Risque individuel de cancer de sein et le triptyque « environnement, génétique et génomique » : une histoire de réparation de l’ADN ?

Abstract

It is currently considered that 90 to 95% of cancers are non-hereditary. However, the mechanisms of cellular transformation that initiate cancer are still unknown and this estimate therefore remains poorly documented. To date, it appears that both misrepaired DNA breaks (produced by the hyper-recombination phenomenon) and cell cycle arrest impairments are required for cells carrying numerous mutations to amplify and lead to a critical mass of transformed cells. In this article, we discussed about a model based on the nucleoshuttling of the ATM protein that could explain this double requirement by the mutation of substrate proteins that might not be directly involved in genomic instability and DNA damage repair.