Ras-driven transformation of human nestin-positive pancreatic epithelial cells.

摘要: Mutational activation of the K-Ras oncogene is well established as a key genetic step in development and growth pancreatic adenocarcinomas. However, means by which aberrant Ras signaling promotes uncontrolled tumor cell remains to be fully elucidated. The recent use primary human cells study Ras-mediated oncogenesis provides important model systems dissect this biology. This chapter describes establishment characterization telomerase-immortalized duct-derived mechanisms transformation. An strength system ability mutationally activated cause potent transformation vitro vivo. We have utilized evaluate antitumor activity small molecule inhibitors Raf-MEK-ERK mitogen-activated protein kinase cascade. will useful for pharmacologic dissection contribution downstream effector Ras-dependent