Ruxolitinib能否抑制TET2-和IDH2-驱动的克隆性造血？

IF 29.7 1区医学 Q1 ONCOLOGY Cancer discovery Pub Date : 2024-10-04 DOI:10.1158/2159-8290.CD-24-1020

Elmira Khabusheva, Margaret A Goodell

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引用次数: 0

摘要

在本期杂志中，Waarts及其同事开发了一种先进的体外CRISPR筛选平台，用于识别克隆造血（CH）中的漏洞。这一独特的系统使作者能够确定 IDH2 和 TET2 CH 突变、组蛋白去甲基化酶和细胞因子信号转导改变之间的联系，从而通过 ruxolitinib 靶向消除 CH 克隆，为预防恶性肿瘤的发展提供了可能的途径。参见Waarts等人的相关文章，第1860页。

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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Can Ruxolitinib Crash TET2- and IDH2-Driven Clonal Hematopoiesis?

In this issue, Waarts and colleagues developed an advanced ex vivo CRISPR screening platform to identify vulnerabilities in clonal hematopoiesis (CH). This unique system allowed the authors to identify a link between IDH2 and TET2 CH mutations, histone demethylases, and altered cytokine signaling, which enabled targeting by ruxolitinib leading to the elimination of CH clones, offering a possible path for preventing the development of malignancy. See related article by Waarts et al., p. 1860.

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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.