ArticleLung cancer (Amsterdam, Netherlands)2017
Emergence of FGFR3-TACC3 fusions as a potential by-pass resistance mechanism to EGFR tyrosine kinase inhibitors in EGFR mutated NSCLC patients.
Article in Lung cancer (Amsterdam, Netherlands), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Oncogenic mutations in non-small cell lung cancer: from molecular mechanisms to clinical practice.Signal transduction and targeted therapy · 2026Review
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- Comprehensive characterization of MET exon 14 skipping mutations in non-small cell lung cancer.Respiratory research · 2026Article
- The resistance landscape of EGFR tyrosine kinase inhibitors in advanced non-small cell lung cancer: molecular mechanisms and novel therapeutic strategies.Translational lung cancer research · 2026Review
- Comprehensive Genomic Profiling for Precision Oncology: Analytical Validation and Clinical Utility in Solid Tumors.Diagnostics (Basel, Switzerland) · 2026Article
- Article
- FGFR3::TACC3 fusions in head and neck carcinomas: a study of nine cases highlighting phenotypic heterogeneity, frequent HPV association, and a morphologically distinct subset in favor of a putative entity.Virchows Archiv : an international journal of pathology · 2025Article
- Single-Cell RNA Sequencing in Unraveling Acquired Resistance to EGFR-TKIs in Non-Small Cell Lung Cancer: New Perspectives.International journal of molecular sciences · 2025Review
- FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway.Frontiers in oncology · 2025Article
- Potential biomarkers of primary resistance to first- and second-generation EGFR-TKIs in non-small-cell lung cancer: a real-world study.Therapeutic advances in medical oncology · 2025Article
- Development and validation of a radiomic prediction model for TACC3 expression and prognosis in non-small cell lung cancer using contrast-enhanced CT imaging.Translational oncology · 2025Article
- Clinical advances and challenges in targeting FGF/FGFR signaling in lung cancer.Molecular cancer · 2024Review
- Adaptive Darwinian off-target resistance mechanisms to selective RET inhibition in RET driven cancer.NPJ precision oncology · 2024Article
- Molecular Targeting of the Fibroblast Growth Factor Receptor Pathway across Various Cancers.International journal of molecular sciences · 2024Review
- Research progress on the role of bypass activation mechanisms in resistance to tyrosine kinase inhibitors in non-small cell lung cancer.Frontiers in oncology · 2024Review
- CRISPR-Cas13a Targeting the FGFR3-TACC3 Fusion Gene Inhibits Proliferation of Bladder Cancer Cells in vitro and in vivo.OncoTargets and therapy · 2024Article
- Review
- A Closer Look at EGFR Inhibitor Resistance in Non-Small Cell Lung Cancer through the Lens of Precision Medicine.Journal of clinical medicine · 2023Review
- Anti-angiogenic therapy for advanced primary pulmonary lymphoepithelioma-like carcinoma: a retrospective multicenter study.Journal of cancer research and clinical oncology · 2023Article
- Therapeutic strategies for EGFR-mutated non-small cell lung cancer patients with osimertinib resistance.Journal of hematology & oncology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
Abstract
Resistance to EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancers (NSCLCs) with activating EGFR mutations generally involve development of acquired secondary or tertiary EGFR mutations, such as T790M or C797S. However, case reports have demonstrated that actionable receptor tyrosine kinase fusions such as EML4-ALK, CCDC6-RET, and FGFR3-TACC3 can potentially confer resistance to EGFR TKIs. We seeked to identify the prevalence of FGFR3-TACC3 fusion transcripts as resistance mechanism to EGFR TKIs. Hybrid-capture based genomic profiling was performed on FFPE tissue samples and circulating tumor DNA isolated from peripheral whole blood in the course of clinical care. We performed a comprehensive survey of 17,319 clinical NSCLC samples (14,170 adenocarcinomas and 3149 NSCLC not otherwise specified (NOS)) and identified 5 cases of FGFR3-TACC3 containing the intact kinase domain of FGFR3 and the coiled-coil domain of TACC3 emerging after treatment with EGFR TKIs, including one previously reported index case. Of the 4 novel cases of FGFR3-TACC3, one emerged after erlotinib, one after afatinib, one after osimertinib, and one after ASP8273. These 5 cases of FGFR3-TACC3 fusions acquired post-EGFR TKI, while rare, indicate that FGFR3-TACC3 is a recurrent resistance mechanism, which can bypass EGFR blockade by all generations of EGFR TKIs in NSCLC. Routine re-biopsy and genomic profiling using platforms capable of detecting kinase fusions has the potential to inform new therapeutic strategies for patients with EGFR-mutant NSCLC progressing on TKIs.
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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.