Journal Basic Info
- Head and Neck Oncology
- Neoadjuvant Therapy
- Breast Cancer
- Pancreatic Cancer
- Kidney Cancer
- Thoracic Oncology
Citation: Clin Oncol. 2023;8(1):2013.DOI: 10.25107/2474-1663.2013
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
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.
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..