ArticleJournal of cancer research and clinical oncology2022
Afatinib, an effective treatment for patient with lung squamous cell carcinoma harboring uncommon EGFR G719A and R776C co-mutations.
Article in Journal of cancer research and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Clinical outcome of Brazilian patients with non-small cell lung cancer in early stage harboring rare mutations in epidermal growth factor receptor.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Case Report: Heterogeneity of Resistance Mechanisms in Different Lesions Co-Mediate Acquired Resistance to First-Line Icotinib in EGFR Mutant Non-Small Cell Lung Cancer.Frontiers in medicine · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpidermal growth factor receptor (EGFR) is a crucial driven gene in non-small cell lung cancer (NSCLC), and the EGFR mutation rate in lung squamous cell carcinoma (SCC) is only 3 ~ 6.92%. Uncommon EGFR mutations, such as S768I, L861Q and G719X, accounting for approximately 15% of NSCLC harboring EGFR mutation. Afatinib, a second-generation EGFR-tyrosine kinase inhibitor (TKI), has been approved for NSCLC harboring uncommon mutations by the FDA in 2018. In our report, the lung SCC patient harboring uncommon compound EGFR mutation (G719A and R776C) benefited from afatinib. CASE PRESENTATION: A case of a lung SCC patient harboring uncommon compound EGFR mutation (G719A and R776C) benefited from afatinib, and new MYC amplification was detected by next-generation sequencing (NGS) after disease progression.
conclusionsThis case first identified a patient with lung squamous cell carcinoma harboring uncommon compound EGFR mutation (G719A and R776C) benefited from afatinib and achieved 11 months of progression-free survival (PFS). Then, new MYC amplification was detected after disease progression, indicating that MYC amplification may be one of the reasons for afatinib resistance.
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