A 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. Issue 5 (10th April 2019)

• Record Type: Journal Article
• Authors: Chen, Lun‐Che; Shih, Jin‐Yuan; Yu, Chong‐Jen; Yang, Ching‐Yao
• Is Part Of: Respirology case reports. Volume 7:Issue 5(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-04-10
• Subjects: Afatinib -- epidermal growth factor receptor -- H773L/V774M -- non‐small‐cell lung cancer -- uncommon mutations; Respiratory organs -- Diseases -- Periodicals; 616.2005
• DOI: 10.1002/rcr2.425
• Languages: English
• ISSNs: 2051-3380

Abstract

Abstract : 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. Abstract : Here, we report a case of advanced non‐small‐cell lung cancer with a rare epidermal growth factor receptor (EGFR) exon 20 H773L/V774M compound mutation, which demonstrated poor clinical response to afatinib, a second‐generation EGFR‐TKI with pan‐human EGFR blocking activity. The anti‐cancer treatment was shifted to platinum‐based chemotherapy, which resulted in a partial response.