神经胶质瘤是一种侵袭性的神经胶质来源的脑肿瘤，具有高度异质性，由于其对传统治疗方案的内在抵抗力，给治疗带来了重大挑战。它的特点是关键信号通路中表观遗传和遗传改变之间的相互作用，这进一步证实了它们的抵抗潜力。异常的 DNA 甲基化模式、组蛋白修饰和非编码 RNA 可能会改变与药物反应和细胞存活相关的基因表达，诱导基因沉默或解除对神经胶质瘤耐药性的关键途径的调节。有证据表明，表观遗传可塑性使神经胶质瘤细胞能够动态适应治疗方案，并形成耐药亚群。此外，肿瘤微环境增加了表观遗传调控的额外输入，增加了耐药机制的复杂性。在此，我们讨论导致神经胶质瘤耐药机制的表观遗传变化，以描绘新的治疗靶点和实现个性化治疗的潜在方法。版权所有 © 2024 Elsevier B.V. 保留所有权利。

Glioma, an aggressive type of brain tumors of glial origin is highly heterogeneous, posing significant treatment challenges due to its intrinsic resistance to conventional therapeutic schemes. It is characterized by an interplay between epigenetic and genetic alterations in key signaling pathways which further endorse their resistance potential. Aberrant DNA methylation patterns, histone modifications and non-coding RNAs may alter the expression of genes associated with drug response and cell survival, induce gene silencing or deregulate key pathways contributing to glioma resistance. There is evidence that epigenetic plasticity enables glioma cells to adapt dynamically to therapeutic schemes and allow the formation of drug-resistant subpopulations. Furthermore, the tumor microenvironment adds an extra input on epigenetic regulation, increasing the complexity of resistance mechanisms. Herein, we discuss epigenetic changes conferring to drug resistance mechanisms in gliomas in order to delineate novel therapeutic targets and potential approaches that will enable personalized treatment.Copyright © 2024 Elsevier B.V. All rights reserved.