Rapid Lorlatinib Response in Lung Adenocarcinoma With a Novel Y Chromosome Intergenic ALK Fusion: A Case Report

IF 3.9 3区医学 Q2 ONCOLOGY

Clinical lung cancer Pub Date : 2026-10-01 Epub Date: 2026-09-07 DOI:10.1016/j.cllc.2026.09.002

Jin-Ming Chen, Yi-Fan Kang, Yue-Can Zeng, Jing-Ru Luo, Shu Lin, Wen-Jun Tang

{"title":"Rapid Lorlatinib Response in Lung Adenocarcinoma With a Novel Y Chromosome Intergenic ALK Fusion: A Case Report","authors":"Jin-Ming Chen, Yi-Fan Kang, Yue-Can Zeng, Jing-Ru Luo, Shu Lin, Wen-Jun Tang","doi":"10.1016/j.cllc.2026.09.002","DOIUrl":null,"url":null,"abstract":"<div><h3>Clinical Practice Points</h3><div><ul><li><span>•</span><span><div>Unexplained rapid disease progression in young, never-smoker patients with lung adenocarcinoma warrants comprehensive large-panel DNA-NGS to detect atypical actionable driver mutations, especially when routine small-panel testing returns negative.</div></span></li><li><span>•</span><span><div>Atypical, focal, or weak ALK immunohistochemistry (IHC) signals should not be readily dismissed as artifacts; they can serve as early indicators of complex, non-canonical intergenic fusions resulting from cross-chromosomal genomic rearrangements.</div></span></li><li><span>•</span><span><div>The third-generation ALK inhibitor lorlatinib demonstrates profound systemic and intracranial efficacy against non-canonical Y-chromosome intergenic-ALK fusions, highlighting its role as a potent therapeutic option for atypical ALK variants.</div></span></li></ul></div></div><div><ul><li><span>•</span><span><div>Unexplained rapid disease progression in young, never-smoker patients with lung adenocarcinoma warrants comprehensive large-panel DNA-NGS to detect atypical actionable driver mutations, especially when routine small-panel testing returns negative.</div></span></li><li><span>•</span><span><div>Atypical, focal, or weak ALK immunohistochemistry (IHC) signals should not be readily dismissed as artifacts; they can serve as early indicators of complex, non-canonical intergenic fusions resulting from cross-chromosomal genomic rearrangements.</div></span></li><li><span>•</span><span><div>The third-generation ALK inhibitor lorlatinib demonstrates profound systemic and intracranial efficacy against non-canonical Y-chromosome intergenic-ALK fusions, highlighting its role as a potent therapeutic option for atypical ALK variants.</div></span></li></ul></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"27 8","pages":"Pages 69-73"},"PeriodicalIF":3.9000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical lung cancer","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S152573042600121X","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/9/7 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Clinical Practice Points

•
Unexplained rapid disease progression in young, never-smoker patients with lung adenocarcinoma warrants comprehensive large-panel DNA-NGS to detect atypical actionable driver mutations, especially when routine small-panel testing returns negative.
•
Atypical, focal, or weak ALK immunohistochemistry (IHC) signals should not be readily dismissed as artifacts; they can serve as early indicators of complex, non-canonical intergenic fusions resulting from cross-chromosomal genomic rearrangements.
•
The third-generation ALK inhibitor lorlatinib demonstrates profound systemic and intracranial efficacy against non-canonical Y-chromosome intergenic-ALK fusions, highlighting its role as a potent therapeutic option for atypical ALK variants.

•
Unexplained rapid disease progression in young, never-smoker patients with lung adenocarcinoma warrants comprehensive large-panel DNA-NGS to detect atypical actionable driver mutations, especially when routine small-panel testing returns negative.
•
Atypical, focal, or weak ALK immunohistochemistry (IHC) signals should not be readily dismissed as artifacts; they can serve as early indicators of complex, non-canonical intergenic fusions resulting from cross-chromosomal genomic rearrangements.
•
The third-generation ALK inhibitor lorlatinib demonstrates profound systemic and intracranial efficacy against non-canonical Y-chromosome intergenic-ALK fusions, highlighting its role as a potent therapeutic option for atypical ALK variants.

查看原文本刊更多论文

Lorlatinib在新型Y染色体基因间ALK融合的肺腺癌中的快速反应：1例报告。

临床实践要点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Clinical lung cancer 医学-肿瘤学

CiteScore

7.00

自引率

2.80%

发文量

159

审稿时长

24 days

期刊介绍： Clinical Lung Cancer is a peer-reviewed bimonthly journal that publishes original articles describing various aspects of clinical and translational research of lung cancer. Clinical Lung Cancer is devoted to articles on detection, diagnosis, prevention, and treatment of lung cancer. The main emphasis is on recent scientific developments in all areas related to lung cancer. Specific areas of interest include clinical research and mechanistic approaches; drug sensitivity and resistance; gene and antisense therapy; pathology, markers, and prognostic indicators; chemoprevention strategies; multimodality therapy; and integration of various approaches.