Journal Basic Info

  • Impact Factor: 2.709**
  • H-Index: 11 
  • ISSN: 2474-1663
  • DOI: 10.25107/2474-1663
**Impact Factor calculated based on Google Scholar Citations. Please contact us for any more details.

Major Scope

  •  Sarcomas
  •  Haemato-Oncology
  •  Paediatric Cancers
  •  Endometrial Cancer
  •  Targeted Therapy
  •  Palliative Care
  •  Carcinomas
  •  Neoadjuvant Therapy


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

*Correspondance to: Portugal GM 

 PDF  Full Text Case Report | Open Access


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..

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