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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.

Systematic review: interactions between aspirin, and other nonsteroidal anti‐inflammatory drugs, and polymorphisms in relation to colorectal cancer