文章：

在融合蛋白驱动的恶性肿瘤中靶向染色质复合物

Targeting chromatin complexes in fusion protein-driven malignancies

原文发布日期：2019-04-08

DOI: 10.1038/s41568-019-0132-x

类型: Review Article

开放获取: 否

英文摘要：

Recurrent chromosomal rearrangements leading to the generation of oncogenic fusion proteins are a common feature of many cancers. These aberrations are particularly prevalent in sarcomas and haematopoietic malignancies and frequently involve genes required for chromatin regulation and transcriptional control. In many cases, these fusion proteins are thought to be the primary driver of cancer development, altering chromatin dynamics to initiate oncogenic gene expression programmes. In recent years, mechanistic insights into the underlying molecular functions of a number of these oncogenic fusion proteins have been discovered. These insights have allowed the design of mechanistically anchored therapeutic approaches promising substantial treatment advances. In this Review, we discuss how our understanding of fusion protein function is informing therapeutic innovations and illuminating mechanisms of chromatin and transcriptional regulation in cancer and normal cells.

摘要翻译： 

导致致癌融合蛋白产生的反复染色体易位是许多癌症的共同特征。这些异常在肉瘤和造血系统恶性肿瘤中尤为普遍，且常涉及染色质调控和转录控制所需的基因。在许多情况下，这些融合蛋白被认为是癌症发展的主要驱动因素，通过改变染色质动力学来启动致癌基因表达程序。近年来，人们对多种致癌融合蛋白的分子功能机制有了深入认识，这些认知使得基于机制锚定的治疗方法得以设计，预示着肿瘤治疗将取得重大进展。本综述将探讨我们对融合蛋白功能的理解如何推动治疗创新，并揭示癌症细胞与正常细胞中染色质和转录调控机制。

原文链接：

Targeting chromatin complexes in fusion protein-driven malignancies