[表观遗传失调驱动多发性骨髓瘤]。

Hiroto Ohguchi
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引用次数: 0

摘要

多发性骨髓瘤(MM)是由遗传改变的积累引发和促进的。然而,MM高度依赖骨髓微环境,这表明表观遗传失调在MM的发病机制中起着重要作用。事实上,最近使用下一代测序的研究已经揭示了MM的表观遗传改变。包括MM在内的癌症发展中涉及的表观遗传调控可以在多种癌症类型中观察到,也可以特异于单一癌症类型。前一种类型的调控与多种癌症类型常见的驱动事件相关,我和我的同事最近发现了kdm5a介导的H3K4甲基化周期在激活myc驱动转录中的重要性。后一种类型与谱系限制表观遗传程序密切相关。在MM中,b细胞分化因子IL-6可能部分介导MM不同的表观遗传程序。本文讨论了MM的表观遗传失调,重点介绍了我们最近的发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Epigenetic dysregulation driving multiple myeloma].

Multiple myeloma (MM) is triggered and promoted by the accumulation of genetic alterations. However, MM is highly dependent on the bone marrow microenvironment, which suggests that epigenetic deregulation plays a significant role in the pathogenesis of MM. Indeed, recent studies using next-generation sequencing have revealed epigenetic alterations in MM. Epigenetic regulation involved in the development of cancers, including MM, can either be observed across multiple cancer types or be specific to a single cancer type. The former type of regulation is associated with driver events common to multiple cancer types, and my colleagues and I have recently identified the importance of the KDM5A-mediated H3K4 methylation cycle in activating MYC-driven transcription. The latter type is closely related to lineage-restricted epigenetic programs. In MM, the B-cell differentiation factor IL-6 may partly mediate the MM-distinct epigenetic program. This article discusses epigenetic deregulation in MM, focusing on our recent findings.

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