Developmental reprogramming of cancer susceptibility
Cet article présente un nouveau modèle d'interaction gènes-environnement dans lequel une exposition environnementale durant le développement induit, par reprogrammation épigénétique, une susceptibilité accrue au cancer à l'âge adulte
Gene–environment interactions have been traditionally understood to promote the acquisition of mutations that drive multistage carcinogenesis, and, in the case of inherited defects in tumour suppressor genes, additional mutations are required for cancer development. However, the developmental origins of health and disease (DOHAD) hypothesis provides an alternative model whereby environmental exposures during development increase susceptibility to cancer in adulthood, not by inducing genetic mutations, but by reprogramming the epigenome. We hypothesize that this epigenetic reprogramming functions as a new type of gene–environment interaction by which environmental exposures target the epigenome to increase cancer susceptibility.