EVI1 induces myelodysplastic syndrome in mice

Journal of Clinical Investigation

Volumn 114, Issue 5, 2004, Pages 713-719

  Buonamici, Silvia ^a   Li, Donglan ^a   Chi, Yiqing ^a   Zhao, Rui ^a   Wang, Xuerong ^a   Brace, Larry ^a   Ni, Hongyu ^a   Saunthararajah, Yogen ^a   Nucifora, Giuseppina ^a  

^a UNIVERSITY OF ILLINOIS AT CHICAGO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

NUCLEAR PROTEIN; PROTEIN EVI1; UNCLASSIFIED DRUG; CYTOKINE; DNA BINDING PROTEIN; EVI1 PROTEIN, MOUSE; TRANSCRIPTION FACTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; C MPL GENE; CHROMOSOME 3Q; CONTROLLED STUDY; EPOR GENE; GENE; GENE ACTIVATION; GENE EXPRESSION REGULATION; MOUSE; MYELODYSPLASTIC SYNDROME; NONHUMAN; PANCYTOPENIA; PRIORITY JOURNAL; PROTEIN EXPRESSION; ANIMAL; BONE MARROW; GENE VECTOR; GENETICS; GROWTH, DEVELOPMENT AND AGING; METABOLISM; PATHOLOGY; PROTO ONCOGENE; RETROVIRUS; TIME;

ANIMALS; BONE MARROW; CYTOKINES; DNA-BINDING PROTEINS; GENETIC VECTORS; MICE; MYELODYSPLASTIC SYNDROMES; PROTO-ONCOGENES; RETROVIRIDAE; TIME FACTORS; TRANSCRIPTION FACTORS;

EID: 85047694750     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI21716     Document Type: Article

References (33)

1. Mucenski, M.L., Taylor, B.A., Copeland, N.G., and Jenkins, N.A. 1988. Chromosomal location of EVI1 in the DNA of AKXD murine myeloid tumors. Oncol. Res. 2:219-233.
2. Morishita, K., Parker, D.S., Mucenski, M.L., Copeland, N.G., and Ihle, J.N. 1988. Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines. Cell. 54:831-840.
3. Chakraborty, S., Senyuk, V., Sitailo, S., Chi, Y., and Nucifora, G. 2001. Interaction of EVI1 with cAMP-responsive element-binding protein-binding protein (CBP) and p300/CBP-associated factor (P/CAF) results in reversible acetylation of EVI1 and in co-localization in nuclear speckles. J. Biol. Chem. 276:44936-44943.
4. Fears, S., et al. 1996. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR family. Proc. Natl. Acad. Sci. U. S. A. 93:1642-1647.
5. Buonamici, S., Chakraborty, S., Vitalyi, S., and Nucifora, G. 2003. The role of EVI1 in normal and leukemic cells. Blood Cells Mol. Dis. 31:206-212.
6. Delwel, R., Funabiki, T., Kreider, B.L., Morishita, K., and Ihle, J.N. 1993. Four of the seven zinc fingers of the EVI1 myeloid-transforming gene are required for sequence-specific binding to GA(C/T)AAGA(T/C)AAGATAA. Mol. Cell. Biol. 13:4291-4300.
7. Funabiki, T., Kreider, B.L., Morishita, K., and Ihle, J.N. 1990. The carboxyl domain of the zinc finger of EVI1 myeloid transforming gene binds a consensus sequence GAAGATGAG. Oncogene. 5:925-927.
8. Morishita, K., Parganas, E., Matsugi, T., and Ihle, J.N. 1992. Expression of the EVI1 zinc finger gene in 32Dd3 myeloid cells blocks granulocytic differentiation in response to granulocyte colony-stimulating factor. Mol. Cell. Biol. 12:183-189.
9. Kreider, B.L., Orkin, S.H., and Ihle, N.J. 1993. Loss of erythropoietin responsiveness in erythroid progenitors due to the expression of the EVI1 myeloid-transforming gene. Proc. Natl. Acad. Sci. U. S. A. 90:6454-6458.
10. Sitailo, S., Sood, R., Barton, K., and Nucifora, G. 1999. Forced expression of the leukemia-associated gene EVI1 in ES cells: model for myeloid leukemia with 3q26 rearrangements. Leukemia. 13:1639-1645.
11. Louz, D., et al. 2000. Erythroid defects and increased retrovirally-induced tumor formation in Evi1 transgenic mice. Leukemia. 14:1876-1884.
12. Chi, Y., Senyuk, V., Chakraborty, S., and Nucifora, G. 2003. EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity. J. Biol. Chem. 278:49806-49811.
13. Barjesteh van Waalwjik van Doorn-Khosrovani, S., et al. 2003. High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients. Blood. 101:837-845.
14. Alessandrino, E.P., et al. 2001. Myelodysplastic syndromes: recent advances. Haematologica. 86:1124-1157.
15. Martinelli, G., et al. 2003. Association of 3q21q26 syndrome with different RPN1/EVII fusion transcripts. Haematologica. 86:1221-1228.
16. Russell, M., et al. 1994. Expression of EVI1 in myelodysplastic syndromes and other hematologic malignancies without 3q26 translocations. Blood. 84:1243-1248.
17. Greenberg, P.L., Young, N.S., and Gattermann, N. 2002. Myelodysplastic syndromes [review]. Hematology (Am. Soc. Hematol. Educ. Program). 136-161.
18. Parker, J.E., and Mufti, G.J. 2004. The myelodysplastic syndromes: a matter of life or death. Acta Haematol. 111:78-99.
19. Matsushima, T., et al. 2003. Prevalence and clinical characteristics of myelodysplastic syndrome with bone marrow eosinophilia or basophilia. Blood. 101:3386-3390.
20. Kurzrock, R., Cortes, J., and Kantarjian, H. 2002. Clinical development of farnesyltransferase inhibitors in leukemias and myelodysplastic syndrome. Semin. Hematol. 39:20-24.
21. List, A.F. 2002. New approaches to the treatment of myelodysplasia. Oncologist. 7:39-49.
22. Mufti, G., List, A.F., Gore, S.D., and Ho, A.Y. 2003. Myelodysplastic syndrome. Hematology (Am. Soc. Hematol. Educ. Program). 176-199.
23. List, A., et al. 2003. Opportunities for Trisenox (arsenic trioxide) in the treatment of myelodysplastic syndromes. Leukemia. 17:1499-1507.
24. Cantor, A.B., and Orkin, S.H. 2002. Transcriptional regulation of erythropoiesis: an affair involving multiple partners. Oncogene. 21:3368-3376.
25. Wu, H., Liu, X., Jaenish, R., and Lodish, H.F. 1995. Generation of committed erythroid and BFU-E and CFU-E progenitors does not require erythropoietin or the erythropoietin receptor. Cell. 83:59-68.
26. Murone, M., Carpenter, D.A., and De Sauvage, F.J. 1998. Hematopoietic deficiencies in c-mpl and TPO knockout mice. Stem Cells. 16:1-6.
27. Mignotte, V., et al. 1994. Structure and transcription of the human c-mpl gene (MPL). Genomics. 20:5-12.
28. Hawley, R.G., Lieu, F.H., Fong, A.Z., and Hawley, T.S. 1994. Versatile retroviral vectors for potential use in gene therapy. Gene Ther. 1:136-138.
29. Wagner, K.U., et al. 2000. Conditional deletion of the Bcl-x gene from erythroid cells results in hemolytic anemia and profound splenomegaly. Development. 127:4949-4958.
30. Senyuk, V., et al. 2002. The leukemia-associated transcription represser AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells. Oncogene. 21:3232-3240.
31. Cuenco, G.M., Nucifora, G., and Ren, R. 2000. Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML. Proc. Natl. Acad. Sci. U. S. A. 97:1760-1765.
32. Buonamici, S., et al. 2002. Real-time quantitation of minimal residual disease in inv(16)-positive acute myeloid leukemia may indicate risk for clinical relapse and may identify patients in a curable state. Blood. 99:443-449.
33. Nucifora, G., et al. 1994. Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and three unrelated genes at 3q26 in the (3;21)(q26;q22) translocation. Proc. Natl. Acad. Sci. U. S. A. 91:4004-4008.