完全抑制 JAK2V617F 可增强骨髓增殖性肿瘤的分子反应

IF 29.7 1区 医学 Q1 ONCOLOGY Cancer discovery Pub Date : 2024-05-01 DOI:10.1158/2159-8290.cd-23-1522
Hamza Celik, Grant A. Challen
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引用次数: 0

摘要

摘要:Dunbar、Bowman 及其同事在此介绍了一种新型遗传小鼠模型,该模型在内源性基因座上可诱导和可逆地表达 JAK2V617F 突变。这项研究的结果清楚地表明,骨髓增生性肿瘤启动细胞的存活对这种突变有绝对的要求,这意味着即使在有其他合作突变的情况下,更有效的抑制剂也能治愈这些患者。参见 Dunbar 等人的相关文章,第 737 页(8)。
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Enhanced Molecular Response in Myeloproliferative Neoplasms with Complete JAK2V617F Inhibition
Summary: Dunbar, Bowman, and colleagues present here a novel genetic mouse model with inducible and reversible expression of the JAK2V617F mutation in the endogenous locus. Results from this study clearly demonstrate an absolute requirement for myeloproliferative neoplasm–initiating cells for this mutation in their survival and imply that more efficacious inhibitors could be curative for these patients even in the setting of additional cooperating mutations. See related article by Dunbar et al., p. 737 (8).
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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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