Tumor-promoting inflammatory networks in pancreatic neoplasia: another reason to loathe Kras.
Oncogenic Kras is increasingly appreciated as an instigator of an inflammatory program that facilitates pancreatic cancer. In this issue of Cancer Cell, McAllister and colleagues use both gain-of-function and loss-of-function studies to demonstrate that oncogenic Kras activates an IL-17-dependent pathway that promotes the initiation and progression of preinvasive pancreatic neoplasia.
Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: rhv@exchange.upenn.edu.
Robert H
RH
Vonderheide
D000818:Animals; D004847:Epithelial Cells / Q000378:metabolism*; D006413:Hematopoietic System / Q000378:metabolism*; D006801:Humans; D020381:Interleukin-17 / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000378:metabolism*; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism*
C098680:Il17a protein, mouse; D020381:Interleukin-17; C495971:Hras protein, mouse; D016283:Proto-Oncogene Proteins p21(ras)