par Saini, Kamal ;Piccart-Gebhart, Martine
Référence The Asia-Pacific Journal of Oncology & Hematology, 2, 2
Publication Publié, 2010
Article révisé par les pairs
Résumé : The phosphatidylinositol 3-kinase (PI 3K)/Akt/mammalian target of rapamycin (mTOR) and the Raf/mitogen-activated and extracellularsignal regulated kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways are commonly dysregulated in breast cancer. Despite their central role in breast cancer cell growth and survival, early trials using single agent targeted therapy against different components of these pathways have generally been disappointing. Preclinical experiments have shown that PI 3K/Akt/mTOR and Raf/MEK/ ERK have significant cross-talk. Inhibition of one cascade upregulates the other, and vice versa. Given this background, it is logical to test if cotargeting both pathways may lead to better clinical outcomes. Indeed several such clinical trials are already underway. In this article, we present an overview of some preclinical work in this rapidly evolving area, and discuss the potential impact of this strategy on the treatment of breast cancer in the future.