The role of aberrant transcription factor in the progression of chronic myeloid leukemia

References

• Daley G Q, Van Etten R A, Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science 1990; 247: 824–830
   PubMed Web of Science ®Google Scholar
• Melo J V, Barnes D J. Chronic myeloid leukaemia as a model of disease evolution in human cancer. Nat Rev Cancer 2007; 7: 441–453
   PubMed Web of Science ®Google Scholar
• Calabretta B, Perrotti D. The biology of CML blast crisis. Blood 2004; 103: 4010–4022
   PubMed Web of Science ®Google Scholar
• Cuenco G M, Ren R. Cooperation of BCR/ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia. Oncogene 2001; 20: 8236–8248
   PubMed Web of Science ®Google Scholar
• Dash A B, Williams I R, Kutok J L, Tomasson M H, Anastasiadou E, Lindahl K, et al. A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9. Proc Natl Acad Sci USA 2002; 99: 7622–7627
   PubMed Web of Science ®Google Scholar
• Mayotte N, Roy D C, Yao J, Kroon E, Sauvageau G. Oncogenic interaction between BCR/ABL and NUP98/HOXA9 demonstrated by the use of an in vitro purging culture system. Blood 2002; 100: 4177–4184
   PubMed Web of Science ®Google Scholar
• Pina C, Enver T. Differential contributions of haematopoietic stem cells to foetal and adult haematopoiesis: insights from functional analysis of transcriptional regulators. Oncogene 2007; 26: 6750–6765
   PubMed Web of Science ®Google Scholar
• Kelly L M, Gilliland D G. Genetics of myeloid leukemias. Annu Rev Genomics Hum Genet 2002; 3: 179–198
   PubMed Web of Science ®Google Scholar
• Gilliland D G, Tallman M S. Focus on acute leukemias. Cancer Cell 2002; 1: 417–420
   PubMed Web of Science ®Google Scholar
• Jamieson C H, Ailles L E, Dylla S J, Muijtjens M, Jones C, Zehnder J L, et al. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N Engl J Med 2004; 351: 657–667
   PubMed Web of Science ®Google Scholar
• Shimizu R, Yamamoto M. Gene expression regulation and domain function of hematopoietic GATA factors. Semin Cell Dev Biol 2005; 16: 129–136
   PubMed Web of Science ®Google Scholar
• Ting C N, Olson M C, Barton K P, Leiden J M. Transcription factor GATA-3 is required for development of the T-cell lineage. Nature 1996; 384: 474–478
   PubMed Web of Science ®Google Scholar
• Grass J A, Boyer M E, Pal S, Wu J, Weiss M J, Bresnick E H. GATA-1-dependent transcriptional repression of GATA-2 via disruption of positive autoregulation and domain-wide chromatin remodeling. Proc Natl Acad Sci U S A 2003; 100: 8811–8816
   PubMed Web of Science ®Google Scholar
• Tsai F Y, Orkin S H. Transcription factor GATA-2 is required for proliferation/survival of early hematopoietic cells and mast cell formation, but not for erythroid and myeloid terminal differentiation. Blood 1997; 89: 3636–3643
   PubMed Web of Science ®Google Scholar
• Tsai F Y, Keller G, Kuo F C, Weiss M, Chen J, Rosenblatt M, et al. An early haematopoietic defect in mice lacking the transcription factor GATA-2. Nature 1994; 371: 221–226
   PubMed Web of Science ®Google Scholar
• Minegishi N, Suzuki N, Yokomizo T, Pan X, Fujimoto T, Takahashi S, et al. Expression and domain-specific function of GATA-2 during differentiation of the hematopoietic precursor cells in midgestation mouse embryos. Blood 2003; 102: 896–905
   PubMed Web of Science ®Google Scholar
• Yuasa H, Oike Y, Iwama A, Nishikata I, Sugiyama D, Perkins A, et al. Oncogenic transcription factor Evi1 regulates hematopoietic stem cell proliferation through GATA-2 expression. EMBO J 2005; 24: 1976–1987
   PubMed Web of Science ®Google Scholar
• Wieser R, Volz A, Vinatzer U, Gardiner K, Jäger U, Mitterbauer M, et al. Transcription factor GATA-2 gene is located near 3q21 breakpoints in myeloid leukemia. Biochem Biophys Res Commun 2000; 273: 239–245
   PubMed Web of Science ®Google Scholar
• Zhang S J, Ma L Y, Huang Q H, Li G, Gu B W, Gao X D, et al. Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia. Proc Natl Acad Sci USA 2008; 105: 2076–2081
   PubMed Web of Science ®Google Scholar
• Zhang P, Behre G, Pan J, Iwama A, Wara-Aswapati N, Radomska H S, et al. Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1. Proc Natl Acad Sci USA 1999; 96: 8705–8710
   PubMed Web of Science ®Google Scholar
• Walsh J C, DeKoter R P, Lee H J, Smith E D, Lancki D W, Gurish M F, et al. Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates. Immunity 2002; 17: 665–676
   PubMed Web of Science ®Google Scholar
• Metcalf D, Dakic A, Mifsud S, Di Rago L, Wu L, Nutt S. Inactivation of PU.1 in adult mice leads to the development of myeloid leukemia. Proc Natl Acad Sci USA 2006; 103: 1486–1491
   PubMed Web of Science ®Google Scholar
• Mueller B U, Pabst T, Osato M, Asou N, Johansen L M, Minden M D, et al. Heterozygous PU.1 mutations are associated with acute myeloid leukemia. Blood 2002; 100: 998–1007
   PubMed Web of Science ®Google Scholar
• Kronenwett R, Butterweck U, Steidl U, Kliszewski S, Neumann F, Bork S, et al. Distinct molecular phenotype of malignant CD34(+) hematopoietic stem and progenitor cells in chronic myelogenous leukemia. Oncogene 2005; 24: 5313–5324
   PubMed Web of Science ®Google Scholar
• de Bruijn M F, Speck N A. Core-binding factors in hematopoiesis and immune function. Oncogene 2004; 23: 4238–4248
   PubMed Web of Science ®Google Scholar
• Pabst T, Mueller B U. Transcriptional dysregulation during myeloid transformation in AML. Oncogene 2007; 26: 6829–6837
   PubMed Web of Science ®Google Scholar
• Harada H, Harada Y, Tanaka H, Kimura A, Inaba T. Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia. Blood 2003; 101: 673–680
   PubMed Web of Science ®Google Scholar
• Preudhomme C, Warot-Loze D, Roumier C, Grardel-Duflos N, Garand R, Lai J L, et al. High incidence of biallelic point mutations in the Runt domain of the AML1/PEBP2 alpha B gene in Mo acute myeloid leukemia and in myeloid malignancies with acquired trisomy 21. Blood 2000; 96: 2862–2869
   PubMed Web of Science ®Google Scholar
• Song W J, Sullivan M G, Legare R D, Hutchings S, Tan X, Kufrin D, et al. Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia. Nat Genet 1999; 23: 166–175
   PubMed Web of Science ®Google Scholar
• Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, Philippe N, et al. RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR/ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood 2008; 111: 3735–3741
   PubMed Web of Science ®Google Scholar
• Mitani K, Ogawa S, Tanaka T, Miyoshi H, Kurokawa M, Mano H, et al. Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia. EMBO J 1994; 13: 504–510
   PubMed Web of Science ®Google Scholar
• Mitani K. Molecular mechanisms of leukemogenesis by AML1/EVI-1. Oncogene 2004; 23: 4263–4269
   PubMed Web of Science ®Google Scholar
• Nucifora G. The EVI1 gene in myeloid leukemia. Leukemia 1997; 11: 2022–2031
   PubMed Web of Science ®Google Scholar
• Izutsu K, Kurokawa M, Imai Y, Ichikawa M, Asai T, Maki K, et al. The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP. Oncogene 2002; 21: 2695–2703
   PubMed Web of Science ®Google Scholar
• Cuenco G M, Nucifora G, Ren R. Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML. Proc Natl Acad Sci USA 2000; 97: 1760–1765
   PubMed Web of Science ®Google Scholar
• Helbling D, Mueller B U, Timchenko N A, Hagemeijer A, Jotterand M, Meyer-Monard S, et al. The leukemic fusion gene AML1-MDS1-EVI1 suppresses C/EBPA in acute myeloid leukemia by activation of Calreticulin. Proc Natl Acad Sci USA 2004; 101: 13312–13317
   PubMed Web of Science ®Google Scholar
• Peterson L F, Boyapati A, Ahn E Y, Biggs J R, Okumura A J, Lo M C, et al. Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts. Blood 2007; 110: 799–805
   PubMed Web of Science ®Google Scholar
• Yin C C, Medeiros L J, Glassman A B, Lin P. t(8;21)(q22;q22) in blast phase of chronic myelogenous leukemia. Am J Clin Pathol 2004; 121: 836–842
   PubMed Web of Science ®Google Scholar
• Kojima K, Yasukawa M, Ishimaru F, Dansako H, Matsuo Y, Kimura Y, et al. Additional translocation (8;21)(q22;q22) in a patient with Philadelphia-positive chronic myelogenous leukaemia in the blastic phase. Br J Haematol 1999; 106: 720–722
   PubMed Web of Science ®Google Scholar
• Wang Y Y, Zhou G B, Yin T, Chen B, Shi J Y, Liang W X, et al. AML1/ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec. Proc Natl Acad Sci USA 2005; 102: 1104–1109
   PubMed Web of Science ®Google Scholar
• Argiropoulos B, Humphries R K. Hox genes in hematopoiesis and leukemogenesis. Oncogene 2007; 26: 6766–6776
   PubMed Web of Science ®Google Scholar
• Nakamura T, Largaespada D A, Lee M P, Johnson L A, Ohyashiki K, Toyama K, et al. Fusion of the nucleoporin gene NUP98 to HOXA9 by the chromosome translocation t(7;11)(p15;p15) in human myeloid leukaemia. Nat Genet 1996; 12: 154–158
   PubMed Web of Science ®Google Scholar
• Borrow J, Shearman A M, Stanton V P, Jr, Becher R, Collins T, Williams A J, et al. The t(7;11)(p15;p15) translocation in acute myeloid leukaemia fuses the genes for nucleoporin NUP98 and class I homeoprotein HOXA9. Nat Genet 1996; 12: 159–167
   PubMed Web of Science ®Google Scholar
• Yamamoto K, Nakamura Y, Saito K, Furusawa S. Expression of the NUP98/HOXA9 fusion transcript in the blast crisis of Philadelphia chromosome-positive chronic myelogenous leukaemia with t(7;11)(p15;p15). Br J Haematol 2000; 109: 423–426
   PubMed Web of Science ®Google Scholar
• Ahuja H G, Popplewell L, Tcheurekdjian L, Slovak M L. NUP98 gene rearrangements and the clonal evolution of chronic myelogenous leukemia. Genes Chromosomes Cancer 2001; 30: 410–415
   PubMed Web of Science ®Google Scholar
• Kasper L H, Brindle P K, Schnabel C A, Pritchard C E, Cleary M L, van Deursen J M. CREB binding protein interacts with nucleoporin-specific FG repeats that activate transcription and mediate NUP98/HOXA9 oncogenicity. Mol Cell Biol 1999; 19: 764–776
   PubMed Web of Science ®Google Scholar
• Takeda A, Goolsby C, Yaseen N R. NUP98/HOXA9 induces long-term proliferation and blocks differentiation of primary human CD34+ hematopoietic cells. Cancer Res 2006; 66: 6628–6637
   PubMed Web of Science ®Google Scholar
• Chung K Y, Morrone G, Schuringa J J, Plasilova M, Shieh J H, Zhang Y, et al. Enforced expression of NUP98/HOXA9 in human CD34(+) cells enhances stem cell proliferation. Cancer Res 2006; 66: 11781–11791
   PubMed Web of Science ®Google Scholar
• Calvo K R, Sykes D B, Pasillas M P, Kamps M P. NUP98/HOXA9 immortalizes myeloid progenitors, enforces expression of HOXa9, HOXa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of HOXa9 and Meis1. Oncogene 2002; 21: 4247–4256
   PubMed Web of Science ®Google Scholar
• Lawrence H J, Rozenfeld S, Cruz C, Matsukuma K, Kwong A, Kömüves L, et al. Frequent co-expression of the HOXA9 and MEIS1 homeobox genes in human myeloid leukemias. Leukemia 1999; 13: 1993–1999
   PubMed Web of Science ®Google Scholar
• Kawagoe H, Humphries R K, Blair A, Sutherland H J, Hogge D E. Expression of HOX genes, HOX cofactors, and MLL in phenotypically and functionally defined subpopulations of leukemic and normal human hematopoietic cells. Leukemia 1999; 13: 687–698
   PubMed Web of Science ®Google Scholar
• Lawrence H J, Helgason C D, Sauvageau G, Fong S, Izon D J, Humphries R K, et al. Mice bearing a targeted interruption of the homeobox gene HOXA9 have defects in myeloid, erythroid, and lymphoid hematopoiesis. Blood 1997; 89: 1922–1930
   PubMed Web of Science ®Google Scholar
• Kroon E, Thorsteinsdottir U, Mayotte N, Nakamura T, Sauvageau G. NUP98/HOXA9 expression in hemopoietic stem cells induces chronic and acute myeloid leukemias in mice. EMBO J 2001; 20: 350–361
   PubMed Web of Science ®Google Scholar
• Bai X T, Gu B W, Yin T, Niu C, Xi X D, Zhang J, et al. Trans-repressive effect of NUP98-PMX1 on PMX1-regulated c-FOS gene through recruitment of histone deacetylase 1 by FG repeats. Cancer Res 2006; 66: 4584–4590
   PubMed Web of Science ®Google Scholar
• Nishii K, Usui E, Sakakura M, Miyata E, Ridge S A, Ford A M, et al. Additional t(11;17)(q23;q21) in a patient with Philadelphia-positive mixed lineage antigen-expressing leukemia. Cancer Genet Cytogenet 2001; 126: 8–12
   PubMed Web of Science ®Google Scholar
• Zhang D E, Zhang P, Wang N D, Hetherington C J, Darlington G J, Tenen D G. Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice. Proc Natl Acad Sci U S A 1997; 94: 569–574
   PubMed Web of Science ®Google Scholar
• Scott L M, Civin C I, Rorth P, Friedman A D. A novel temporal expression pattern of three C/EBP family members in differentiating myelomonocytic cells. Blood 1992; 80: 1725–1735
   PubMed Web of Science ®Google Scholar
• Cheng T, Shen H, Giokas D, Gere J, Tenen D G, Scadden D T. Temporal mapping of gene expression levels during the differentiation of individual primary hematopoietic cells. Proc Natl Acad Sci USA 1996; 93: 13158–13163
   PubMed Web of Science ®Google Scholar
• Pabst T, Mueller B U, Zhang P, Radomska H S, Narravula S, Schnittger S, et al. Dominant-negative mutations of C/EBPA, encoding CCAAT/enhancer binding protein-alpha (C/EBP alpha), in acute myeloid leukemia. Nat Genet 2001; 27: 263–270
   PubMed Web of Science ®Google Scholar
• Preudhomme C, Sagot C, Boissel N, Cayuela J M, Tigaud I, de Botton S, et al. Favorable prognostic significance of CEBPA mutations in patients with de novo acute myeloid leukemia: a study from the Acute Leukemia French Association (ALFA). Blood 2002; 100: 2717–2723
   PubMed Web of Science ®Google Scholar
• Fröhling S, Schlenk R F, Stolze I, Bihlmayr J, Benner A, Kreitmeier S, et al. CEBPA mutations in younger adults with acute myeloid leukemia and normal cytogenetics: prognostic relevance and analysis of cooperating mutations. J Clin Oncol 2004; 22: 624–633
   PubMed Web of Science ®Google Scholar
• Pabst T, Stillner E, Neuberg D, Nimer S, Willman C L, List A F, et al. Mutations of the myeloid transcription factor C/EBPA are not associated with the blast crisis of chronic myeloid leukaemia. Br J Haematol 2006; 133: 400–402
   PubMed Web of Science ®Google Scholar
• Perrotti D, Cesi V, Trotta R, Guerzoni C, Santilli G, Campbell K, et al. BCR/ABL suppresses C/EBPalpha expression through inhibitory action of hnRNP E2. Nat Genet 2002; 30: 48–58
   PubMed Web of Science ®Google Scholar
• Chang J S, Santhanam R, Trotta R, Neviani P, Eiring A M, Briercheck E, et al. High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP-E2 dependent suppression of C/EBPalpha-driven myeloid differentiation. Blood 2007; 110: 994–1003
   PubMed Web of Science ®Google Scholar
• Tavor S, Park D J, Gery S, Vuong P T, Gombart A F, Koeffler H P. Restoration of C/EBPalpha expression in a BCR/ABL+ cell line induces terminal granulocytic differentiation. J Biol Chem 2003; 278: 52651–52659
   PubMed Web of Science ®Google Scholar
• Radich J P, Dai H, Mao M, Oehler V, Schelter J, Druker B, et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci USA 2006; 103: 2794–2799
   PubMed Web of Science ®Google Scholar
• Skorski T. BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability. Oncogene 2002; 21: 8591–8594
   PubMed Web of Science ®Google Scholar
• Sattler M, Verma S, Shrikhande G, Byrne C H, Pride Y B, Winkler T, et al. The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells. J Biol Chem 2000; 275: 24273–24278
   PubMed Web of Science ®Google Scholar
• Weisberg E, Manley P W, Cowan-Jacob S W, Hochhaus A, Griffin J D. Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia. Nat Rev Cancer 2007; 7: 345–356
   PubMed Web of Science ®Google Scholar
• Quintás-Cardama A, Kantarjian H, Cortes J. Flying under the radar: the new wave of BCR-ABL inhibitors. Nat Rev Drug Discov 2007; 6: 834–848
   PubMed Web of Science ®Google Scholar
• Shen Z X, Shi Z Z, Fang J, Gu B W, Li J M, Zhu Y M, et al. All-trans retinoic acid/As2O3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia. Proc Natl Acad Sci USA 2004; 101: 5328–5335
   PubMed Web of Science ®Google Scholar
• Yin T, Wu Y L, Sun H P, Sun G L, Du Y Z, Wang K K, et al. Combined effects of As4S4 and imatinib on chronic myeloid leukemia cells and BCR/ABL oncoprotein. Blood 2004; 104: 4219–4225
   PubMed Web of Science ®Google Scholar