Path and Evolution of Drug-Resistant Clones in Lung Cancer
Posted: Tuesday, January 23, 2018
New insight into the evolution of acquired resistance in non–small cell lung cancers to EGFR inhibitors has presented opportunities to intercept developing resistance in the clinic. Research conducted by Jeffrey Engelman, MD, PhD; Aaron N. Hata, MD, PhD; and colleagues at the Massachusetts General Hospital, Boston, addresses the complex interactions that lead to clonal resistance and the potential for future targeted therapies. These research findings were presented by Dr. Hata at the American Association for Cancer Research–International Association for the Study of Lung Cancer (AACR-IASLC) International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic (Abstract IA18).
In a previous study, cultures from EGFR inhibitor–resistant patient tumors were used to determine apoptotic responses of drug-tolerant cells. The investigators identified cells that showed suppressed apoptotic responses (low-BIM cells) and treated them to stimulate apoptosis. The cancers then demonstrated an increased sensitivity to original targeted therapies. Findings from this previous study and ongoing research present an opportunity for novel therapeutic strategies to target processes such as adaptive signaling changes and epigenetic plasticity to prevent or perhaps delay the development of drug resistance.
Findings from this previous study and ongoing research present an opportunity for novel therapeutic strategies to target processes such as adaptive signaling changes and epigenetic plasticity to prevent or perhaps delay the development of drug resistance.
