Overcoming Resistance to Egfr Inhibitors in Egfr-Mutant Nsclc

Volume 19
Erscheinungsjahr 2023
ISBN: 978-0-12-822833-3
Verlag: Elsevier Science

Buch, Englisch, 250 Seiten, Format (B × H): 191 mm x 235 mm, Gewicht: 450 g

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.

This book is a valuable resource for cancer researchers, clinicians, graduate students and other members of the biomedical field who are interested in promising treatments for lung cancer.

Autoren/Hrsg.

Faber, Anthony

Fachgebiete

• Naturwissenschaften Biowissenschaften Biowissenschaften

Inhaltsverzeichnis

1. The EGFR in NSCLC: Biology, activation and targeting2. Background of the EGFR receptor, biology of activation, regulation of EGFR in normal cells and cancer cells, mutations as oncogenic in NSCLC3. Background of EGFR inhibitor development and implementation, assessment of how EGFR inhibitors have been implemented and are currently implemented4. YAP signalling in EGFR inhibitor resistance5. Apoptosis resistance in EGFR inhibitor resistance6. EGFR mutations and resistance to EGFR inhibitors7. SCLC transformation and resistance to EGFR inhibitors8. EMT and resistance to EGFR inhibitors in EGFR mutant NSCLC9. Intratumoral heterogeneity and resistance10. Clinical trials of EGFR inhibitors in EGFR mutant lung cancer11. Methodology of the detection of resistant mechanisms in the lung cancer clinic

Über Autor(innen)

Faber, Anthony
Dr. Faber's research program includes studying resistance mechanisms to targeted therapies in lung cancer. During his postdoctoral training, he discovered that low expression levels of functional BIM, a pro-apoptotic protein, was sufficient to impart resistance to EGFR inhibitors in EGFR mutant lung cancer through loss of a cell death response. Loss of functional BIM is now part of clinical decision making for EGFR mutant lung cancer patients and combination therapy of EGFR inhibitors with BH3 mimetics to rescue or improve cell death responses are being explored clinically. Dr. Faber's laboratory more recently linked epithelial-to-mesenchymal related EGFR inhibitor resistance with low levels of BIM, and a deficient cell death response.