Increase in PI3K signalling mimics mutated-Kras induction of pancreatic cancer

摘要

Activation of PI3K/Akt pathway is described in 50% of pancreatic adenocarcinomas (measured through the increase in phosphorylation of its kinase substrate Akt) and is associated with a poor prognosis [1]. Phosphoinositide-3-kinases (PI3Ks) are positioned at the crossroad of several genetic alterations and oncogenic pathways found in pancreatic cancer, and are thus considered as major possible therapeutic target candidates. However, the demonstration of the implication of PI3K pathway in pancreatic carcinogenesis in vivo has not been yet provided. This question has now been partly answered by the findings of Eiser et al. [2]. In the March issue of Cancer Cell, the authors showed that increase of PI3K signalling is the driving force for initiation of Kras-mutated pancreatic cancers.