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

IF 29.7 1区 医学 Q1 ONCOLOGY
Elmira Khabusheva, Margaret A Goodell
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引用次数: 0

Abstract

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.

Ruxolitinib能否抑制TET2-和IDH2-驱动的克隆性造血?
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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来源期刊
Cancer discovery
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.
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