Identification of a EML4-ALK exon 19 fusion variant in lung adenocarcinoma and alectinib resistance. (October 2021)

• Record Type: Journal Article
• Authors: Liu, Di; Xu, Xinyan; Wen, Junmiao; Zhang, Chi; Fan, Min
• Is Part Of: Lung cancer. Volume 160(2021)
• Page Start: 32
• Page End: 35
• Publication Date: 2021-10
• Subjects: Lung cancer -- ALK variants -- ALK TKIs -- Case report; Lungs -- Cancer -- Periodicals; Lung Neoplasms -- Abstracts; Lung Neoplasms -- Periodicals; Poumons -- Cancer -- Périodiques; Lungs -- Cancer; Periodicals; Electronic journals; Electronic journals; 616.99424
• DOI: 10.1016/j.lungcan.2021.07.020
• Languages: English
• ISSNs: 0169-5002

Abstract

Highlights: Most ALK variants are sensitive to ALK TKIs, refractory subtype is uncommon. The additional protein coded by ALK exon 19 could compete with ALK TKI binging site. The identified ALK variant may be correlated with poor response to ALK TKIs . Abstract: Alectinib, a highly selective inhibitor of anaplastic lymphoma kinase (ALK), has shown a high response rate and long progression-free survival in primary treatment of ALK-positive non-small-cell lung cancer (NSCLC). De novo resistance or refractory subtype is rare event. Herein, we identify the first case with serial next-generation sequencing (NGS) results that harboured a rare echinoderm microtubule associated protein like 4 gene ( EML4 ) -ALK (breaking site at exon 19) fusion in a lung adenocarcinoma (LUAD) patient who acquired alectinib resistance rapidly (less than 3 months), followed by multi-drug resistance and short survival time.