Aspirin and NSAID chemoprevention, gene-environment interactions, and risk of colorectal cancer
Menée à partir des données de 5 études cas-témoins et de 5 études de cohorte ayant débuté entre 1976 et 2003 aux Etats-Unis, au Canada, en Australie ou en Allemagne et incluant au total 8 634 patients atteints d'un cancer colorectal et 8 553 témoins, cette étude évalue, en fonction de la présence ou non de variants génétiques, l'association entre l'utilisation régulière d'aspirine ou d'autres anti-inflammatoires non stéroïdiens et le risque de développer la maladie
In this issue of JAMA, Nan and colleagues1 report the results of a gene-environment interaction study examining an interaction between a genetic polymorphism and the regular use of aspirin or other nonsteroidal anti-inflammatory agents (NSAIDs) and the association with risk of colorectal cancer. This case-control study is scientifically noteworthy for 4 distinct reasons. First, the study advances understanding of how to conduct research designed to detect gene-environment interactions. Second, the study illustrates that interventions can be genetically targeted not just to direct treatment but also to direct preventive interventions. Third, the study provides insight into the mechanistic understanding of how aspirin alters colon cancer risk. Fourth, the study highlights the need to conduct implementation research to ensure clinicians are prepared to apply gene-environment research in daily practice.
JAMA , éditorial, 2014