Longitudinal Assessment of EGFR and MET Transcriptional Activity Using Cell-Free Chromatin Immunoprecipitation in Two Patients with EGFR-Mutated Non-Small Cell Lung Cancer

Background/Objectives: MET amplification represents the most common bypass resistance mechanism to EGFR tyrosine kinase inhibitor (TKI) treatment in EGFR-mutated non-small cell lung cancer (NSCLC). Combination therapy with the EGFR-TKI, osimertinib, and the MET-TKI, crizotinib, has demonstrated clinical efficacy in overcoming this resistance. However, assessing MET transcriptional activity during treatment remains challenging.