized approaches in cancer prevention.
While the findings do not support a chemopreventive role for statins, they emphasize the importance of incorporating genetic profiling into future research. Larger, more diverse studies examining the type, dose, and duration of statin use could further illuminate whether subsets of the population might benefit from such treatment.
The authors concluded, "Ultimately, the research adds clarity to a complex issue and encourages continued exploration into gene-environment interactions in the context of cancer risk and prevention."
Reference:
Amiri, A., Xu, W., Zhang, Q., Jeong, J. H., Freedland, S. J., Fleshner, N. E., Finelli, A., & Hamilton, R. J. (2025). The association between statin use, genetic variation, and prostate cancer risk. Prostate Cancer and Prostatic Diseases, 1-7. https://doi.org/10.1038/s41391-025-00964-x
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