Summary Background Nonsteroidal anti‐inflammatory drugs ( NSAID s) include aspirin (acetylsalicylic acid, ASA ). Long‐term use of NSAID s has been associated with lowered risk of colorectal cancer ( CRC ), but the use is hampered by adverse effects. Also, the anti‐carcinogenic effects of NSAID s are incompletely understood. Understanding biological effects of NSAID s may help developing new preventive medical strategies. Aim To identify gene–environment interactions between genetic variation and NSAID use in relation to risk of CRC . Methods We performed a PubMed literature search and all studies reporting original data on interactions between NSAID s and polymorphisms in relation to CRC were evaluated. Results We found indications that aspirin interacted with rs6983267 close to MYC (encoding a transcription factor involved in cell cycle progression, apoptosis and cellular transformation) and NSAID s interacted with rs3024505 and rs1800872 in or close to IL 10 (encoding IL ‐10) in preventing CRC . Homozygous carriers of the variant allele of rs6983267 (ca. 25% of the population) halved their risk for CRC by aspirin use compared to homozygous wildtype carriers who did not benefit from aspirin intake. No interaction between use of NSAID s and PTGS ‐2 (encoding COX ‐2) in relation to CRC risk was detected. Other findings of interactions between genes in inflammatory and oncogenic pathways and NSAID s were considered suggestive. Conclusions Knowledge of underlying biological effects of NSAID s in relation to CRC 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 CRC are warranted in large well‐characterised prospective cohorts.

Nonsteroidal anti-inflammatory drugs (NSAID) are members of a therapeutic drug class which reduces pain, decreases inflammation, decreases fever, and prevents Nonsteroidal anti-inflammatory drugs (NSAID) are members of a therapeutic drug class which reduces pain, decreases inflammation, decreases fever, and prevents blood clots. Side effects depend on the specific drug, its dose and duration of use, but largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack, and kidney disease. Well-known nonsteroidal anti-inflammatory dru Nonsteroidal anti-inflammatory drugs (NSAID) are members of a therapeutic drug class which reduces pain, decreases inflammation, decreases fever, and prevents blood clots. Side effects depend on the specific drug, its dose and duration of use, but largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack, and kidney disease. Well-known nonsteroidal anti-inflammatory drugs include aspirin, ibuprofen, diclofenac, and naproxen, all of which are available over the counter (OTC). Paracetamol (acetaminophen) is generally not considered an NSAID because it has only minor anti-inflammatory activity. The term nonsteroidal, common from around 1960, distinguishes these drugs from corticosteroids, another class of anti-inflammatory drugs, which during the 1950s had acquired a bad reputation due to overuse and side-effect problems after their introduction in 1948. Nonsteroidal anti-inflammatory drugs work by inhibiting the activity of cyclooxygenase enzymes (the COX-1 and COX-2 isoenzymes). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins, which are involved in inflammation, and thromboxanes, which are involved in blood clotting. "Nons…

INTERACTIONS None OTHER DRUGS • Other nonsteroidal anti-inflammatory drugs (NSAIDs) • Folic acid … choline-magnesium salicylate • Other nonsteroidal anti-inflammatory drugs (NSAIDs) • Narcotic painkillers: … PRESCRIBED DRUGS • Early disease or acute/chronic inflammation: aspirin or other nonsteroidal anti-inflamma-

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