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- The EGFR in NSCLC: Biology, activation and targeting
2. Background of the EGFR receptor, biology of activation, regulation of EGFR in normal cells and cancer cells, mutations as oncogenic in NSCLC
3. Background of EGFR inhibitor development and implementation, assessment of how EGFR inhibitors have been implemented and are currently implemented
4. YAP signalling in EGFR inhibitor resistance
5. Apoptosis resistance in EGFR inhibitor resistance
6. EGFR mutations and resistance to EGFR inhibitors
7. SCLC transformation and resistance to EGFR inhibitors
8. EMT and resistance to EGFR inhibitors in EGFR mutant NSCLC
9. Intratumoral heterogeneity and resistance
10. Clinical trials of EGFR inhibitors in EGFR mutant lung cancer
11. Methodology of the detection of resistant mechanisms in the lung cancer clinic
Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC, Volume 17 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.
- Presents historical context on how NSCLC and SCLC has been treated, with an emphasis on NSCLC and how the concept of EGFR inhibitors has been implemented
- Discusses critical resistant mechanisms seen in the clinic to 1st, 2nd and 3rd generation EGFR inhibitors
- Encompasses the current state of affairs in clinical trials to address resistance
Cancer researchers, medical scientists, clinicians, graduate students
- No. of pages:
- © Academic Press 2021
- 1st March 2021
- Academic Press
- Hardcover ISBN:
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.
Co-leader. Developmental therapeutics, Massey Cancer Center, Associate Professor, Virginia Commonwealth University, USA
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