Abstract The central function of phosphoinositide 3- kinase (PI3K) activation in tumour cell biology has urged a sizeable trouble to target PI3K and/ or downstream kinases similar as AKT and mammalian target of rapamycin
(mTOR) in cancer. still, arising clinical data show limited single- agent exertion of impediments targeting PI3K, AKT or mTOR at permitted boluses. One exception is the response to PI3Kδ impediments in habitual lymphocytic leukaemia, where a combination of cell- natural and- foreign conditioning drive efficacity. Then, we review crucial challenges and openings for the clinical development of impediments targeting the PI3K – AKT – mTOR pathway. Through a lesser focus on patient selection, increased understanding of vulnerable modulation and strategic operation of rational combinations, it should be possible to realize the eventuality of this promising class of targeted anticancer agents.
Keywords Cancer, mTOR, PI3K, Ras, Signaling.