Giuseppina Nucifora

Summary

Affiliation: University of Illinois at Chicago
Country: USA

Publications

  1. ncbi request reprint Association of 3q21q26 syndrome with different RPN1/EVI1 fusion transcripts
    Giovanni Martinelli
    Institute of Hematology and Medical Oncology L and A Seragnoli, University of Bologna, Italy
    Haematologica 88:1221-8. 2003
  2. ncbi request reprint EVI1 and hematopoietic disorders: history and perspectives
    Giuseppina Nucifora
    Department of Pathology, University of Illinois at Chicago, 60607, United States
    Gene 368:1-11. 2006
  3. ncbi request reprint Corepressor CtBP1 interacts with and specifically inhibits CBP activity
    Vitalyi Senyuk
    Department of Pathology, The Cancer Center, University of Illinois at Chicago, Chicago, IL, USA
    Arch Biochem Biophys 441:168-73. 2005
  4. ncbi request reprint P/CAF and GCN5 acetylate the AML1/MDS1/EVI1 fusion oncoprotein
    Vitalyi Senyuk
    Department of Pathology, Molecular Biology Research Building, M C 737, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607, USA
    Biochem Biophys Res Commun 307:980-6. 2003
  5. doi request reprint EVI1 Impairs myelopoiesis by deregulation of PU.1 function
    Leopoldo Laricchia-Robbio
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    Cancer Res 69:1633-42. 2009
  6. pmc Significant increase of self-renewal in hematopoietic cells after forced expression of EVI1
    Leopoldo Laricchia-Robbio
    Department of Medicine, University of Illinois at Chicago M C 737, 909 South Wolcott Avenue, Chicago, IL 60612, USA
    Blood Cells Mol Dis 40:141-7. 2008
  7. ncbi request reprint Combinatorial action of RUNX1 and PU.1 in the regulation of hematopoiesis
    Yogen Saunthararajah
    Department of Medicine and Cancer Center, University of Illinois at Chicago, Chicago, IL 60612, USA
    Crit Rev Eukaryot Gene Expr 16:183-92. 2006
  8. ncbi request reprint The distal zinc finger domain of AML1/MDS1/EVI1 is an oligomerization domain involved in induction of hematopoietic differentiation defects in primary cells in vitro
    Vitalyi Senyuk
    Department of Pathology and The Cancer Center, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    Cancer Res 65:7603-11. 2005
  9. pmc The oncoprotein EVI1 and the DNA methyltransferase Dnmt3 co-operate in binding and de novo methylation of target DNA
    Vitalyi Senyuk
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America
    PLoS ONE 6:e20793. 2011
  10. ncbi request reprint The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells
    Vitalyi Senyuk
    Department of Pathology, The Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607, USA
    Oncogene 21:3232-40. 2002

Research Grants

  1. TEL, AML1, and TEL/AML1 in Hematopoiesis
    Giuseppina Nucifora; Fiscal Year: 2006
  2. Inactivating EVI1 for the Treatment of Myelodysplastic *
    Giuseppina Nucifora; Fiscal Year: 2007
  3. Role of EVI1 Modifications in Cell Transformation
    Giuseppina Nucifora; Fiscal Year: 2009
  4. MOLECULAR ANALYSIS OF TEL AND TEL/AML1 IN PREB LEUKEMIA
    Giuseppina Nucifora; Fiscal Year: 2001
  5. EVI1 Expression is a Prognostic Marker of CML
    Giuseppina Nucifora; Fiscal Year: 2004
  6. ANALYSIS OF MULTIPLE CHIMERIC TRANSCRIPTS IN THE T(3;21)
    Giuseppina Nucifora; Fiscal Year: 2004
  7. INTERFERON ALPHA-INDUCED BIOLOGICAL RESPONSES IN CML
    Giuseppina Nucifora; Fiscal Year: 2004
  8. A Mouse Model of Myelodysplastic Syndrome Progression
    Giuseppina Nucifora; Fiscal Year: 2009

Collaborators

Detail Information

Publications26

  1. ncbi request reprint Association of 3q21q26 syndrome with different RPN1/EVI1 fusion transcripts
    Giovanni Martinelli
    Institute of Hematology and Medical Oncology L and A Seragnoli, University of Bologna, Italy
    Haematologica 88:1221-8. 2003
    ..Other genes that have been implicated at the rearrangement breakpoint are GR6 and RPN1 (both on 3q21). The aim of this study was to investigate the expression of the EVI1 fusion genes in AML patients with 3q21q26 syndrome...
  2. ncbi request reprint EVI1 and hematopoietic disorders: history and perspectives
    Giuseppina Nucifora
    Department of Pathology, University of Illinois at Chicago, 60607, United States
    Gene 368:1-11. 2006
    ..In this review, we summarize the biochemical properties of EVI1 and the effects of EVI1 in biological models...
  3. ncbi request reprint Corepressor CtBP1 interacts with and specifically inhibits CBP activity
    Vitalyi Senyuk
    Department of Pathology, The Cancer Center, University of Illinois at Chicago, Chicago, IL, USA
    Arch Biochem Biophys 441:168-73. 2005
    ..Based on these results, we propose that CtBP1 mediates repression by blocking histone acetylation by HAT complexes...
  4. ncbi request reprint P/CAF and GCN5 acetylate the AML1/MDS1/EVI1 fusion oncoprotein
    Vitalyi Senyuk
    Department of Pathology, Molecular Biology Research Building, M C 737, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607, USA
    Biochem Biophys Res Commun 307:980-6. 2003
    ..AME acetylation has no effect on its interaction with the co-repressor CtBP1. Finally, we demonstrate that the co-expression of AME and either P/CAF or GCN5 abrogates the repression of an AML1-dependent reporter gene...
  5. doi request reprint EVI1 Impairs myelopoiesis by deregulation of PU.1 function
    Leopoldo Laricchia-Robbio
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    Cancer Res 69:1633-42. 2009
    ..After mapping the PU.1-EVI1 interaction sites, we show that an EVI1 point mutant, unable to bind PU.1, restores the activation of PU.1-regulated genes and allows a normal differentiation of BM progenitors in vitro...
  6. pmc Significant increase of self-renewal in hematopoietic cells after forced expression of EVI1
    Leopoldo Laricchia-Robbio
    Department of Medicine, University of Illinois at Chicago M C 737, 909 South Wolcott Avenue, Chicago, IL 60612, USA
    Blood Cells Mol Dis 40:141-7. 2008
    ....
  7. ncbi request reprint Combinatorial action of RUNX1 and PU.1 in the regulation of hematopoiesis
    Yogen Saunthararajah
    Department of Medicine and Cancer Center, University of Illinois at Chicago, Chicago, IL 60612, USA
    Crit Rev Eukaryot Gene Expr 16:183-92. 2006
    ..Here we describe the relationship of RUNX1 with PU.1 as a facet of the combinatorial relationships that determine hematopoietic lineage commitment...
  8. ncbi request reprint The distal zinc finger domain of AML1/MDS1/EVI1 is an oligomerization domain involved in induction of hematopoietic differentiation defects in primary cells in vitro
    Vitalyi Senyuk
    Department of Pathology and The Cancer Center, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    Cancer Res 65:7603-11. 2005
    ....
  9. pmc The oncoprotein EVI1 and the DNA methyltransferase Dnmt3 co-operate in binding and de novo methylation of target DNA
    Vitalyi Senyuk
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America
    PLoS ONE 6:e20793. 2011
    ....
  10. ncbi request reprint The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells
    Vitalyi Senyuk
    Department of Pathology, The Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607, USA
    Oncogene 21:3232-40. 2002
    ....
  11. ncbi request reprint A new translocation that rearranges the AML1 gene in a patient with T-cell acute lymphoblastic leukemia
    Fady M Mikhail
    Department of Clinical Pathology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
    Cancer Genet Cytogenet 135:96-100. 2002
    ..By metaphase fluorescence in situ hybridization analysis, the AML1 breakpoint was mapped using recombinant phage clones, and shown to be either immediately upstream or downstream of exon 5...
  12. ncbi request reprint Repression of RUNX1 activity by EVI1: a new role of EVI1 in leukemogenesis
    Vitalyi Senyuk
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    Cancer Res 67:5658-66. 2007
    ....
  13. ncbi request reprint RUNX1-RUNX1 homodimerization modulates RUNX1 activity and function
    Donglan Li
    Department of Medicine, University of Illinois, Chicago, Illinois 60612, USA
    J Biol Chem 282:13542-51. 2007
    ....
  14. pmc Point mutations in two EVI1 Zn fingers abolish EVI1-GATA1 interaction and allow erythroid differentiation of murine bone marrow cells
    Leopoldo Laricchia-Robbio
    University of Illinois at Chicago M C 737, 909 South Wolcott Avenue, Chicago, IL 60612, USA
    Mol Cell Biol 26:7658-66. 2006
    ..Point mutations that disrupt the geometry of two zinc fingers of EVI1 abolish the protein-protein interaction, leading to normal erythroid differentiation of normal murine bone marrow in vitro...
  15. pmc Small ubiquitin-like modifier conjugation regulates nuclear export of TEL, a putative tumor suppressor
    Lauren D Wood
    Department of Biochemistry and Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 100:3257-62. 2003
    ..We propose that the ability of TEL to repress transcription and suppress growth is regulated by sumoylation and nuclear export...
  16. ncbi request reprint Meeting report: Sixth International Workshop on Molecular Aspects of Myeloid Stem Cell Development and Leukemia, Annapolis, May 1-4, 2005
    Linda Wolff
    National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Exp Hematol 33:1436-42. 2005
  17. ncbi request reprint SUV39H1 interacts with AML1 and abrogates AML1 transactivity. AML1 is methylated in vivo
    Soumen Chakraborty
    Department of Pathology and The Cancer Center, University of Illinois at Chicago, Chicago, IL 60607, USA
    Oncogene 22:5229-37. 2003
    ..Our data suggest that other enzymes are also involved in gene regulation by AML1 activity by modulating the affinity of AML1 for DNA...
  18. ncbi request reprint Normal and transforming functions of RUNX1: a perspective
    Fady M Mikhail
    Department of Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Cell Physiol 207:582-93. 2006
    ..Here, we provide an overview of the many roles of RUNX1 in hematopoietic self-renewal and differentiation and summarize the information that is currently available on the many mechanisms of RUNX1 deregulation in human leukemia...
  19. ncbi request reprint The role of EVI1 in normal and leukemic cells
    Silvia Buonamici
    Department of Pathology and Cancer Center, University of Illinois at Chicago, Chicago, IL 60607, USA
    Blood Cells Mol Dis 31:206-12. 2003
    ....
  20. ncbi request reprint EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity
    Yiqing Chi
    Department of Pathology and The Cancer Center, University of Illinois, Chicago, Illinois 60607, USA
    J Biol Chem 278:49806-11. 2003
    ..Taken together, these data support the hypothesis that the interaction with BRG1 is important for up-regulation of cell-growth by EVI1...
  21. ncbi request reprint EVI1 abrogates interferon-alpha response by selectively blocking PML induction
    Silvia Buonamici
    Department of Pathology and Cancer Center, University of Illinois, Chicago, Illinois 60607, USA
    J Biol Chem 280:428-36. 2005
    ..These results point to a novel mechanism utilized by an oncogene to escape normal cell response to growth-controlling cytokines...
  22. pmc EVI1 induces myelodysplastic syndrome in mice
    Silvia Buonamici
    Department of Pathology and Cancer Center, University of Illinois at Chicago, Chicago, Illinois, USA
    J Clin Invest 114:713-9. 2004
    ..These defects are not fatal, and the mice survive for about 10 months with compensated hematopoiesis. Over this time, compensation fails, and the mice succumb to fatal peripheral cytopenia...
  23. ncbi request reprint Arsenic trioxide and thalidomide combination produces multi-lineage hematological responses in myelodysplastic syndromes patients, particularly in those with high pre-therapy EVI1 expression
    Azra Raza
    Section of Myeloid Diseases and MDS Center, Rush University, Rush Presbyterian St Luke s Medical Center, 2242 West Harrison Street, Suite 108, Chicago, IL 60612 3515, USA
    Leuk Res 28:791-803. 2004
    ..Both low/high risk MDS may benefit significantly from therapy with ATO/thalidomide, and those with high pre-therapy EVI1 expression may be uniquely sensitive...
  24. ncbi request reprint A novel gene, FGA7, is fused to RUNX1/AML1 in a t(4;21)(q28;q22) in a patient with T-cell acute lymphoblastic leukemia
    Fady M Mikhail
    Department of Clinical Pathology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
    Genes Chromosomes Cancer 39:110-8. 2004
    ..It is possible that the expression of a constitutively shortened AML1 could compete with full-length AML1 and act as a dominant negative inhibitor of the promoters that the core binding factor activates...
  25. pmc Genomic DNA breakpoints in AML1/RUNX1 and ETO cluster with topoisomerase II DNA cleavage and DNase I hypersensitive sites in t(8;21) leukemia
    Yanming Zhang
    Section of Hematology Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA
    Proc Natl Acad Sci U S A 99:3070-5. 2002
    ..These sites correlated with genomic DNA breakpoints in both AML1 and ETO, thus implicating them in the de novo 8;21 translocation...
  26. doi request reprint Meeting report: Seventh International Workshop on Molecular Aspects of Myeloid Stem Cell Development and Leukemia, Annapolis, MD, May 13-16, 2007
    Linda Wolff
    National Cancer Institute, Bethesda, MD 20892, USA
    Exp Hematol 36:523-32. 2008

Research Grants28

  1. TEL, AML1, and TEL/AML1 in Hematopoiesis
    Giuseppina Nucifora; Fiscal Year: 2006
    ....
  2. Inactivating EVI1 for the Treatment of Myelodysplastic *
    Giuseppina Nucifora; Fiscal Year: 2007
    ..The third aim will be focused on the role of arsenic trioxide in the treatment of EVI1-positive MDS and on the isolation of small molecules that inhibit EVI1. ..
  3. Role of EVI1 Modifications in Cell Transformation
    Giuseppina Nucifora; Fiscal Year: 2009
    ..2. To identify the components and the functions of the nuclear EVI1 multiprotein complexes. 3. To characterize the sumoylation and acetylation of EVI1 in vivo and to define their role in EVI1- induced transformation. ..
  4. MOLECULAR ANALYSIS OF TEL AND TEL/AML1 IN PREB LEUKEMIA
    Giuseppina Nucifora; Fiscal Year: 2001
    ..The experiments outlined in this proposal will allow them to begin to dissect the effects of TEL/AML1 in hematopoiesis and its contribution to leukogenesis. ..
  5. EVI1 Expression is a Prognostic Marker of CML
    Giuseppina Nucifora; Fiscal Year: 2004
    ..Real-time RT-PCR analysis and statistical analysis of CML and control samples will be used for this study. ..
  6. ANALYSIS OF MULTIPLE CHIMERIC TRANSCRIPTS IN THE T(3;21)
    Giuseppina Nucifora; Fiscal Year: 2004
    ..In addition, our results will provide insight in the study of leukemias in which either AML 1 or MDS1/EVI1 are rearranged. ..
  7. INTERFERON ALPHA-INDUCED BIOLOGICAL RESPONSES IN CML
    Giuseppina Nucifora; Fiscal Year: 2004
    ..The ability to identify CML patients who will not respond to IFNalpha-therapy will be a very valuable clinical tool that could affect their treatment and their overall survival. ..
  8. A Mouse Model of Myelodysplastic Syndrome Progression
    Giuseppina Nucifora; Fiscal Year: 2009
    ..We plan to use a combination of molecular biology and in vivo systems to dissect the molecular pathways of EVI1 and identify steps that can be used for the development of new treatments. ..