ArticleThoracic cancer2017
Concurrent epidermal growth factor receptor T790M secondary mutation and epithelial-mesenchymal transition in a lung adenocarcinoma patient with EGFR-TKI drug resistance.
Article in Thoracic cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- MZT2A drives epithelial-mesenchymal transition in lung adenocarcinoma via the LGALS3BP/ITGB1/TGF-β/smad2 axis.iScience · 2026Article
- Histological transformation in lung adenocarcinoma: Insights of mechanisms and therapeutic windows.Journal of translational internal medicine · 2024Article
- Retroperitoneal Metastasis, with Marked Fibrosis, of Lung Adenocarcinoma after Afatinib Treatment: An Autopsy Case Report.Internal medicine (Tokyo, Japan) · 2020Article
- Specificity Assessment of CRISPR Genome Editing of Oncogenic EGFR Point Mutation with Single-Base Differences.Molecules (Basel, Switzerland) · 2019Article
- Approaches to Tumor Classification in Pulmonary Sarcomatoid Carcinoma.Lung Cancer (Auckland, N.Z.) · 2019Review
- Radiation-induced sarcoma in a 10-year survivor with stage IV EGFR-mutated lung adenocarcinoma.Respiratory medicine case reports · 2019Article
- Cytokine-induced killer cells as a feasible adoptive immunotherapy for the treatment of lung cancer.Cell death & disease · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Almost all epidermal growth factor receptor (EGFR)-mutant lung cancers develop resistance to EGFR-tyrosine kinase inhibitors. Several mechanisms for this acquired resistance have been identified, including development of an EGFR T790M mutation, MET amplification, hepatocyte growth factor overexpression, loss of phosphatase and tensin homolog expression, epithelial-mesenchymal transition, and transformation to small cell lung cancer. Herein, we report a case of a lung cancer patient with EGFR exon 19 deletion who was resistant to EGFR-tyrosine kinase inhibitor treatment during disease progression. Using histological and gene sequencing analysis, we observed that the primary adenocarcinoma acquired T790M mutation in EGFR exon 20, and a secondary sarcomatoid carcinoma developed in the vicinity. Assessment of E-cadherin and Vimentin expression confirmed that the sarcomatoid carcinoma had undergone an epithelial-mesenchymal transition. Therefore, it is important to perform a tissue re-biopsy after the development of resistance to identify the best treatment options. Surgical resection might be a better "salvage" treatment in cases of oligometastatic progression.
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Registered trials
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