Table 1. Bypass resistance pathways after first-line osimertinib in EGFR-mutant NSCLC.
Bypass mechanism | Prevalence (%) | References |
---|---|---|
MET amplifications | 7–15 | (9,10) |
RET rearrangements | 3.7 | (9) |
ALK rearrangements | 3.0 | (9) |
BRAF rearrangements | 3.7 | (9) |
HER2 amplifications | 2.0 | (10) |
KRAS mutations | 2–7 | (9,10) |
PIK3CA mutations | 4.0 | (9) |
EGFR, epidermal growth factor receptor; NSCLC, non-small cell lung cancer; MET, mesenchymal-epithelial transition; RET, rearranged during transfection; ALK, anaplastic lymphoma kinase; BRAF, v-raf murine sarcoma viral oncogene homologue B; HER2, human epidermal growth factor receptor 2; KRAS, Kirsten rat sarcoma viral oncogene homolog; PIK3CA, PI3K P110α catalytic subunit.