MET Fusions in NSCLC: Clinicopathologic Features and Response to MET Inhibition

医学 腺癌 队列 内科学 肿瘤科 融合基因 癌症 置信区间 疾病 突变 人口统计学的 基因 遗传学 人口学 生物 社会学
作者
Richard Riedel,Jana Fassunke,Andreas H. Scheel,Matthias Scheffler,Carina Heydt,Lucia Nogová,Sebastian Michels,Rudolf‐Josef Fischer,Anna Eisert,Heather Scharpenseel,Felix John,Lea Ruge,Diana Schaufler,Janna Siemanowski,Michaela A. Ihle,Svenja Wagener‐Ryczek,Roberto Pappesch,Jan Rehker,Alexander C. Bunck,Carsten Kobe,Felix Keil,Sabine Merkelbach‐Bruse,Reinhard Büttner,Jürgen Wolf
出处
期刊:Journal of Thoracic Oncology [Elsevier]
卷期号:19 (1): 160-165 被引量:9
标识
DOI:10.1016/j.jtho.2023.06.020
摘要

Introduction MET fusions have been described only rarely in NSCLC. Thus, data on patient characteristics and treatment response are limited. We here report histopathologic data, patient demographics, and treatment outcome including response to MET tyrosine kinase inhibitor (TKI) therapy in MET fusion-positive NSCLC. Methods Patients with NSCLC and MET fusions were identified mostly by RNA sequencing within the routine molecular screening program of the national Network Genomic Medicine, Germany. Results We describe a cohort of nine patients harboring MET fusions. Among these nine patients, two patients had been reported earlier. The overall frequency was 0.29% (95% confidence interval: 0.15–0.55). The tumors were exclusively adenocarcinoma. The cohort was heterogeneous in terms of age, sex, or smoking status. We saw five different fusion partner genes (KIF5B, TRIM4, ST7, PRKAR2B, and CAPZA2) and several different breakpoints. Four patients were treated with a MET TKI leading to two partial responses, one stable disease, and one progressive disease. One patient had a BRAF V600E mutation as acquired resistance mechanism. Conclusions MET fusions are very rare oncogenic driver events in NSCLC and predominantly seem in adenocarcinomas. They are heterogeneous in terms of fusion partners and breakpoints. Patients with MET fusion can benefit from MET TKI therapy.
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