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Science Signaling|September 26, 2013
Bypass mechanisms of resistance to receptor tyrosine kinase inhibition in lung cancerMatthew J Niederst, Jeffrey A EngelmanThe FEBS Journal|February 21, 2012
Suppression of survival signalling pathways by the phosphatase PHLPPAudrey K O'Neill, Matthew J Niederst, Alexandra C NewtonThe Lancet. Oncology|April 8, 2015
Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of originMatthew G Oser, Matthew J Niederst, Lecia V Sequist, et al.Clinical Cancer Research : an Official Journal of the American Association for Cancer Research|May 13, 2015
The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment StrategiesMatthew J Niederst, Haichuan Hu, Hillary E Mulvey, et al.Blood Cancer Discovery|June 27, 2025
DLBCL cells emerge post CD19 CAR-T with cross-antigen resistance and a gene signature predictive of clinical CAR-T responseFabiana Lϋӧnd, Jeanne Whalen, Youngchul Song, et al.Cell Reports|March 24, 2023
Integrated CRISPR screening and drug profiling identifies combination opportunities for EGFR, ALK, and BRAF/MEK inhibitorsRalph Tiedt, Frederick J King, Christelle Stamm, et al.JCO Precision Oncology|August 21, 2018
Heterogeneity and Coexistence of T790M and T790 Wild-Type Resistant Subclones Drive Mixed Response to Third-Generation Epidermal Growth Factor Receptor Inhibitors in Lung CancerZofia Piotrowska, Mehlika Hazar-Rethinam, Coleen Rizzo, et al.Biorxiv : the Preprint Server for Biology|February 8, 2024
Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancerLeslie Duplaquet, Kevin So, Alexander W Ying, et al.Cancer Discovery|May 3, 2015
Heterogeneity Underlies the Emergence of EGFRT790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR InhibitorZofia Piotrowska, Matthew J Niederst, Chris A Karlovich, et al.Pageof 3