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埃罗替尼对JAK2V617F阳性细胞体外增殖分化的影响 被引量:1

Effect of Erlotinib on Proliferation and Differentiation of JAK2V617F-Positive Cells in vitro
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摘要 本研究探讨埃罗替尼对JAK2V617F阳性细胞体外增殖分化的影响,为埃罗替尼用于真性红细胞增多症靶向治疗提供实验依据。采用体外集落形成试验检测埃罗替尼在体外对真性红细胞增多症患者骨髓造血祖细胞增殖分化的影响,MTT比色法检测埃罗替尼对含有JAK2V617F纯合突变的HEL细胞株增殖的作用。结果表明:埃罗替尼在5μmol/L对真性红细胞增多症患者JAK2V617F突变阳性的造血祖细胞体外增殖分化具有抑制作用,而对患者正常造血祖细胞无明显抑制作用。埃罗替尼可以抑制HEL细胞株的增殖活性,IC50为4.1μmol/L。结论:埃罗替尼对JAK2V617F阳性细胞体外增殖分化具有一定的抑制作用。 The aim of this study was to investigate the effect of erlotinib on proliferation and differentiation of JAK2V617F-positive cells in vitro,and to provide experimental evidence of erlotinib for potential target therapy in polycythemia vera.Colony forming assays were used to detect the effect of erlotinib on differentiation of hematopoietic progenitor cells from bone marrow of polycythemia vera patients,and MTT method was used to measure the proliferation of HEL cell line containing the JAK2V617F mutation.The results showed that erlotinib 5 μmol/L inhibited the differentiation of JAK2V617F-positive hematopoietic progenitor cells into hematopoietic colonies in vitro,while it had almost no effect on normal hematopoietic progenitor cells from the patients.Erlotinib had inhibitory effect on the proliferation of HEL cell line in a dose dependent manner.The IC50 was 4.1 μmol/L.It is concluded that erlotinib can inhibit proliferation and differentiation of JAK2V617F-positive cells to a certain extent in vitro.
出处 《中国实验血液学杂志》 CAS CSCD 北大核心 2012年第2期368-371,共4页 Journal of Experimental Hematology
基金 山东省自然科学基金(编号Y2007C059)
关键词 埃罗替尼 JAK2V617F突变 真性红细胞增多症 HEL细胞株 erlotinib JAK2V617F mutation polycythemia vera HEL cell line
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参考文献14

  • 1Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet, 2005 ; 365 (9496) : 1054 - 1061.
  • 2Levine RL, Wadleigh M, Cools J, et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythe-mia, and myeloid metaplasia with myelofibrosis. Cancer Cell, 2005 ; 7(4) : 387 -397.
  • 3Vizmanos JL, Onnazabal C, Larrayoz MJ, et al. JAK2V617F muta- tion in classic chronic myeloproliferative diseases : a report on a series of 349 patients. Leukemia, 2006 ; 20 (3) : 534 - 535.
  • 4梅丽娜,王季石,卢英豪,李建勇.141例慢性骨髓增生性疾病中JAK2基因V617F点突变的研究[J].临床血液学杂志,2009,22(3):244-249. 被引量:8
  • 5何祥萌,张凌岩,李英.BCR-ABL阴性骨髓增殖性疾病患者JAK2 V617F突变的检测及其临床意义[J].中国肿瘤生物治疗杂志,2009,16(5):507-511. 被引量:4
  • 6Tefferi A, Vardiman JW. Classification and diagnosis of myeloprolif- erative neoplasms : The 2008 World Health Organization criteria and point-of-care diagnostic algorithms. Leukemia, 2008 ;22 ( 1 ) : 14 - 22.
  • 7Tsao MS, Sakurada A, Cutz JC, et al. Erlotinib in lung cancer -mo- lecular and clinical predictors of outcome. N Engl J Med, 2005 ; 353 (2) :133 - 144.
  • 8Li Z, Xu M, Xing S, et al. Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth. J Biol Chem, 2007;282 (6) : 3428 -3432.
  • 9Finazzi G, Barbui T. How I treat patients with polyeythemia vera. Blood, 2007;109(12) :5104-5111.
  • 10Janmaat ML, Giaccone G. Small-molecule epidermal growth factor receptor tyrosine kinase inhibitors. Oncologist, 2003 ; 8 ( 6 ) : 576 - 586.

二级参考文献48

  • 1宋君红,李建勇,张苏江.骨髓增殖性疾病JAK2基因V617F点突变研究[J].中华血液学杂志,2006,27(9):632-633. 被引量:18
  • 2CAMPBELL P J, BAXTER E J, BEER P A, et al. Mutation of JAK2 in the myelop roliferative disorders: timing, clonality studies, cytogenetic associations and role in leukemic transformation[J]. Blood, 2006,108 3548--3555.
  • 3ROSSI D, DEAMBROGI C, CAPELLO D, et al. JAK2V617F mutation in leukaemic transformation of philadelphia negative chronic myeloproliferative disorders[J]. Blood (ASH Annual Meeting Abstracts), 2006,108 : 3605-- 3605.
  • 4VILLEVAL J L,JAMES C,PISANI D F,et al. New insights into the pathogenesis of JAK2 V617F-posirive myeloproliferative disorders and consequences for the management of patients[J]. Serm Thromh Haemost,2006,32:341--351.
  • 5LIPPERT E, BOISSINOT M, KRALOVICS R, et al. The JAK2-V617F mutation is frequently present at diagnosis in patients withessential thrombocythemia and polyeythemia vera[J]. Blood, 2006, 108: 1865- 1867.
  • 6PARDANANI A. JAK2 inhibitor therapy in myeloproliferative disorders: rationale, preclinical studies and ongoing clinical trials[J].Leukemia, 2008,22:23 --30.
  • 7JOHN M G,JUNIA V M. Chronic myeloid leukemiaadvances in biology and new approaches to treatment[J]. N Engl J Med,2003,349:1451--1464.
  • 8KRALOVICS R, PASSAMONTI F, BUSER A S, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders[J]. N Engl J Med, 2005,352 : 1779 --1790.
  • 9LEVINE R L, WADLEIGH M. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera,essential thrombocythemia and myeloid metaplasia with myetofibrosis[J]. Cancer Cell, 2005,7 : 387-- 397.
  • 10JAMES C,UGO V,LE COUEDIC J P,et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera[J]. Nature, 2005,434 : 1144 --1148.

共引文献12

同被引文献49

  • 1James C,Ugo V,Le Couedic JP, et al. A unique clonal JAK2 mutationleading to Constitutive signaling causes polycythemia vera [ J ]. Na-ture, 2005 ,434(7037) :1144-1148.
  • 2Levine RL,Wadleigh M,Cools J,et al. Activating mutation of the tyro—sine Kinase JAK2 in Polycythemia vera,essential thrombocythe-mia,and Myeloid Metaplasia with myelofibrosis [ J ]. Cancer Cell,2005,7(4) :387 -397.
  • 3Baxter EJ,Scott LM,Campbell PJ,et al. Acquired mutation of the tyro—sine Kinase JAK2 in human myeloproliferative disorders [ J ]. TheLancet,2005,365(9464) : 1054 -1061.
  • 4Kralovics R,Passaraonti F,Buser AS,et al. A gain - of - function mu-tation of JAK2 in myeloproliferative disorders [ J]. N Engl J Med,2005,35(17) :1779 -1790.
  • 5ZhaoR,Xing S,LI Z,et al. Identification of an acquired JAK2 muta-tion in Polycythemia vera[ J]. J Biol Chem,2005 ,280(24) ;22788 -22792.
  • 6Renata Mendes de Freitas,Marcelo de Oliveira Santos, Carlos Magnoda Costa Maranduba. The JAK2 gene as a protagonist in chronic my -eloproliferative neoplasms [ J ]. Rev Bras Hematol Hemoter, 2013 ,3 5(4):278 -279.
  • 7Ann Mullally, Steven W. Lane, Brian Ball, et al. PhysiologicalJak2V617F Expression Causes a Lethal Myeloproliferative Neoplasmwith Differential Effects on Hematopoietic Stem and Progenitor Cells[J]. Cancer Cell,2010,17(6) :584 -596.
  • 8Kralovics R,Teo SS,Li S,et al. A Acquisition of the V617F Muta-tion of JAK2 is a Late Genetic Event in a Subset of Patients WithMyeloproliferative Disorders [ J ]. Blood, 2006,108 ( 4 ) : 1377-1380.
  • 9Quintdis - Cardama A, Vaddi K, Liu P, et al. Preclinical character-ization of the selective JAK1/2 inhibitor INCB018424 : therapeuticimplications for the treatment of myeloproliferative neoplasms [ J ].Blood,2010,115(15) :3109 -3117.
  • 10Verstovsek S, Kantarjian H, Mesa RA, et al. Safety and efficacy ofINCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis [ J ]. NEngl J Med,2010 ,363( 12) :1117 -1127.

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