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急性髓细胞白血病多步骤发病机制及分子靶向研究进展 被引量：2

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作者 孙雪梅 李晓惠
机构地区 南京中医药大学附属医院血液科
出处 《临床血液学杂志》 CAS 2008年第4期398-400,共3页 Journal of Clinical Hematology
基金 江苏省科技厅社会发展项目资助(No:BS2003603)
关键词 白血病 基因突变 发病机制
分类号 R733.7 [医药卫生—肿瘤]
  • 相关文献

参考文献17

  • 1VALK PJM, VERHAAK RGW, BEIJEN MA, et al. Prognostically useful gene-expression profiles in acute myeloid leukemia[J]. New Engl J Med, 2004, 350:1617-1628.
  • 2孙雪梅.急性白血病FLT3基因突变及其靶向抑制的研究进展[J].江苏医药,2004,30(10):774-775. 被引量：3
  • 3王莉红,周春林,张新伟,陈森,王敏,王建祥.FLT3基因内部串联重复突变与急性白血病的关系及临床意义[J].中华血液学杂志,2004,25(7):393-396. 被引量：35
  • 4SHIH L Y, LIN T L, WANG P N, et al. Internal tandem duplication of fms-like tyrosine kinase 3 is associated with poor outcome in patients with myelodysplastic syndrome [J]. Cancer, 2004,101:989-998.
  • 5KANG H J, HONGSH, KIMI H, etal. Prognostic significance of FLT3 mutations in pediatric nonpromyelocytic acute myeloid leukemia [J]. Leuk Res, 2005,29:617-623.
  • 6KELLYLM, LIU Q, KUTOKJ L, etal. FLT3internal tandem duplication mutations associated with human acute myeloid leukemias induce myelo-proliferative disease in a murine bone marrow transplant model[J]. Blood,2002, 99:310-318.
  • 7SHIH L Y, HUANG C F, WANG P N, et al. Acquisition of FLT3 or N-ras mutations is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia [J]. Leukemia, 2004,18:466-475.
  • 8SPECK N A, GILLILAND D G. Core-binding factors in haematopoiesis and leukaemia [J]. Nat Rev Cancer, 2002,2:502-513.
  • 9MICHAUD J, WU F, OSATO M, et al. In vitro analyses of known and novel RUNX1/AML1 mutations in dominant familial platelet disorder with predisposition to acute myelogenous leukemia: implications for mechanisms of pathogenesis[J]. Blood, 2002,99 : 1364 -1372.
  • 10HIGUCHI M, O'BRIEN D, KUMARAVELU P, et al. Expression of a conditional AML1-ETO oncogene bypasses embryonic lethality and establishes a murine model of human t(8-21) acute myeloid leukemia [J]. Cancer Cell, 2002,1 : 63-74.

二级参考文献21

  • 1Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood, 2002,100:1532-1542.
  • 2Griffithin J, Black J, Faerman C, et al. The structural basis for autoinhibition of FLT3 by the juxtamembrane domain. Mol Cell, 2004,13:169-178.
  • 3Shih LY, Huang CF,Wang PN, et al. Acquisition of FLT3 or Nras mutations is frquently associated with progression of myelodysplastic syndrome to acute myeloid leukemia. Leukemia,2004,18: 466-475.
  • 4Zheng R,Friedman AD, Levis M,et al. Internal tandem duplication mutation of FLT3 blocks myeloid differentiation through suppression of C/EBPalpha expression. Blood, 2004,103:1883-1890.
  • 5Li Y, Li H,Wang MN, et al. Suppression of feukemia expressing wild-type or ITD-mutant FLT3 receptor by a fully human antiFLT3 neutralizing antibody. Blood, 2004,104:1 137-1144.
  • 6Smith B D,Levis M,Beran M,et al. Single agent CEP-701,a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia.Blood, 2004,103: 3669-3676.
  • 7Fiedler W, Mesters R, Tinnefeld H, et al. A phase 2 clinical study of SU5416 in patients with refractory acute myeloid leukemia. Blood, 2003,102: 2763-2767.
  • 8O'Farrell AM, Foran JM, Fiedler W, et al. An innovative phase I clinical study demonstrates inhibition of FLT3 phosphorylation by SU11248 in acute myeloid leukemia patients. Clin Cancer Res, 2003,9: 5465-5476.
  • 9Kelly LM, Yu JC, Boulton Cl, et al. CT53518, a novel selective FLT3 antagonist for the treatment of acute myelogenous leukemia(AML). Cancer Cell, 2002,1: 421-432.
  • 10Stone,RM et al. PKC412,an oral FLT3 inhibitor,has activity in mutant FLT3 acute myeloid leukemia(AML) :a phase Ⅱ clinical trial. Blood, 2002,100: 316a.

共引文献35

同被引文献13

引证文献2

二级引证文献6

临床血液学杂志
2008年 第4期

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