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Genetic Modifiers such as Fas Regulate Tumor-Cell Dependence on Mutant EGFRGrant Why?
Grandis, JenniferPerson Why?
Acquired Resistance of EGFR-Mutant Lung Cancer to a T790M-Specific EGFR Inhibitor: Emergence of a Third Mutation (C797S) in the EGFR Tyrosine Kinase Domain.Academic Article Why?
Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers.Academic Article Why?
Local therapy with continued EGFR tyrosine kinase inhibitor therapy as a treatment strategy in EGFR-mutant advanced lung cancers that have developed acquired resistance to EGFR tyrosine kinase inhibitors.Academic Article Why?
A urokinase receptor-Bim signaling axis emerges during EGFR inhibitor resistance in mutant EGFR glioblastoma.Academic Article Why?
Co-activation of STAT3 and YES-Associated Protein 1 (YAP1) Pathway in EGFR-Mutant NSCLC.Academic Article Why?
EGFR-targeted therapies in the post-genomic era.Academic Article Why?
EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.Academic Article Why?
Resistance to EGFR-targeted therapy by Ets-1 inactivation.Academic Article Why?
Targeted Inhibition of EGFR and Glutaminase Induces Metabolic Crisis in EGFR Mutant Lung Cancer.Academic Article Why?
AUY922 effectively overcomes MET- and AXL-mediated resistance to EGFR-TKI in lung cancer cells.Academic Article Why?
Erlotinib versus radiation therapy for brain metastases in patients with EGFR-mutant lung adenocarcinoma.Academic Article Why?
Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers.Academic Article Why?
Programmed death-ligand 1 expression and T790M status in EGFR-mutant non-small cell lung cancer.Academic Article Why?
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