Open AccessA rare epidermal growth factor receptor H773L/V774M compound mutation in advanced non‐small‐cell lung cancer with poor response to epidermal growth factor receptor tyrosine kinase inhibitor
Author(s) -
Chen LunChe,
Shih JinYuan,
Yu ChongJen,
Yang ChingYao
Publication year - 2019
Publication title -
respirology case reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.304
H-Index - 9
ISSN - 2051-3380
DOI - 10.1002/rcr2.425
Subject(s) - afatinib , epidermal growth factor receptor , medicine , gefitinib , pemetrexed , lung cancer , t790m , cancer research , adenocarcinoma , tyrosine kinase inhibitor , oncology , tyrosine kinase , erlotinib , pathology , chemotherapy , cisplatin , cancer , receptor
Uncommon mutations account for 10–15% of epidermal growth factor receptor (EGFR) mutations in patients with non‐small‐cell lung cancer. Afatinib is currently the most efficient EGFR‐tyrosine kinase inhibitor (TKI) against uncommon EGFR mutations. Here we report a 56‐year‐old woman presenting with persistent cough for one month. She was diagnosed with stage IV lung adenocarcinoma by bronchoscopic biopsy to the left lower lung tumour and serial image modalities. A rare H773L/V774M compound mutation in exon 20 was detected by gene sequencing. The patient received first‐line afatinib but primary resistance was noted with rapid left lower lung tumour progression. Second‐line chemotherapy combined with bevacizumab, pemetrexed, and cisplatin demonstrated more durable response. Our case suggests that H773L/V774M may be one of the EGFR‐TKI‐resistant uncommon EGFR mutations.