Many cancers are driven by mutations in the guanosine triphosphatase KRAS; however, mutant KRAS proteins have proven to be extremely difficult to target therapeutically. By bringing together this collection of freely available Research Articles published by Science Signaling, we highlight new potential ways to target mutant KRAS, strategies that preempt the possibility of resistance to such drugs, and the identification of other components in KRAS pathways that could be potential therapeutic targets. If you perform research in this or a related area, we would be very interested in considering your work for publication. Please contact us at: email@example.com.
By Kevin Lou, Veronica Steri, Alex Y. Ge, Y. Christina Hwang, Christopher H. Yogodzinski, Arielle R. Shkedi, Alex L. M. Choi, Dominique C. Mitchell, Danielle L. Swaney, Byron Hann, John D. Gordan, Kevan M. Shokat, and Luke A. Gilbert
Functional genomics reveals paths to enhancing combination therapies in KRAS-mutant cancers.
By Devon R. Blake, Angelina V. Vaseva, Richard G. Hodge, McKenzie P. Kline, Thomas S. K. Gilbert, Vikas Tyagi, Daowei Huang, Gabrielle C. Whiten, Jacob E. Larson, Xiaodong Wang, Kenneth H. Pearce, Laura E. Herring, Lee M. Graves, Stephen V. Frye, Michael J. Emanuele, Adrienne D. Cox, and Channing J. Der
CDK9 inhibitors may treat KRAS-mutant cancers by inducing MYC protein degradation.
By Anita K. Mehta, Kevin Hua, William Whipple, Minh-Thuy Nguyen, Ching-Ti Liu, Johannes Haybaeck, Joanne Weidhaas, Jeff Settleman, and Anurag Singh
The loss of microRNA miR-124 enables prosurvival autophagy signaling and metastatic features in KRAS mutant mesenchymal lung cancer cells.
By Erin Sheffels, Nancy E. Sealover, Chenyue Wang, Do Hyung Kim, Isabella A. Vazirani, Elizabeth Lee, Elizabeth M. Terrell, Deborah K. Morrison, Ji Luo, and Robert L. Kortum
Mutant RAS–selective dependence on the GEF SOS2 reveals tumor cell sensitivity to kinase inhibitors.
By Marco Biancucci, George Minasov, Avik Banerjee, Alfa Herrera, Patrick J. Woida, Matthew B. Kieffer, Lakshman Bindu, Maria Abreu-Blanco, Wayne F. Anderson, Vadim Gaponenko, Andrew G. Stephen, Matthew Holderfield, and Karla J. F. Satchell
A bacterial toxin effector domain disrupts RAS-ERK signaling by cleaving RAS through an unusual mechanism.
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