Reprogramming to resist
Menées à l'aide de modèles murins de cancer de la prostate, ces deux études mettent en évidence des mécanismes par lesquels la perte d'expression de deux gènes suppresseurs de tumeurs (RB1 et TP53) favorise, via le facteur de transcription SOX2, la résistance aux traitements anti-androgènes
One means by which cancer cells evade therapies involves their ability to reprogram to a cell type that no longer depends on the cellular pathway being targeted by the treatments. Hormone deprivation therapies that suppress androgen receptor (AR) signaling are the mainstay of treatment for metastatic prostate cancer. However, prostate cancers can become resistant to this approach by losing dependence on androgen hormones. On pages 84 and 78 of this issue, Mu et al. (1) and Ku et al. (2), respectively, contribute to our mechanistic understanding of this remarkable plasticity in cell identity, which allows cancers to thrive.
Science , commentaire, 2016