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1
Transformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transduced TEL/JAK2 fusion genes.通过逆转录病毒转导的TEL/JAK2融合基因，造血细胞系转化为生长因子非依赖性，并在小鼠中诱发致命的骨髓和淋巴增殖性疾病。
EMBO J. 1998 Sep 15;17(18):5321-33. doi: 10.1093/emboj/17.18.5321.
2
Fusion of the ets transcription factor TEL to Jak2 results in constitutive Jak-Stat signaling.ets转录因子TEL与Jak2融合导致组成型Jak-Stat信号传导。
Blood. 1999 Jun 15;93(12):4354-64.
3
Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2.Stat5对于由TEL/JAK2诱导的骨髓和淋巴细胞增殖性疾病至关重要。
Mol Cell. 2000 Sep;6(3):693-704. doi: 10.1016/s1097-2765(00)00067-8.
4
Transforming properties of chimeric TEL-JAK proteins in Ba/F3 cells.嵌合TEL-JAK蛋白在Ba/F3细胞中的转化特性。
Blood. 2000 Mar 15;95(6):2076-83.
5
Constitutive activation of STAT3 and STAT5 is induced by leukemic fusion proteins with protein tyrosine kinase activity and is sufficient for transformation of hematopoietic precursor cells.具有蛋白酪氨酸激酶活性的白血病融合蛋白可诱导STAT3和STAT5的组成性激活，这足以使造血前体细胞发生转化。
Exp Hematol. 2002 Mar;30(3):262-71. doi: 10.1016/s0301-472x(01)00787-1.
6
Socs-1 inhibits TEL-JAK2-mediated transformation of hematopoietic cells through inhibition of JAK2 kinase activity and induction of proteasome-mediated degradation.Socs-1通过抑制JAK2激酶活性并诱导蛋白酶体介导的降解来抑制TEL-JAK2介导的造血细胞转化。
Mol Cell Biol. 2001 May;21(10):3547-57. doi: 10.1128/MCB.21.10.3547-3557.2001.
7
Constitutively active STAT5 variants induce growth and survival of hematopoietic cells through a PI 3-kinase/Akt dependent pathway.组成型激活的STAT5变体通过PI 3激酶/Akt依赖性途径诱导造血细胞的生长和存活。
Oncogene. 2001 Apr 19;20(17):2080-90. doi: 10.1038/sj.onc.1204308.
8
TEL/PDGFbetaR fusion protein activates STAT1 and STAT5: a common mechanism for transformation by tyrosine kinase fusion proteins.TEL/血小板衍生生长因子β受体融合蛋白激活信号转导和转录激活因子1及信号转导和转录激活因子5：酪氨酸激酶融合蛋白介导细胞转化的共同机制
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9
Signal transduction and transforming properties of the TEL-TRKC fusions associated with t(12;15)(p13;q25) in congenital fibrosarcoma and acute myelogenous leukemia.先天性纤维肉瘤和急性髓性白血病中与t(12;15)(p13;q25)相关的TEL-TRKC融合蛋白的信号转导及转化特性
EMBO J. 2000 Apr 17;19(8):1827-38. doi: 10.1093/emboj/19.8.1827.
10
The TEL/PDGFbetaR fusion in chronic myelomonocytic leukemia signals through STAT5-dependent and STAT5-independent pathways.慢性粒单核细胞白血病中的TEL/PDGFβR融合蛋白通过STAT5依赖和非依赖途径发出信号。
Blood. 2001 Dec 1;98(12):3390-7. doi: 10.1182/blood.v98.12.3390.

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The role of the Janus-faced transcription factor PAX5-JAK2 in acute lymphoblastic leukemia.两面神转录因子PAX5-JAK2在急性淋巴细胞白血病中的作用
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6
The tyrosine phosphatase SHP2 is required for cell transformation by the receptor tyrosine kinase mutants FIP1L1-PDGFRα and PDGFRα D842V.受体酪氨酸激酶突变体FIP1L1-PDGFRα和PDGFRα D842V介导的细胞转化需要酪氨酸磷酸酶SHP2。
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7
Signal transducer and activator of transcription-1 localizes to the mitochondria and modulates mitophagy.信号转导和转录激活因子1定位于线粒体并调节线粒体自噬。
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8
Identification of Ponatinib as a potent inhibitor of growth, migration, and activation of neoplastic eosinophils carrying FIP1L1-PDGFRA.鉴定泊那替尼是一种有效的抑制剂，可抑制携带 FIP1L1-PDGFRA 的肿瘤性嗜酸性粒细胞的生长、迁移和激活。
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9
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10
Combined targeting of JAK2 and Bcl-2/Bcl-xL to cure mutant JAK2-driven malignancies and overcome acquired resistance to JAK2 inhibitors.联合靶向 JAK2 和 Bcl-2/Bcl-xL 以治愈突变 JAK2 驱动的恶性肿瘤并克服对 JAK2 抑制剂的获得性耐药。
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本文引用的文献

1
Fusion of Huntingtin interacting protein 1 to platelet-derived growth factor beta receptor (PDGFbetaR) in chronic myelomonocytic leukemia with t(5;7)(q33;q11.2).在伴有t(5;7)(q33;q11.2)的慢性粒单核细胞白血病中，亨廷顿相互作用蛋白1与血小板衍生生长因子β受体（PDGFβR）融合。
Blood. 1998 Jun 15;91(12):4419-26.
2
Cloning and characterization of the human homolog of mouse Jak2.小鼠Jak2的人类同源物的克隆与特性分析
Blood. 1998 Feb 1;91(3):844-51.
3
Induction of epithelial tubules by growth factor HGF depends on the STAT pathway.生长因子HGF诱导上皮小管的形成依赖于STAT信号通路。
Nature. 1998 Jan 15;391(6664):285-8. doi: 10.1038/34657.
4
FGFR1 is fused with a novel zinc-finger gene, ZNF198, in the t(8;13) leukaemia/lymphoma syndrome.在t(8;13)白血病/淋巴瘤综合征中，成纤维细胞生长因子受体1（FGFR1）与一种新的锌指基因ZNF198发生融合。
Nat Genet. 1998 Jan;18(1):84-7. doi: 10.1038/ng0198-84.
5
B lymphocytes from patients with chronic lymphocytic leukemia contain signal transducer and activator of transcription (STAT) 1 and STAT3 constitutively phosphorylated on serine residues.慢性淋巴细胞白血病患者的B淋巴细胞含有信号转导子和转录激活子（STAT）1和STAT3，其丝氨酸残基持续磷酸化。
J Clin Invest. 1997 Dec 15;100(12):3140-8. doi: 10.1172/JCI119869.
6
Retrovirus-mediated gene transfer of NPM-ALK causes lymphoid malignancy in mice.逆转录病毒介导的NPM-ALK基因转移可导致小鼠发生淋巴恶性肿瘤。
Blood. 1997 Oct 15;90(8):2901-10.
7
Constitutive activation of JAKs and STATs in BCR-Abl-expressing cell lines and peripheral blood cells derived from leukemic patients.在表达BCR-Abl的细胞系以及白血病患者来源的外周血细胞中JAKs和STATs的组成性激活。
J Immunol. 1997 Nov 15;159(10):4720-8.
8
A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia.一种在人类白血病中具有组成性激酶活性的TEL-JAK2融合蛋白。
Science. 1997 Nov 14;278(5341):1309-12. doi: 10.1126/science.278.5341.1309.
9
Fusion of TEL, the ETS-variant gene 6 (ETV6), to the receptor-associated kinase JAK2 as a result of t(9;12) in a lymphoid and t(9;15;12) in a myeloid leukemia.由于在淋巴细胞白血病中存在t(9;12)以及在髓系白血病中存在t(9;15;12)，导致ETS变异基因6（ETV6）的TEL与受体相关激酶JAK2融合。
Blood. 1997 Oct 1;90(7):2535-40.
10
Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.BCR/ABL对造血细胞的转化需要激活PI-3k/Akt依赖的信号通路。
EMBO J. 1997 Oct 15;16(20):6151-61. doi: 10.1093/emboj/16.20.6151.

通过逆转录病毒转导的TEL/JAK2融合基因，造血细胞系转化为生长因子非依赖性，并在小鼠中诱发致命的骨髓和淋巴增殖性疾病。

Transformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transduced TEL/JAK2 fusion genes.

作者信息

Schwaller J, Frantsve J, Aster J, Williams I R, Tomasson M H, Ross T S, Peeters P, Van Rompaey L, Van Etten R A, Ilaria R, Marynen P, Gilliland D G

机构信息

Division of Hematology and Oncology, Harvard Medical School, Boston, MA 02115, USA.

出版信息

EMBO J. 1998 Sep 15;17(18):5321-33. doi: 10.1093/emboj/17.18.5321.

DOI:10.1093/emboj/17.18.5321
PMID:9736611
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1170859/
Abstract

Recent reports have demonstrated fusion of the TEL gene on 12p13 to the JAK2 gene on 9p24 in human leukemias. Three variants have been identified that fuse the TEL pointed (PNT) domain to (i) the JAK2 JH1-kinase domain, (ii) part of and (iii) all of the JH2 pseudokinase domain. We report that all of the human TEL/JAK2 variants, and a human/mouse chimeric hTEL/mJAK2(JH1) fusion gene, transform the interleukin-3 (IL-3)-dependent murine hematopoietic cell line Ba/F3 to IL-3-independent growth. Transformation requires both the TEL PNT domain and JAK2 kinase activity. Furthermore, all TEL/JAK2 variants strongly activated STAT 5 by phosphotyrosine Western blots and by electrophoretic mobility shift assays (EMSA). Mice (n = 40) transplanted with bone marrow infected with the MSCV retrovirus containing either the hTEL/mJAK2(JH1) fusion or its human counterpart developed a fatal mixed myeloproliferative and T-cell lymphoproliferative disorder with a latency of 2-10 weeks. In contrast, mice transplanted with a TEL/JAK2 mutant lacking the TEL PNT domain (n = 10) or a kinase-inactive TEL/JAK2(JH1) mutant (n = 10) did not develop the disease. We conclude that all human TEL/JAK2 fusion variants are oncoproteins in vitro that strongly activate STAT 5, and cause lethal myelo- and lymphoproliferative syndromes in murine bone marrow transplant models of leukemia.

摘要

最近的报告显示，在人类白血病中12p13上的TEL基因与9p24上的JAK2基因发生了融合。已鉴定出三种变体，它们将TEL尖（PNT）结构域与（i）JAK2 JH1激酶结构域、（ii）部分JH2假激酶结构域以及（iii）全部JH2假激酶结构域融合。我们报告称，所有人类TEL/JAK2变体以及一个人/鼠嵌合hTEL/mJAK2（JH1）融合基因，均可将依赖白细胞介素-3（IL-3）的小鼠造血细胞系Ba/F3转化为不依赖IL-3的生长状态。转化需要TEL PNT结构域和JAK2激酶活性。此外，所有TEL/JAK2变体通过磷酸酪氨酸免疫印迹法和电泳迁移率变动分析（EMSA）均能强烈激活STAT 5。用含有hTEL/mJAK2（JH1）融合基因或其人类对应基因的MSCV逆转录病毒感染骨髓后进行移植的小鼠（n = 40），会在2 - 10周的潜伏期后发展出致命的混合性骨髓增殖性和T细胞淋巴增殖性疾病。相比之下，移植了缺乏TEL PNT结构域的TEL/JAK2突变体（n = 10）或激酶失活的TEL/JAK2（JH1）突变体（n = 10）的小鼠并未发病。我们得出结论，所有人类TEL/JAK2融合变体在体外都是癌蛋白，能强烈激活STAT 5，并在白血病小鼠骨髓移植模型中引发致命的骨髓和淋巴增殖综合征。