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Overcoming resistance to EGFR inhibitors in EGFR mutant NSCLC
Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC presents updated information on how EGFR mutant lung cancers evolve to evade EGFR inhibitors, clinical strategies that identify these mechanisms, and how to implement newer therapeutic strategies to combat resistance and improve patient survival. As resistance to EGFR inhibitors is often through re-activation of MEK/ERK and PI3K pathways, or through loss of cell death responses, there is much overlap with resistance to targeted therapies in other paradigms, such as BRAF inhibitors in BRAF mutant melanoma, and HER2 inhibitors in HER2 amplified breast cancer.
Intro -- Cancer Sensitizing Agents for Chemotherapy: Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC -- Copyright -- Cover Image Insert -- Aims and Scope for Series ``Cancer Sensitizing Agents for Chemotherapy´´ -- About the Series Editor -- Aims and Scope of the Volume -- About the Volume Editor -- Preface -- Contents -- Contributors -- Chapter 1: Historical development of EGFR-targeted therapy -- Introduction -- Pan-cancer preclinical studies and phase I trials of EGFR TKIs -- Early phase II/III clinical trials of gefitinib and erlotinib on lung cancer -- EGFR mutations as biomarker of TKI response and approval of EGFR TKIs in EGFR-mutated lung cancer -- Development of second-generation EGFR TKIs -- Development of third-generation EGFR TKIs -- EGFR TKI in early-stage completely resected lung cancer patients -- References -- Chapter 2: The development and implementation of EGFR inhibitors in advanced NSCLC -- Introduction -- A brief overview of EGFR structure and signaling -- First-generation EGFR tyrosine kinase inhibitors -- Gefitinib -- Erlotinib -- First-generation EGFR inhibitors in patients with an activating EGFR mutation -- Second-generation EGFR inhibitors -- Third-generation EGFR inhibitors -- Osimertinib in brain metastases of patients with EGFR-mutant NSCLC -- Exon 20 insertions -- Checkpoint inhibitor therapy in patients with EGFR mutations -- Current standard management of EGFR-mutant patients -- Conclusions -- Future directions -- References -- Chapter 3: YAP/TAZ-mediated resistance to EGFR inhibitors -- Introduction -- Regulation of YAP/TAZ through the Hippo pathway-dependent and -independent mechanisms -- The role of YAP/TAZ in human cancer -- Interplay between YAP/TAZ and the EGFR signaling pathway -- The role of YAP/TAZ in resistance to EGFR inhibitors.
Key signaling changes induced by EMT in EGFR-mutant NSCLC -- Receptor tyrosine kinases that are active specifically in mesenchymal-like EGFR-mutant NSCLC AXL and FGFR -- Other molecules outside of RTKs that become active in mesenchymal EGFR mutant NSCLC -- Integrins -- CD44 -- CDK7 -- YAP1 -- NOTCH1 -- Acquired resistance to targeted therapies and BCL2 family members -- Cell death and EMT in EGFR inhibitor resistance in EGFR-mutant NSCLC -- Targeting BCL-xL to resensitize to EGFR inhibitors in EMT EGFR-mutant NSCLC -- Conclusions -- References -- Index.
Includes bibliographical references and index.
Cancer sensitizing agents for chemotherapy ; v. 19