Vanessa Rodrik-Outmezguine

TL;DR: It is shown that AKT inhibition induces the expression and phosphorylation of multiple receptor tyrosine kinases (RTKs), and combined inhibition of AKT and HER kinase activity is more effective than either alone alone.

TL;DR: The adaptive capabilities of oncogenic signaling networks are revealed, as AKT signaling becomes reactivated through a feedback-induced AKT species phosphorylated on T308 but lacking S473, highlighting the possible need for combinatorial approaches to block feedback-regulated pathways.

TL;DR: Three distinct functional classes of BRAF mutants in human tumours are defined—those that have impaired kinase activity or are kinase-dead, whose activation of signalling is RAS-dependent, and those that activate ERK signalling by different mechanisms that dictate their sensitivity to therapeutic inhibitors of the pathway.

TL;DR: A new class of mTOR inhibitors is reported which overcomes resistance to existing first and second generation inhibitors and exploits the unique juxtaposition of two drug binding pockets to create a bivalent interaction that allows inhibition of these resistant mutants.

TL;DR: The authors have discovered that breast cancers resistant to the PI3K inhibitor BYL719 had persistently active mTOR signaling, and found that growth factors such as insulin-like growth factor 1 and neuregulin 1 can activate mammalian target of rapamycin (mTOR) and mediate resistance to BYL 719.