Despite the efficacy of osimertinib in the first-line treatment of advanced EGFR-mutated NSCLC, the development of resistance is nearly inevitable. BRAF mutations and fusions are reported in 1% to 3% of patients with EGFR-mutated NSCLC receiving osimertinib and represent potential targetable alterations. In this case report, we discuss the rationale for EGFR-MEK co-inhibition in a patient with EGFR-mutated NSCLC treated with osimertinib that developed a CTNNA1-BRAF fusion at progression. In addition, we provide a brief overview of the current evidence of BRAF fusions as an acquired resistance mechanism to osimertinib and potential treatment strategies.
BRAF Fusion as Resistance Mechanism to Osimertinib in EGFR-Mutated NSCLC: A Case Report and Review of Literature / Peroni, M.; Leonetti, A.; Minari, R.; Verze, M.; Gnetti, L.; Bottarelli, L.; Azzoni, C.; Galaverni, M.; Simoni, N.; Missale, G.; Biasini, E.; Tiseo, M.. - In: JTO CLINICAL AND RESEARCH REPORTS. - ISSN 2666-3643. - 6:8(2025). [10.1016/j.jtocrr.2025.100867]
BRAF Fusion as Resistance Mechanism to Osimertinib in EGFR-Mutated NSCLC: A Case Report and Review of Literature
Peroni M.;Leonetti A.;Gnetti L.;Azzoni C.;Simoni N.;Missale G.;Biasini E.;Tiseo M.
2025-01-01
Abstract
Despite the efficacy of osimertinib in the first-line treatment of advanced EGFR-mutated NSCLC, the development of resistance is nearly inevitable. BRAF mutations and fusions are reported in 1% to 3% of patients with EGFR-mutated NSCLC receiving osimertinib and represent potential targetable alterations. In this case report, we discuss the rationale for EGFR-MEK co-inhibition in a patient with EGFR-mutated NSCLC treated with osimertinib that developed a CTNNA1-BRAF fusion at progression. In addition, we provide a brief overview of the current evidence of BRAF fusions as an acquired resistance mechanism to osimertinib and potential treatment strategies.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
