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亚塑性甲状腺癌的一小组含有MET变化,具有潜在的治疗选择

Sarah Theurer¹, Hans-Ulrich Schildhaus², Thomas Herold¹

¹Institute of Pathology, University Hospital Essen and Faculty of Medicine, University of Duisburg-Essen, Essen, Germany.

Pathology, research and practice

|September 26, 2025

概括

无塑性甲状腺癌 (ATC) 在10%的病例中存在MET变异,包括基因放大和融合. 早期的分子测试可以在临床试验中确定有资格接受向抗MET疗法的患者.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

无塑性甲状腺癌 (ATC) 是一种具有有限治疗选择的侵袭性癌症.
针对特定基因变异 (BRAFV600E,NTRK,ALK,RET) 的向疗法已被批准用于ATC.
在其他癌症中发现了MET变化,并且已获得批准的治疗方法,但在ATC中了解得很少.

研究的目的:

调查ATC中MET变化的频率和治疗相关性.
提供MET基因放大,融合和ATC中的蛋白质表达的全面概述.
为了将分子发现与临床数据和瘤形态相关联.

主要方法:

分析了28个ATC样本,使用MET免疫组织化学 (IHC),光在位杂交 (FISH) 和RNA/DNA下一代测序.
分子发现与瘤形态和临床随访的相关性.
评估MET基因放大 (≥10.0平均基因数) 和ETV6-MET融合.

主要成果:

在10% (3/28) 的ATC样本中发现了MET变化,包括顶级基因放大和ETV6-MET融合.
在具有MET变化的样本中,IHC证实了MET蛋白的过度表达.
MET变异与BRAF,RAS和PIK3CA突变相互排斥,但与TP53和TERT促进子突变同时发生.

结论:

MET顶级放大和MET基因融合发生在ATC的一个子集中.
这些MET变化可能可以通过现有的抗MET疗法来向.
基于RNA的测序和FISH是推的生物标记测试,用于识别ATC中的MET变化,以获得临床试验资格.

关键词:

无塑性甲状腺癌是一种甲状腺癌.这就是CAPZA2-MET.在 ETV6-MET 播放.在MET中,MET是MET.在MET中,融合是MET.分子瘤瘤董事会分子瘤瘤董事会

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