Abstract
Quo vadis, Kras?
Highlights
Günter Schneider: Technische Universität München, Klinikum rechts der Isar, II
Conditional deletion of the Phosphatidylinositol 3-kinase (PI3K) effector PDK1 in the pancreas completely blocks KrasG12D-driven preneoplastic lesion and cancers, demonstrating an essential contribution of PI3K signaling in Kras-dependent pancreatic carcinogenesis [4]
Recent in vitro work with a large cell line platform representing common human tumor entities revealed that Kras mutations correlate with increased sensitivity towards MEK inhibitors and a decreased sensitivity towards inhibitors of the PI3K pathway [6]
Summary
Günter Schneider: Technische Universität München, Klinikum rechts der Isar, II. Medizinische Klinik, Ismaninger Str. 22, 81675 Munich, Germany. Due to this high mutation frequency and the recent observation that survival of KrasG12D-driven cancer cells depends on the continuous expression of the oncogene in vivo [1, 2], mutant Kras is an excellent therapeutic target. The role of Kras effectors for cancer initiation and development has been clarified using genetic gain and loss of function models in vivo.
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