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Lyla J. Stanland on Muck Rack

Lyla J. Stanland

As seen in: Cell Press, The Journal of Clinical Investigation
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Articles

Inverted chimeric RNAi molecules synergistically co-target MYC and KRAS in KRAS-driven cancers

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By Yogitha Chareddy, Hayden P Huggins, Snehasudha S. Sahoo, Lyla J. Stanland
| The Journal of Clinical Investigation
ResearchOncology Open Access | 10.1172/JCI187204 J Clin Invest. https://doi.org/10.1172/JCI187204. Copyright © 2025, Chareddy et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. View PDF Abstract Mutant KRAS has been implicated in driving a quarter of all cancer types.
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A first-in-class EGFR-directed KRAS G12V selective inhibitor

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By Lyla J. Stanland, Hayden P Huggins, Snehasudha S. Sahoo, Alessandro Porrello, Yogitha Chareddy, Salma H. Azam, Jillian Perry, Pradeep S. Pallan, Kristina M. Whately, Lincy Edatt, WIlliam Green, William Green, Matthew Fleming, Jonah Im, Christina Gutierrez-Ford, Imani Simmons, Alyaa Dawoud, Katherine Zhou, Vandanaa Jayaprakash, Albert Wielgus, Justin Milner, Martin Egli, Albert A. Bowers, Chad V. Pecot
| Cell Press Verified
Keywords KRAS siRNA RNA interference mutant-selective cancer ligand conjugation EGFR angiogenesis siRNA delivery lung cancer Introduction The Kirsten rat sarcoma (KRAS) proto-oncogene encodes a small GTPase that is crucial for the activation of numerous intracellular signaling pathways that regulate cell proliferation, survival, and differentiation.
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Identification of Host Biomarkers of Epstein-Barr Virus Latency IIb and Latency III

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By Joshua E. Messinger, Joanne Dai, Alexander M. Price, Lyla J. Stanland
| asm.org
Research Article | Host-Microbe Biology Joshua E. Messinger, Joanne Dai, Lyla J. Stanland, Alexander M. Price, Micah A. Luftig Richard Frederick Ambinder, Invited Editor, Diane E. Griffin, Editor DOI: 10.1128/mBio.01006-19 ABSTRACT Deciphering the molecular pathogenesis of virally induced cancers is challenging due, in part, to the heterogeneity of both viral gene expression and host gene expression.
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