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急性髓系白血病基因突变研究进展 被引量:3

Research progress on gene mutation of acute myeloid leukemia
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摘要 急性髓系白血病(AML)是获得性造血祖细胞变异而引起的克隆性疾病。在造血干、祖细胞遗传学变异累积的结果下,造血干、祖细胞最终恶性变为具有自我更新能力和增生、生存优势的白血病干细胞。目前多认为细胞、分子遗传学异常是AML的致病基础。近年来人们在血液肿瘤中发现了较多的原癌基因和抑癌基因,基因组学的研究极大推动了疾病分子标记的发现以及临床应用。 Summary Acute myeloid leukemia (AML) is a kind of malignant clonal blood system disease caused by ab- beration of hematopoietic stem and progenitor cells. The relationship between gene mutation and AML has been re- peatedly reported in recent years. Recent studies show the importance of individual gene mutations in AML. This review makes a simpler overview focusing on the recent progress of gene mutation in AML.
作者 向国强 曾云
出处 《临床血液学杂志》 CAS 2013年第6期808-812,共5页 Journal of Clinical Hematology
基金 国家自然科学基金(No:40110012) 云南省联合专项基金(No:40210015)
关键词 白血病 髓系 急性 基因突变 进展 acute myeloid leukemia gene mutation progress
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参考文献27

  • 1成人急性髓系白血病(非急性早幼粒细胞白血病)中国诊疗指南(2011年版)[J].中华血液学杂志,2011,32(11):804-807. 被引量:183
  • 2BULLINGER L, DOHNER K, KRANZ R, et al. An FL T3 gene-expression signature predicts clinical out?come in normal karyotype AML[J]. Blood, 2008 , 111 : 4490-4495.
  • 3MEAD AJ ,GALE R E,KOTTARIDIS P D,et al. A?cute myeloid leukaemia blast cells with a tyrosine ki?nase domain mutation of FL T3 are less sensitive to lestaurtinib than those with a FL T3 internal tandem duplication[J]. BrJ Haematol,2008,141:454-460.
  • 4ZARRINKAR P P,GUNAWARDANE R N,CRAM?ER M D, et al. AC220 is a uniquely potent and selec?tive inhibitor of FL T3 for the treatment of acute mye?loid leukemia (AML)[J]. Blood, 2009,114: 2984 - 2992.
  • 5KRONKEJ ,SCHLENK R F ,JENSEN KO,et al. Mo?nitoring of minimal residual disease in NPM1-mutated acute myeloid leukemia[J].J Clin Oncol , 2011, 29: 2709-2716.
  • 6HAFERLACH LBACHER U,ALPERMANN Let al. Amount of bone marrow blasts is strongly correla?ted to NPM1 and FL T3- lTD mutation rate in AML with normal karyotype[J]. Leuk Res, 2012,36: 51- 58.
  • 7FALINI B,BOLLI N,LISO Av et al. Altered nucleo?phosmin transport in acute myeloid leukaemia with mutated NPM1[J]. Leukemia, 2009 ,23: 1731-1743.
  • 8PARSONS D W,JONES S,ZHANG x, al. An inte?grated genomic analysis of humanglioblastoma multi?forme[J]. Science, 2008 ,321: 1807 -1812.
  • 9DANG L, WHITE D W ,GROSS Sv et al. Cancer-asso?ciated IDH1 mutations produce 2-hydroxyglutarate[J]. Nature,2009,462:739-744.
  • 10GROSS S,CAIRNS R A, MINDEN M D, et al. Canc?er-associated metabolite 2-hydroxyglutarate accumu?lates in acute myelogenous leukemia with is ocitrate dehydrogenase 1 and 2 mutations[J].J Exp Med, 2010,207: 339 - 344.

二级参考文献12

  • 1Gouqopoulou D M, Kiari S H, Erqazaki M, et al. Mutations and expression of the ras family genes in leukemias[ J]. Stem Cells, 1996,14 (6) :725-729.
  • 2Levis M. Recent advances in the development of small-molecule inhibitors for the treatment of acute myeloid leukemia[ J ]. Curr Opin Hematol,2005,12 ( 1 ) :55-61.
  • 3Perentesis J P, Bhatia S, Boyle E, et al. RAS oncogene mutations and outcome of therapy for childhood acute lymphoblastic leukemia [ J ]. Leukemia,2004,18 (4) :685-692.
  • 4Gilliland D G. FLT3-activating mutations in acute promyelocytic leukaemia: a rationale for risk-adapted therapy with FLT3 inhibitors [ J ]. Best Pract & Res Clin Haematol, 2003,16 ( 3 ) : 409-417.
  • 5Barletta G, Gorini G, Vineis P, et al. Ras gene mutations in patients with acute myeloid leukaemia and exposure to chemical agents [ J ]. Carcinogenesis ,2004,25 ( 5 ) :749-755.
  • 6Bowen D T, Frew M E, Hills R. et al. Ras mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years [ J ]. Blood,2005,106 (6) :2113- 2119.
  • 7Molina J R, Adjei A A. The Ras/Raf/MAPK Pathway [ J ]. J Thorac Oncol,2006,1 ( 1 ) :7-9.
  • 8Martelli A M, Nyakern M, Tabellini G, et al. Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia[ J]. Leukemia, 2006,20(6) :911-928.
  • 9Le D T, Shannon K M. Ras processing as a therapeutic target in hematologic malignancies [ J ]. Curr Opin Hematol, 2002,9 (4) : 308-315.
  • 10Gills J J, Dennis P A. The development of phosphatidylinositol ether lipid analogues as inhibitors of the serine/threonine kinase, Akt [ J ]. Expert Opin Investig Drugs,2004,13 (7) :787- 797.

共引文献186

同被引文献47

  • 1柴晓阳,朱元深,高晓宁.索拉非尼对FMS样酪氨酸激酶3-基因内部串联重复突变急性髓系白血病患者的疗效观察[J].解放军医学院学报,2020,0(1):45-49. 被引量:2
  • 2于力.DNA甲基化与肿瘤[J].中华内科杂志,2005,44(6):403-404. 被引量:12
  • 3周助人,孙开来.肿瘤细胞中基因选择性剪接的研究进展[J].中华医学遗传学杂志,2006,23(2):177-180. 被引量:2
  • 4Warzecha CC, Jiang P, Amirikian K, et al. An ESRP-regulated splicing programming is abrogated during the epithelial-mesenchymal transition[ J/OL]. EMBO J, 2010, 29 (19) : 3286 - 3300.
  • 5Lin SH, Wang J, Saintigny P, et al. Genes suppressed by DNA methylation in non - small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition [ J/OL]. BMC Genomies, 2014, 15 : 1079.
  • 6Ishii H, Saitoh M, Sakamoto K, et al. Epithelial splicing regulatory proteins 1 ( ESRP1 ) and 2 (ESRP2) suppress cancer cell motility v/a different mechanisms [ J ]. J Biol Chem, 2014, 289 ( 40 ) : 27386 - 27399.
  • 7Ivanov I, Lo KC, Hawthorn L, et al. Identifying candidate colon cancer rumor suppressor genes using inhibition of nonsense-mediated mRNA decay in colon cancer cells[J]. Oncogene, 2007,26(20) : 2873 - 2884.
  • 8Lekva T, Berg JP, Lyle R, et al. Epithelial splicing regulator protein 1 and alternative splicing in somatotmph adenomas [ J ]. Endocrinology, 2013, 154(9) : 3331 -3343.
  • 9Osorio J. Pituitary gland: ESRPI-a regulator of epithelial-mesenchymal transition in somatotreph adenomas[ J] ? Nat Rev Endocrinol, 2012, 8(8) : 444.
  • 10Lekva T, Berg JP, Fougner SL, et al. Gene expression profiling identifies ESRP1 as a potential regulator of epithelia[ mesenchymal transition in somatotroph adenomas from a large cohort of patients with aeromegaly[ J]. J Clin Endoerinol Metab, 2012, 97 (8) : E1506- E1514.

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