MYB/MYBL1基因改变的神经胶质瘤经常携带MYB和MYBL1基因的截断和非生产性融合

IF 9.3 1区 医学 Q1 CLINICAL NEUROLOGY Acta Neuropathologica Pub Date : 2024-10-18 DOI:10.1007/s00401-024-02803-0
Hye-Jung Chung, Sharika Rajan, Zhichao Wu, Christina K. Ferrone, Mark Raffeld, Ina Lee, Jeffrey Gagan, Christopher Dampier, Zied Abdullaev, Manoj Tyagi, Patrick. J. Cimino, Martha Quezado, Kenneth Aldape
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引用次数: 0

摘要

携带MYB或MYBL1复发性基因组改变的星形细胞瘤是2021年《世界卫生组织中枢神经系统肿瘤分类》中新认定的一类儿科型弥漫低级别胶质瘤。这些肿瘤在WHO分类中被描述为携带MYB或MYBL1融合。在本报告中,我们研究了14例连续发现MYB或MYBL1改变的病例(6例血管中心型胶质瘤和8例弥漫型星形细胞瘤,MYB或MYBL1改变),每个病例都通过全基因组DNA甲基化图谱进行了诊断确认,并研究了这些基因的特定基因组改变。通过 RNA 测序,我们发现仅有 5/14 个病例的 MYB 或 MYBL1 基因发生了有成效的框架内融合。其余 9 个病例的基因组发生了改变,导致基因截断,但没有证据表明存在框架内融合的伴侣。基因表达分析表明,无论是否存在生产性融合,MYB(L1)基因都会过度表达。此外,QKI是血管中心性胶质瘤中常见的公认融合伙伴,与由1000个不同类型的中枢神经系统肿瘤组成的队列相比,无论QKI是否存在基因组改变,这14个病例中的QKI都普遍上调。总之,研究结果表明,在没有产生融合的情况下,MYB(L1)基因的截短很可能会驱动肿瘤的发生,这对分析和诊断血管中心型胶质瘤和弥漫性星形细胞瘤、MYB或MYBL1基因改变的病例具有重要意义,尤其是对那些通过旨在重点检测融合的检测板进行检测的病例。
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MYB/MYBL1-altered gliomas frequently harbor truncations and non-productive fusions in the MYB and MYBL1 genes

Astrocytomas that harbor recurrent genomic alterations in MYB or MYBL1 are a group of Pediatric-type diffuse low-grade gliomas that were newly recognized in the 2021 WHO Classification of Tumors of the Central Nervous System. These tumors are described in the WHO classification as harboring fusions in MYB or MYBL1. In this report, we examine 14 consecutive cases in which a MYB or MYBL1 alteration was identified, each with diagnostic confirmation by genome-wide DNA methylation profiling (6 Angiocentric gliomas and 8 Diffuse astrocytomas, MYB- or MYBL1-altered), for their specific genomic alterations in these genes. Using RNA sequencing, we find productive in-frame fusions of the MYB or MYBL1 genes in only 5/14 cases. The remaining 9 cases show genomic alterations that result in truncation of the gene, without evidence of an in-frame fusion partner. Gene expression analysis showed overexpression of the MYB(L1) genes, regardless of the presence of a productive fusion. In addition, QKI, a recognized fusion partner common in angiocentric glioma, was generally up-regulated in these 14 cases, compared to a cohort comprising >1000 CNS tumors of various types, regardless of whether a genomic alteration in QKI was present. Overall, the results show that truncations, in the absence of a productive fusion, of the MYB(L1) genes can likely drive the tumors and have implications for the analysis and diagnosis of Angiocentric glioma and Diffuse astrocytoma, MYB- or MYBL1-altered, especially for cases that are tested on panels designed to focus on fusion detection.

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来源期刊
Acta Neuropathologica
Acta Neuropathologica 医学-病理学
CiteScore
23.70
自引率
3.90%
发文量
118
审稿时长
4-8 weeks
期刊介绍: Acta Neuropathologica publishes top-quality papers on the pathology of neurological diseases and experimental studies on molecular and cellular mechanisms using in vitro and in vivo models, ideally validated by analysis of human tissues. The journal accepts Original Papers, Review Articles, Case Reports, and Scientific Correspondence (Letters). Manuscripts must adhere to ethical standards, including review by appropriate ethics committees for human studies and compliance with principles of laboratory animal care for animal experiments. Failure to comply may result in rejection of the manuscript, and authors are responsible for ensuring accuracy and adherence to these requirements.
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