ETV6-NTRK3 as a resistance mechanism to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors: favorable response after combination of osimertinib and entrectinib: a case report and literature review.

Wei Xie, Han Luo, Huan Wang, Guangqing Shi, Jiajun Tang, Lijie Ma, Jing Zhou

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In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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5 · Who and what money

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7 authors.

Wei Xie *Department of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Han Luo *Department of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Huan WangDepartment of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Guangqing ShiDepartment of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Jiajun TangDepartment of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Lijie MaDepartment of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Jing ZhouDepartment of Respiratory and Critical Care Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), typified by osimertinib, yield substantial efficacy in non-small cell lung cancer (NSCLC) with sensitizing EGFR mutations. However, acquired tumor resistance to these agents is unavoidable and driven by heterogeneous mechanisms, which dictate subsequent therapeutic selection. A key resistance pathway involves activation of alternative oncogenic signaling; beyond classic alterations (C797S mutation, MET amplification, HER2 variants), rare oncogenic drivers may also emerge. We report a case of an EGFR exon 19 deletion-positive NSCLC patient who developed osimertinib resistance after first-line therapy. Second-line rebiopsy identified an ETV6-NTRK3 (neurotrophic tyrosine receptor kinase [NTRK]) fusion. Combination therapy with osimertinib and entrectinib induced regression of pulmonary lesions, but the patient ultimately discontinued all targeted agents due to the development of severe hepatorenal failure and

Indexed as

acquired resistance to EGFR-TKIentrectinibnon-small cell lung cancerNTRK fusionosimertinib

Identifiers

PMID41948726

DOI10.3389/fphar.2026.1762137

PMCPMC13050915

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.