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Published byIne Thorvaldsen Modified over 6 years ago
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Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench Kenichi Suda, MD, PhD, Paul A. Bunn, MD, Christopher J. Rivard, PhD, Tetsuya Mitsudomi, MD, PhD, Fred R. Hirsch, MD, PhD Journal of Thoracic Oncology Volume 12, Issue 1, Pages (January 2017) DOI: /j.jtho Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions
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Figure 1 Molecular mechanisms that support residual tumor cells in the early phase of EGFR tyrosine kinase inhibitor (TKI) monotherapy. Preexistence of a minor resistance subpopulation that will survive frontline EGFR TKI monotherapy (A), reversible drug-tolerant state mainly observed in cell line models (B), survival signaling from microenvironment (fibroblasts or dying cancer cells) (C), and role of poor vascularization (D) are shown. MET, MET proto-oncogene, receptor tyrosine kinase gene; IGF-1R, insulin-like growth factor 1 receptor; NF-κB, nuclear factor kappa light-chain enhancer of activated B cells; STAT3, signal transducer and activator of transcription 3; YAP, yes-associated protein; BIM, BCL2 like 11; HGF, human growth factor. Journal of Thoracic Oncology , 27-35DOI: ( /j.jtho ) Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions
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