Unravelling the complexity of -mutated lung adenocarcinoma: a unique case report with histological transformations and co-alteration acquisition.

Date publication

février 2025

Journal

Translational lung cancer research

Auteurs

Membres identifiés du Cancéropôle Est :
Pr CLAVEL Christine , Dr DALSTEIN Véronique , Dr OUDART Jean-Baptiste

Tous les auteurs :
Boutahir A, Dalstein V, Oudart JB, Deslee G, Clavel C, Dewolf M, Durlach A, Ancel J

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/40114956

Résumé

Osimertinib, a third-generation tyrosine kinase inhibitor that targets epidermal growth factor receptor (EGFR), specifically inhibits both EGFR tyrosine kinase inhibitor-sensitive mutations and T790M resistance mutations. Despite initial positive responses to EGFR tyrosine kinase inhibitors, nearly all patients eventually experience disease progression. Mechanisms of resistance are classically divided into EGFR-dependent and EGFR-independent mechanisms, such as the activation of alternative pathways and histological changes. We report a case of histological transformation into large cell carcinoma associated with the subsequent acquisition of an anaplastic lymphoma kinase (ALK) rearrangement after osimertinib exposure.

Mots clés

Epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), case report, large-cell neuroendocrine carcinoma (LCNEC), transformation

Référence

Transl Lung Cancer Res. 2025 02 28;14(2):639-648