Dual TKI Therapy in Acquired ALK Gene Fusion as Mechanism of Resistance to Osimertinib in EGFR-Mutant Advanced NSCLC

Portugal GM, Sousa AC2 and Alves P

Hospital Pulido Valente, Centro Hospitalar Universitário Lisboa Norte (CHULN), Portugal
GenoMed—Diagnosticos De Medicina Molecular, S.A., Avenida Professor Egas Moniz, Portugal

^*Correspondance to: Portugal GM 

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Abstract:

Epidermal Growth Factor Receptor (EGFR) gene somatic activating mutations account for approximately 20% of lung adenocarcinomas. Tyrosine Kinase Inhibitors (TKIs) are the standard therapy of advanced Non-Small Lung Cancer (NSCLC) harboring EGFR gene mutations. Response to TKI is inevitably followed by acquired resistance and disease progression. The mechanisms of resistance to EGFR-TKIs are remarkably heterogeneous. In recent years, the mutual exclusive possibility of EGFR mutations and ALK rearrangements has been questioned. In fact, several reports show a prevalence of 1.6% of these concomitant mutations in advanced NSCLC with only 0.13% of EGFR-mutated NSCLC developing TKI resistance by acquired ALK translocation. Inhere, a case of an acquired ALK rearrangement following the development of resistance to Osimertinib treatment is reported as well as the efficacy and safety of dual TKI therapy.

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Cite the Article:

Portugal GM, Sousa AC, Alves P. Dual TKI Therapy in Acquired ALK Gene Fusion as Mechanism of Resistance to Osimertinib in EGFR-Mutant Advanced NSCLC. Clin Oncol. 2023;8:2013..