细胞周期：开启 EZH2 靶向疗法抗药性的钥匙

IF 29.7 1区医学 Q1 ONCOLOGY

Cancer discovery Pub Date : 2024-06-03 DOI:10.1158/2159-8290.CD-24-0186

Rachel L Paolini, George P Souroullas

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引用次数: 0

摘要

摘要：本期，Kazansky及其同事的一项研究探讨了恶性横纹肌瘤（MRT）和上皮样肉瘤（ES）抑制EZH2后的耐药机制。研究发现了EZH2本身的基因改变，以及汇聚于RB1-E2F介导的细胞周期控制的改变，并证明抑制细胞周期激酶（如极光激酶B (AURKB)）可以绕过EZH2抑制剂的耐药性，提高疗效。参见 Kazansky 等人的相关文章，第 965 页（6）。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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The Cell Cycle: a Key to Unlock EZH2-targeted Therapy Resistance.

Summary: In this issue, a study by Kazansky and colleagues explored resistance mechanisms after EZH2 inhibition in malignant rhabdoid tumors (MRT) and epithelioid sarcomas (ES). The study identified genetic alterations in EZH2 itself, along with alterations that converge on RB1-E2F-mediated cell-cycle control, and demonstrated that inhibition of cell-cycle kinases, such as Aurora Kinase B (AURKB) could bypass EZH2 inhibitor resistance to enhance treatment efficacy. See related article by Kazansky et al., p. 965 (6).

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来源期刊

Cancer discovery ONCOLOGY-

CiteScore

22.90

自引率

1.40%

发文量

838

审稿时长

6-12 weeks

期刊介绍： Cancer Discovery publishes high-impact, peer-reviewed articles detailing significant advances in both research and clinical trials. Serving as a premier cancer information resource, the journal also features Review Articles, Perspectives, Commentaries, News stories, and Research Watch summaries to keep readers abreast of the latest findings in the field. Covering a wide range of topics, from laboratory research to clinical trials and epidemiologic studies, Cancer Discovery spans the entire spectrum of cancer research and medicine.