Abstract
MET exon14 skipping mutations (METex14s) are rarely reported as a potential resistance mechanism to EGFR tyrosine kinase inhibitors (TKIs). The efficacy of targeted therapy against METex14s emerging after osimertinib resistance is uncertain. Herein, we report a case of EGFR-mutated metastatic lung adenocarcinoma in which METex14 was detected in a re-biopsy upon first-line osimertinib resistance. The patient received capmatinib monotherapy as third-line therapy, which was ineffective, followed by an exceptional response to salvage therapy with afatinib. This report highlights the heterogeneity of EGFR-TKI resistance and that targeting rare resistance mechanisms remains challenging.
Keywords:
Capmatinib; MET; Osimertinib; Resistance; exon14 skipping.
Copyright © 2024 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.
MeSH terms
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Acrylamides* / therapeutic use
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Adenocarcinoma of Lung* / drug therapy
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Adenocarcinoma of Lung* / genetics
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Afatinib / administration & dosage
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Afatinib / therapeutic use
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Aniline Compounds* / therapeutic use
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Antineoplastic Agents / therapeutic use
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Benzamides / therapeutic use
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Drug Resistance, Neoplasm* / genetics
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ErbB Receptors* / genetics
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Exons / genetics
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Humans
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Imidazoles
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Indoles
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Lung Neoplasms* / drug therapy
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Lung Neoplasms* / genetics
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Lung Neoplasms* / pathology
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Male
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Protein Kinase Inhibitors / therapeutic use
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Proto-Oncogene Proteins c-met* / genetics
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Pyrimidines
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Salvage Therapy
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Triazines / administration & dosage
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Triazines / therapeutic use
Substances
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Acrylamides
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Afatinib
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Aniline Compounds
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Antineoplastic Agents
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Benzamides
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capmatinib
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EGFR protein, human
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ErbB Receptors
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Imidazoles
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Indoles
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MET protein, human
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osimertinib
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Protein Kinase Inhibitors
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Proto-Oncogene Proteins c-met
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Pyrimidines
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Triazines