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恶性神经胶质瘤发病机制中的表观遗传功能障碍。

The epigenetic dysfunction underlying malignant glioma pathogenesis.

机构信息

Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.

出版信息

Lab Invest. 2022 Jul;102(7):682-690. doi: 10.1038/s41374-022-00741-7. Epub 2022 Feb 12.

DOI:10.1038/s41374-022-00741-7
PMID:35152274
Abstract

Comprehensive molecular profiling has dramatically transformed the diagnostic neuropathology of brain tumors. Diffuse gliomas, the most common and deadly brain tumor variants, are now classified by highly recurrent biomarkers instead of histomorphological characteristics. Several of the key molecular alterations driving glioma classification involve epigenetic dysregulation at a fundamental level, implicating fields of biology not previously thought to play major roles glioma pathogenesis. This article will review the major epigenetic alterations underlying malignant gliomas, their likely mechanisms of action, and potential strategies for their therapeutic targeting.

摘要

全面的分子谱分析极大地改变了脑肿瘤的诊断神经病理学。弥漫性神经胶质瘤是最常见和最致命的脑肿瘤变体,现在根据高度复发的生物标志物进行分类,而不是根据组织形态学特征。驱动神经胶质瘤分类的几个关键分子改变涉及基本水平的表观遗传失调,暗示以前认为在神经胶质瘤发病机制中不起主要作用的生物学领域。本文将综述恶性神经胶质瘤的主要表观遗传改变、它们的可能作用机制以及针对它们的治疗靶点的潜在策略。

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