Turning the focus to EGFR inhibitors, Sandip P. Patel, MD, discusses their mechanism action and the improved toxicity profile of next-generation inhibitors.
Case: A 60-Year-Old Woman with Early-Stage Non–Small Cell Lung Cancer
Initial presentation and Clinical Workup
This is a video synopsis/summary of a Case-Based Peer Perspectives featuring Sandip P. Patel, MD.
EGFR small-molecule inhibitors work by inhibiting the mutated, hyperactivated EGFR kinase in cancer cells. These oral targeted therapies essentially turn off an oncogenic signaling switch promoting uncontrolled growth. By shutting down aberrant EGFR activity, the drugs can induce cancer cell cycle arrest and death.
There are multiple generations of EGFR inhibitors. Later-generation agents have better central nervous system penetration to control brain metastases and are more selective, sparing wild-type EGFR inhibition that causes adverse effects like rash and diarrhea. By improving tolerability along with antitumor efficacy, these treatments can enhance patient quality of life compared to traditional chemotherapy.
Obtaining molecular profiling to identify EGFR mutations is thus critical to delivering optimal-quality, personalized therapy in non–small cell lung cancer (NSCLC). Pairing the right drug with the right patient molecular profile is imperative whether considering metastatic or localized disease settings. EGFR testing helps identify those who may derive profound benefit from genotype-directed therapy.
Video synopsis is AI-generated and reviewed by Targeted Oncology™ editorial staff.