Antitumor mechanisms when pRb and p53 are genetically inactivated
Cet article passe en revue les perspectives thérapeutiques offertes par les travaux récents sur les mécanismes antitumoraux dont l'efficacité est indépendante de l'inactivation des gènes suppresseurs de tumeurs pRb et p53
pRb and p53 are the two major tumor suppressors. Their inactivation is frequent when cancers develop and their reactivation is rationale of most cancer therapeutics. When pRb and p53 are genetically inactivated, cells irreparably lose the antitumor mechanisms afforded by them. Cancer genome studies document recurrent genetic inactivation of RB1 and TP53, and the inactivation becomes more frequent in more advanced cancers. These findings may explain why more advanced cancers are more likely to resist current therapies. Finding successful treatments for more advanced and multi-therapy-resistant cancers will depend on finding antitumor mechanisms that remain effective when pRb and p53 are genetically inactivated. Here, we review studies that have begun to make progress in this direction.