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EVI1基因在白血病中的研究进展 被引量：5

The gene of EVI 1 in leukemia
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摘要 EVI1基因主要控制胚胎的发育，3q重排、MLL易位、7号染色单体或者与其他基因的相互作用都可使其异常表达或户生融合基因。新近研究发现，EVI1基因在部分急性淋巴细胞性白血病、急性髓细胞性白血病和慢性粒细胞性白血病中都有异常表达，并且与不良预后相关，其致白血病机制有表观遗传学的修饰、调控转录、调节信号通路、提高白血病细胞黏附、增殖、集落形成和抗凋亡能力。基因治疗药物有表观遗传学制剂、mTOR抑制剂、抗人ITGA6／ITGB4复合物抗体、抗CD52单克隆抗体。 EVI1 gene mainly controls embryo development. 3q rearrangement, MLL translocations, monosomy 7, which react with other genes, can lead to EVIl aberrant expresion or fusion gene. Recent studies have shown aberrant expression of EVIl gene in parts of acute lymphatic leukemia,acute myeloid leukemia and chronic granulocytic Leukemia and correlation with poor prognosis. Leukemogenic mechanism include epigenetic modifications,transcriptional control, regulation of signaling pathways, upregulation of cell adhesion, prolifera- tion, and colony formation and antiapoptosis. Drugs of genetic therapy include epigenetic agents, tuTOR inhibi- tor,human ITGA6/ITGB4 complex antibody and CD52 monoclonal antibody.
作者 姜敏(综述) 吴介洪 金润铭(审校)
机构地区 华中科技大学同济医学院附属协和医院儿科
出处 《国际儿科学杂志》 2013年第4期398-401,共4页 International Journal of Pediatrics
关键词 EVI1基因 白血病 Ecotropic viral integration site Leukemia
分类号 R733.71 [医药卫生—肿瘤]
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参考文献37

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同被引文献109

  • 1顾龙君.儿童急性淋巴细胞白血病诊疗建议(第三次修订草案)[J].中华儿科杂志,2006,44(5):392-395. 被引量：476
  • 2王东侠,吕志强,张文艺,杨淑芝,雷蕊,候伟,乔子剑,杨淑莲.CD41诊断急性巨核细胞白血病假阳性原因探讨[J].临床误诊误治,2006,19(8):54-56. 被引量：6
  • 3李六红,孙延河,阴志琦.儿童期急性巨核细胞白血病（AML—M7）及脐血移植1例报告[J].中国医师杂志,2007,9(2):150-150. 被引量：1
  • 4Groschel S, Schlenk RF, Engelmann J, et al. Deregulated expression of EVIl defines a poor prognostic subset of MLL-rearranged acute myeloid leukemias: a study of the German-Austrian Acute Myeloid Leukemia Study Group and the Dutch-Belgian-Swiss HOVON/ SAKK Cooperative Group [ J ]. J Clin Oncol, 2013,31 ( 1 ) :95-103.
  • 5Vfzquez I, Maicas M, Cervera J,et al. Down-regulation of EVIl is associated with epigenetic alterations and good prognosis in patients with acute myeloid leukemia [ J ]. Haematologica, 2011,96 ( 10 ) : 1448-1456.
  • 6Konantz M,Andre MC, Ebinger M, et al. EVI-1 modulates leukemo- genic potential and apoptosis sensitivity in human acute lymphoblastic leukemia[ J]. Leukemia,2013,27( 1 ) :56-65 .
  • 7Pallisgaard N, Holdand P, Riishcbj DC,et al. Multiplex reverse tran- scription-polymerase chain reaction for simultaneous screening of 29 Iranslocations and chromosomal aberrations in acute leukemia. Blood, 1998 ,92(2) :574-588.
  • 8De Weer A, Poppe B, Cauwelier B, et al. Screening for EVIl: ectopic expression absent in T-cell acute lymphoblastic leukemia patients and cell lines[ J ]. Cancer Genet Cytogenet , 2006, 171 : 79-80.
  • 9Ba Q, Zhou N, Duan J, et al. Dihydroartemisinin exerts its anticancer activity through depleting cellular iron via transferrin receptor-I [ J]. PLoS One,2012,7(8) : 042703.
  • 10Moura IC, Lepelletier Y, Amulf B ,et al. A neutralizing monoclonal antibody (mAb A24) directed agaimt the transferrin receptor induces apoptosis of tumor T lymphocytes from ATL patients[ J ]. Blood, 2004, 103(5) :1838-1845.

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国际儿科学杂志
2013年 第4期

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