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).

中文翻译：

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完全抑制 JAK2V617F 增强骨髓增殖性肿瘤的分子反应

摘要：Dunbar、Bowman 及其同事在此提出了一种新型遗传小鼠模型，该模型在内源基因座中可诱导且可逆地表达 JAK2V617F 突变。这项研究的结果清楚地表明，骨髓增生性肿瘤起始细胞的生存绝对需要这种突变，并且意味着即使在存在其他协同突变的情况下，更有效的抑制剂也可以对这些患者起到治疗作用。请参阅 Dunbar 等人的相关文章，第 17 页。 737（8）。