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白血病细胞内重现性基因突变

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摘要 白血病细胞内基因突变对白血病的发生发展起着十分重要的作用。近年来,随着白血病发病“双重打击”学说的提出,对白血病细胞内基因突变的研究报道日益增多。主要的重现性基因突变有RUNX1、FLT3、CEBPA、PTPN11、SHIP、RAS、KIT、NPM1和NOTCH1等;其中CEBPA、NPM1和NOTCH1突变的患者预后较好,而RUNX1、FLT3、PTPN11和RAS突变的患者预后较差;SHIP和KIT等突变的预后意义尚不明确。
出处 《国际输血及血液学杂志》 CAS 2007年第3期231-234,共4页 International Journal of Blood Transfusion and Hematology
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  • 1Matsuno N, Osato M, Yamashita N, et al. Dual mutations in the AMLI and FLT3 genes are associated with leukemogenesis in acute myeloblastic leukemia of the M0 subtype. Leukemia, 2003, 17(12) :2492-2499.
  • 2Langabeer SE, Gale RE, Rollinson SJ, et al. Mutations of the AML1 gene in acute myeloid leukemia of FAB types M0 and M7. J Biol Chem,2004,279(4) :2873-2884.
  • 3Harada H, Harada Y, Niimi H, et al. High incidence of somatic mutations in the AMLI/RUNX1 gene in myelodysplastic syndrome and low blast percentage myeloid leukemia with myelodysplasia. Blood, 2004,103(6) :2316-2324.
  • 4Ichikawa M, Asai T, Saito T, et al. RUNX1/AML1 ranks as a master regulater of adult hematopoiesis. Nat Med, 2004, 10 (3) : 299-304.
  • 5Lyman SD, James L, Zappone J, et al. Characterization of the protein encoded by the flt3 (flk2) recepyor-like tyrosine kinase gene. Oncogene, 1993,8 ( 4 ) : 815-822.
  • 6Rosnet O,Buhring HJ ,deLapeyiere O,et al. Expression and singal transduction of the FLT3 tyrosine kinase receptor. Acta Haematol, 1996,95(3) : 218-223.
  • 7Zheng R, Levis M, Piloto O,et al. FLT3 ligand causes autocrine signaling in acute myeloid leukemia cells. Blood, 2004, 103 (1) : 267-274.
  • 8Kindler T, Breitenbuecher F, Kasper S, et al. Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML). Blood, 2005,105 (1) : 335-340.
  • 9Taketani T, Taki T, Sugita K, et al. Flt3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy. Blood, 2004,103 (3): 1085-1088.
  • 10Naoe T,Kiyoi H. Normal and oncogenic FLT3. Cell Mol Life Sci, 2004,61 (23) : 2932-2938.

二级参考文献8

  • 1Kelly LM,Gilliland DG.Genetics of myeloid leukemias.Annu Rev Genomics Hum Genet,2002,3:179-198.
  • 2Vardiman JW,Harris NL,Brunning RD.The World Health Organization (WHO) classification of the myeloid neoplasms.Blood,2002,100:2292-2302.
  • 3Steer E J,Cross NC.Myeloproliferative disorders with translocations of chromosome 5q31-35:role of the platelet-derived growth factor receptor Beta.Acta Haematol,2002,107:113-122.
  • 4Apperley JF,Gardembas M,Melo JV,et al.Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta.N Engl J Med,2002,347:481-487.
  • 5Odai H,Sasaki K,Iwamatsu A,et al.Purification and molecular cloning of SH2-and SH3-containing inositol polyphosphate-5-phosphatase,which is involved in the signaling pathway of granulocytemacrophage colony-stimulating factor,erythropoietin,and Bcr-Abl.Blood,1997,89:2745-2756.
  • 6Luo JM,Yoshida H,Komura S,et al.Possible dominant-negative mutation of the SHIP gene in acute myeloid leukemia.Leukemia,2003,17:1-8.
  • 7Tartaglia M,Niemeyer CM,Fragale A,et al.Somatic mutations in PTPN11 in juvenile myelomonocytic leukemia,myelodysplastic syndromes and acute myeloid leukemia.Nature Genet,2003,34:148-150.
  • 8Skorski T.Oncogenic tyrosine kinases and the DNA-damage response.Nat Rev Cancer,2002,2:351-360.

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