PU.1 表达降低与 Tet2 缺失协同作用触发髓系白血病发生。
Reduced PU.1 Expression Collaborates with Tet2 Loss to Trigger Myeloid Leukemogenesis.
机构信息
Division of Hematology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Department of Microbiology and Immunology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
出版信息
Blood Cancer Discov. 2022 Sep 6;3(5):378-381. doi: 10.1158/2643-3230.BCD-22-0100.
Abstract
The leukemic transformation of hematopoietic stem and progenitor cells in the setting of Tet2 deficiency is driven by PU.1 gene network loss through complementary reduction in PU.1 expression and hypermethylation of ETS loci at the enhancers of PU.1 target genes. See related article by Aivalioti et al., p. 444 (6).
摘要
Tet2 缺陷情况下造血干祖细胞的白血病转化是由 PU.1 基因网络缺失驱动的，其机制是 PU.1 表达降低和 PU.1 靶基因增强子上 ETS 位点的超甲基化作用形成互补。见 Aivalioti 等人的相关文章，第 444 页（6）。
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2
Clonal hematopoiesis: Mutation-specific adaptation to environmental change.克隆性造血：突变特异性适应环境变化。
Cell Stem Cell. 2022 Jun 2;29(6):882-904. doi: 10.1016/j.stem.2022.05.006.
3
The Cell Type-Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia.健康人类造血和 TET2 突变性白血病的细胞类型特异性 5hmC 景观和动态。
Blood Cancer Discov. 2022 Jul 6;3(4):346-367. doi: 10.1158/2643-3230.BCD-21-0143.
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TET2 mutations are associated with hypermethylation at key regulatory enhancers in normal and malignant hematopoiesis.TET2 突变与正常和恶性造血中关键调节增强子的高甲基化有关。
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