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adrienne cox

As seen in: Nature, USA Today, Science Magazine, Cell Reports, The Journal of Clinical Investigation, Times Record News, Genes and Development Journal, The News-Star, The Journal of Biological Chemistry

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Articles

Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition

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By Andrew Waters, Bjoern Papke, Craig Goodwin, G. Aaron Hobbs, J. Nathaniel Diehl, Runying Y. Yang, Katherine Walsh, Rita Sulahian, James M McFarland, Kevin S. Kapner, Thomas Gilbert, Clint A. Stalnecker, Sehrish Javaid, Anna Barkovskaya, Kajal R Grover, Devon R. Blake, Antje Schaefer, Katherine Nowak, Jennifer E. Klomp, Tikvah K Hayes, Nanyun Tang, Kaisheng Chen, Yingyao Zhou, Manpreet Kalkat, Laura Herring, Lee Graves, Linda Z. Penn, Hongwei Yin, Andrew J. Aguirre, William Hahn, adrienne cox, Channing J. Der, A. Cole Edwards, Priya S. Hibshman, Michelle Kassner, Olga Tanaseichuk
| Cell Reports Verified
Main text (Cell Reports 35, 109291; June 29, 2021) There are errors in two figures of this paper. In Figure 6C, the p130Cas, total ERK, and phospho-p130Cas immunoblots inadvertently display alternative exposures from Figure 3D. In Figure S10B, images of four KX2-391-treated ex vivo tumors were inadvertently duplicated in the ERKi-treated ex vivo tumors.
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KRAS: the Achilles’ heel of pancreas cancer biology

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By Kristina Drizyte-Miller, Taiwo Talabi, Ashwin Somasundaram, adrienne cox
| The Journal of Clinical Investigation
Abstract The genetic landscape of pancreatic ductal adenocarcinoma (PDAC) is well-established and dominated by four key genetic driver mutations. Mutational activation of the KRAS oncogene is the initiating genetic event, followed by genetic loss of function of the CDKN2A, TP53, and SMAD4 tumor suppressor genes.
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Drugging mutant KRAS by disrupting binding to effectors and GTP - Nature Cancer

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By adrienne cox, Channing J. Der
| Nature Verified
Although enhancing the GTPase activity of KRAS is an attractive approach to inhibit constitutively active, GTP-bound mutant KRAS, so far this has not been achieved. Now, a RAS inhibitor thought to act by preventing engagement of downstream effectors is shown to also reactivate cycling to the inactive GDP-bound state.
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