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Anil K. Rustgi on Muck Rack

Anil K. Rustgi

As seen in: Nature, MDPI, Science Magazine, Cell Press, Cell Stem Cell, HemOnc Today, Genes and Development Journal
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Articles

Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis

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By Adrien Grimont, David J. Falvo, Whitney J. Sisso, Francisco Santos, Christopher Chan, Paul Zumbo, William Fall, Katherine R Ferrick, Grace A. Pan, Megan Cleveland, Tomer M. Yaron-Barir, Alexa Osterhoudt, Yinuo Meng, Maria Paz Zafra, André F. Rendeiro, Erika Hissong, Rhonda K. Yantiss, Doron Betel, Mark A. Magnuson Verified, Steven Leach, Anil K. Rustgi, Lukas Dow, Rohit Chandwani
| Cell Press Verified
Keywords pancreatic ductal adenocarcinoma KRAS inflammation lineage reversion epigenetic reprogramming acinar-ductal metaplasia EGFR RAC1 VAV1 G12R Get full text access Log in, subscribe or purchase for full access. References 1. Means, A.L. ∙ Meszoely, I.M. ∙ Suzuki, K. ... Pancreatic epithelial plasticity mediated by acinar cell transdifferentiation and generation of nestin-positive intermediates Development. 2005; 132:3767-3776 2. Fendrich, V. ∙ Esni, F. ∙ Garay, M.V.R. ...
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Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia

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By Michael Quante, Govind Bhagat, Julian Abrams, Pamela Good, Michele Lee, Yoomi Lee, Richard D. Friedman, Samuel Asfaha, Zinaida A. Dubeykovskaya, Umar Mahmood, Jose-Luiz Figueiredo, Jan K. Kitajewski, Carrie J. Shawber, Charles J. Lightdale, Anil K. Rustgi, Timothy C. Wang, Frederic Marache
| Cell Press Verified
Main text (Cancer Cell 21, 36–51; January 17, 2012) This publication reports that bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia, identifying Lgr5+ and Dclk1+ cells at the squamocolumnar junction as a potential origin of Barrett-like metaplasia and esophageal adenocarcinoma. We, the editors of Cancer Cell, were made aware of a query regarding Figure 7A, in which the mouse Barrett and adenocarcinoma panels appear to overlap.
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High-throughput screening identifies NT-1 that synergizes with MRTX1133 against acquired resistant KRAS G12D colorectal cancer

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By Ning Wei, Emiko Nagai, Michele Houston, Leonard H Augenlicht, Alice E. Shin, Joel T. Gabre, Anil K. Rustgi, Grace Ha, Lindsay M. LaFave, Edward Chu, Seiya Kitamura, Natalie Thielen, Chaoyuan Kuang
| Nature Verified
Abstract Metastatic colorectal cancer (mCRC) remains a significant clinical challenge, with a 5-year survival rate of 10%. Approximately 40% of CRCs harbor mutations in the KRAS gene, leading to poor response to standard therapy. This underscores the crucial need for novel therapeutics targeting KRAS and overcoming the growing barrier of resistance.
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