Open AccessResponse to tyrosine kinase inhibitors in lung adenocarcinoma with the rare epidermal growth factor receptor mutation S768I and G724S : A case report and literature review
Author(s) -
Zhang Cuicui,
Lin Li,
Zuo Ran,
Wang Yajie,
Chen Peng
Publication year - 2020
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13606
Subject(s) - afatinib , osimertinib , medicine , epidermal growth factor receptor , lung cancer , adenocarcinoma , cancer research , tyrosine kinase , gefitinib , mutation , erlotinib , oncology , epidermal growth factor , tyrosine kinase inhibitor , targeted therapy , chemotherapy , cancer , receptor , gene , biology , genetics
Mutations in the epidermal growth factor receptor (EGFR) are drivers of a subset of lung cancers. In recent years, the treatment of non‐small cell lung cancer (NSCLC), especially with EGFR inhibitors, has made rapid progress, and the median progression‐free survival (PFS) of patients with EGFR gene‐sensitive mutations has been significantly prolonged. However, the response effect of some uncommon EGFR mutations to tyrosine kinase inhibitors (TKIs) remains unclear. Here, we present a patient with multiple EGFR mutations that highlights tumor heterogeneity leading to a mixed molecular response to targeted drugs and emphasizes the complexity of EGFR‐driven lung cancer. He received chemotherapy and molecular‐targeted treatment including icotinib, afatinib, osimertinib and afatinib + osimertinib. In conclusion, patients with lung adenocarcinoma harboring the EGFR S768I and G724S mutations appear less sensitive to icotinib than patients with sensitive EGFR. However, the patient in our report benefited from treatment with afatinib. Here, we hope to provide information for the treatment of rare and compound mutations in patients.