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. 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.

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.