Journal
CANCER CELL
Volume 37, Issue 4, Pages 543-550Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2020.03.013
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Funding
- European Research Council [ERC-AG/695566]
- Spanish Ministry of Science, Innovation and Universities [RTI2018-094664-B-I00, RTC2017-6576-1]
- Autonomous Community of Madrid [B2017/BMD-3884 iLUNG-CM]
- Asociacion Espanola contra el Cancer [GC166173694BARB]
- AXA Research Fund
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KRAS mutations occur in a quarter of all of human cancers, yet no selective drug has been approved to treat these tumors. Despite the recent development of drugs that block KRAS(G12C), the majority of KRAS oncoproteins remain undruggable. Here, we review recent efforts to validate individual components of the mitogenactivated protein kinase (MAPK) pathway as targets to treat KRAS-mutant cancers by comparing genetic information derived from experimental mouse models of KRAS-driven lung and pancreatic tumors with the outcome of selective MAPK inhibitors in clinical trials. We also review the potential of RAF1 as a key target to block KRAS-mutant cancers.
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