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Cancer Cell|December 19, 2012
Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer modelsRyan B Corcoran, Katherine A Cheng, Aaron N Hata, et al.
Nature|August 12, 2021
Cycling cancer persister cells arise from lineages with distinct programsYaara Oren, Michael Tsabar, Michael S Cuoco, et al.
Biorxiv : the Preprint Server for Biology|May 7, 2026
Dual inhibition of GTP-bound (ON) and GDP-bound (OFF) KRAS G12C suppresses PI3Kα and leads to potent tumor inhibitionKatherine Parker, Samar Ghorbanpoor, Wafa Malik, et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|February 23, 2020
MET Alterations Are a Recurring and Actionable Resistance Mechanism in ALK-Positive Lung CancerIbiayi Dagogo-Jack, Satoshi Yoda, Jochen K Lennerz, et al.
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology|January 27, 2018
Impact of EML4-ALK Variant on Resistance Mechanisms and Clinical Outcomes in ALK-Positive Lung CancerJessica J Lin, Viola W Zhu, Satoshi Yoda, et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|June 4, 2025
STX-721, a Covalent EGFR/HER2 Exon 20 Inhibitor, Utilizes Exon 20-Mutant Dynamic Protein States and Achieves Unique Mutant Selectivity Across Human Cancer ModelsRaymond A Pagliarini, Jack A Henderson, Benjamin C Milgram, et al.
Cell|February 7, 2025
GUK1 activation is a metabolic liability in lung cancerJaime L Schneider, Kiran Kurmi, Yutong Dai, et al.
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