title: Wild-type RAS: keeping mutant RAS in CHK.
abstract: Mutant RAS-driven tumorigenesis was thought for decades to arise independently of wild-type RAS isoforms, but recent evidence indicates wild-type isoforms are involved. In this issue of Cancer Cell, Grabocka and colleagues report how the loss of wild-type RAS alters oncogenic signaling and dampens the DNA-damage response, thereby affecting tumor progression and chemosensitivity.
authors: Abramson Family Cancer Research Institute, Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
authors: Theonie
authors: T
authors: Anastassiadis
authors: Abramson Family Cancer Research Institute, Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA. Electronic address: brownej@upenn.edu.
authors: Eric J
authors: EJ
authors: Brown
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D004249:DNA Damage / Q000235:genetics*; D005260:Female; D020558:GTP Phosphohydrolases / Q000378:metabolism*; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism*; D009369:Neoplasms / Q000473:pathology*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism*; D018631:ras Proteins / Q000235:genetics*
chemical_list: C117307:KRAS protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D020558:GTP Phosphohydrolases; C579846:NRAS protein, human; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins