Nonsteroidal anti-inflammatory drugs (NSAIDs) include aspirin (acetylsalicylic acid, ASA).
Long-term use of NSAIDs has been associated with lowered risk of colorectal cancer, but the use is hampered by adverse effects.
Also, the anti-carcinogenic effects of NSAIDs are incompletely understood.
Understanding biological effects of NSAIDs may help developing new preventive medical strategies.
Dr Andersen and colleagues from Denmark identified gene–environment interactions between genetic variation and NSAID use in relation to risk of colorectal cancer.
The researchers performed a PubMed literature search, and all studies reporting original data on interactions between NSAIDs and polymorphisms in relation to colorectal cancer were evaluated.
|Homozygous carriers of the variant allele of rs6983267 halved their risk for colorectal cancer by aspirin use |
|Alimentary Pharmacology & Therapeutics|
The research team found indications that aspirin interacted with rs6983267 close to MYC, and NSAIDs interacted with rs3024505 and rs1800872 in or close to IL10 in preventing colorectal cancer.
The team observed that homozygous carriers of the variant allele of rs6983267 halved their risk for colorectal cancer by aspirin use compared to homozygous wildtype carriers who did not benefit from aspirin intake.
No interaction between use of NSAIDs and PTGS-2 in relation to colorectal cancer risk was detected.
Other findings of interactions between genes in inflammatory and oncogenic pathways and NSAIDs were considered suggestive.
Dr Andersen's team concludes, "Knowledge of underlying biological effects of NSAIDs in relation to colorectal cancer is scarce and the basis for stratifying the patients for preventive treatment is not yet available."
"Further studies assessing interactions between long-term NSAID exposure and genetic variation in relation to colorectal cancer are warranted in large well-characterized prospective cohorts."