Aberrant expression of ecotropic viral integration site-1 in acute myeloid leukemia and acute lymphoblastic leukemia

References

• Estey E, Dohner H. Acute myeloid leukaemia. Lancet 2006;368: 1894–1907.
   PubMed Web of Science ®Google Scholar
• Vardiman JW, Thiele J, Arber DA, et al. The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. Blood 2009; 114:937–951.
   PubMed Web of Science ®Google Scholar
• Gilliland DG, Tallman MS. Focus on acute leukemias. Cancer Cell 2002;1:417–420.
   PubMed Web of Science ®Google Scholar
• Yin B, Delwel R, Valk PJ, et al. A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood 2009;113:1075–1085.
   PubMed Web of Science ®Google Scholar
• Lowenberg B. Acute myeloid leukemia: the challenge of capturing disease variety. Hematology Am Soc Hematol Educ Program 2008: 1–11.
   Google Scholar
• Morishita K, Parker DS, Mucenski ML, et al. Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines. Cell 1988;54:831–840.
   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
• Senyuk V, Sinha KK, Li D, et al. Repression of RUNX1 activity by EVI1: a new role of EVI1 in leukemogenesis. Cancer Res 2007;67: 5658–5666.
   PubMed Web of Science ®Google Scholar
• Spensberger D, Delwel R. A novel interaction between the proto-oncogene Evi1 and histone methyltransferases, SUV39H1 and G9a. FEBS Lett 2008;582:2761–2767.
   PubMed Web of Science ®Google Scholar
• Goyama S, Nitta E, Yoshino T, et al. EVI-1 interacts with histone methyltransferases SUV39H1 and G9a for transcriptional repression and bone marrow immortalization. Leukemia 2010;24: 81–88.
   PubMed Web of Science ®Google Scholar
• Kurokawa M, Mitani K, Irie K, et al. The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3. Nature 1998;394:92–96.
   PubMed Web of Science ®Google Scholar
• Izutsu K, Kurokawa M, Imai Y, et al. The corepressor CtBP interacts with Evi-1 to repress transforming growth factor beta signaling. Blood 2001;97:2815–2822.
   PubMed Web of Science ®Google Scholar
• Palmer S, Brouillet JP, Kilbey A, et al. Evi-1 transforming and repressor activities are mediated by CtBP co-repressor proteins. J Biol Chem 2001;276:25834–25840.
   PubMedGoogle Scholar
• Vinatzer U, Taplick J, Seiser C, et al. The leukaemia-associated transcription factors EVI-1 and MDS1/EVI1 repress transcription and interact with histone deacetylase. Br J Haematol 2001;114: 566–573.
   PubMed Web of Science ®Google Scholar
• Chakraborty S, Senyuk V, Sitailo S, et al. 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 2001;276:44936–44943.
   PubMed Web of Science ®Google Scholar
• Lugthart S, Figueroa ME, Bindels E, et al. Aberrant DNA hypermethylation signature in acute myeloid leukemia directed by EVI1. Blood 2011;117:234–241.
   PubMed Web of Science ®Google Scholar
• Senyuk V, Premanand K, Xu P, et al. The oncoprotein EVI1 and the DNA methyltransferase Dnmt3 co-operate in binding and de novo methylation of target DNA. PloS One 2011;6:e20793.
   PubMed Web of Science ®Google Scholar
• Spensberger D, Vermeulen M, Le Guezennec X, et al. Myeloid transforming protein Evi1 interacts with methyl-CpG binding domain protein 3 and inhibits in vitro histone deacetylation by Mbd3/Mi-2/NuRD. Biochemistry 2008;47:6418–6426.
   PubMed Web of Science ®Google Scholar
• Yuasa H, Oike Y, Iwama 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
• Laricchia-Robbio L, Nucifora G. Significant increase of self-renewal in hematopoietic cells after forced expression of EVI1. Blood Cell Mol Dis 2008;40:141–147.
   PubMed Web of Science ®Google Scholar
• Goyama S, Yamamoto G, Shimabe M, et al. Evi-1 is a critical regulator for hematopoietic stem cells and transformed leukemic cells. Cell Stem Cell 2008;3:207–220.
   PubMed Web of Science ®Google Scholar
• Arai S, Yoshimi A, Shimabe M, et al. Evi-1 is a transcriptional target of mixed-lineage leukemia oncoproteins in hematopoietic stem cells. Blood 2011;117:6304–6314.
   PubMed Web of Science ®Google Scholar
• Kataoka K, Sato T, Yoshimi A, et al. Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity. J Exp Med 2011;208:2403–2416.
   PubMed Web of Science ®Google Scholar
• Buonamici S, Li D, Chi Y, et al. EVI1 induces myelodysplastic syndrome in mice. J Clin Invest 2004;114:713–719.
   PubMed Web of Science ®Google Scholar
• Jin G, Yamazaki Y, Takuwa M, et al. Trib1 and Evi1 cooperate with Hoxa and Meis1 in myeloid leukemogenesis. Blood 2007;109: 3998–4005.
   PubMedGoogle Scholar
• Haas K, Kundi M, Sperr WR, et al. Expression and prognostic significance of different mRNA 5’-end variants of the oncogene EVI1 in 266 patients with de novo AML: EVI1 and MDS1/EVI1 overexpression both predict short remission duration. Genes Chromosomes Cancer 2008;47:288–298.
   PubMed Web of Science ®Google Scholar
• Lugthart S, van Drunen E, van Norden Y, et al. High EVI1 levels predict adverse outcome in acute myeloid leukemia: prevalence of EVI1 overexpression and chromosome 3q26 abnormalities underestimated. Blood 2008;111:4329–4337.
   PubMed Web of Science ®Google Scholar
• Groschel S, Lugthart S, Schlenk RF, et al. High EVI1 expression predicts outcome in younger adult patients with acute myeloid leukemia and is associated with distinct cytogenetic abnormalities. J Clin Oncol 2010;28:2101–2107.
   PubMed Web of Science ®Google Scholar
• Morishita K, Parganas E, William CL, et al. Activation of EVI1 gene expression in human acute myelogenous leukemias by translocations spanning 300-400 kilobases on chromosome band 3q26. Proc Natl Acad Sci USA 1992;89:3937–3941.
   PubMed Web of Science ®Google Scholar
• Barjesteh van Waalwijk van Doorn-Khosrovani S, Erpelinck C, van Putten WL, et al. High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients. Blood 2003;101:837–845.
   PubMed Web of Science ®Google Scholar
• Russell M, List A, Greenberg P, et al. Expression of EVI1 in myelodysplastic syndromes and other hematologic malignancies without 3q26 translocations. Blood 1994;84:1243–1248.
   PubMed Web of Science ®Google Scholar
• Vinatzer U, Mannhalter C, Mitterbauer M, et al. Quantitative comparison of the expression of EVI1 and its presumptive antagonist, MDS1/EVI1, in patients with myeloid leukemia. Genes Chromosomes Cancer 2003;36:80–89.
   PubMedGoogle Scholar
• Balgobind BV, Lugthart S, Hollink IH, et al. EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia. Leukemia 2010;24:942–949.
   PubMed Web of Science ®Google Scholar
• Ho PA, Alonzo TA, Gerbing RB, et al. High EVI1 expression is associated with MLL rearrangements and predicts decreased survival in paediatric acute myeloid leukaemia: a report from the children’s oncology group. Br J Haematol 2013;162:670–677.
   PubMed Web of Science ®Google Scholar
• Bindels EM, Havermans M, Lugthart S, et al. EVI1 is critical for the pathogenesis of a subset of MLL-AF9-rearranged AMLs. Blood 2012;119:5838–5849.
   PubMed Web of Science ®Google Scholar
• Valk PJ, Verhaak RG, Beijen MA, et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. N Engl J Med 2004;350:1617–1628.
   PubMed Web of Science ®Google Scholar
• Liu D, Chen S, Pan J, et al. Acquired EVI1 rearrangement involved in the transformation from 5q- syndrome to pre-B lymphocytic leukemia in a Chinese patient. Int J Hematol 2012;96:806–809.
   PubMed Web of Science ®Google Scholar
• Caudell D, Harper DP, Novak RL, et al. Retroviral insertional mutagenesis identifies Zeb2 activation as a novel leukemogenic collaborating event in CALM-AF10 transgenic mice. Blood 2010; 115:1194–1203.
   PubMed Web of Science ®Google Scholar
• Ott MG, Schmidt M, Schwarzwaelder K, et al. Correction of X-linked chronic granulomatous disease by gene therapy, augmented by insertional activation of MDS1-EVI1, PRDM16 or SETBP1. Nat Med 2006;12:401–409.
   PubMed Web of Science ®Google Scholar
• Konantz M, Andre MC, Ebinger M, et al. EVI-1 modulates leukemogenic potential and apoptosis sensitivity in human acute lymphoblastic leukemia. Leukemia 2013;27:56–65.
   PubMed Web of Science ®Google Scholar
• Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative C(T) method. Nat Protoc 2008;3:1101–1108.
   PubMed Web of Science ®Google Scholar
• Daghistani M, Marin D, Khorashad JS, et al. EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors. Blood 2010;116:6014–6017.
   PubMed Web of Science ®Google Scholar
• Santamaria CM, Chillon MC, Garcia-Sanz R, et al. Molecular stratification model for prognosis in cytogenetically normal acute myeloid leukemia. Blood 2009;114:148–152.
   PubMed Web of Science ®Google Scholar
• Groschel S, Schlenk RF, Engelmann J, et al. Deregulated expression of EVI1 defines a poor prognostic subset of MLL- rearranged acute myeloid leukemias: a study of the German-Austrian Acute Myeloid Leukemia Study Group and the Dutch-Belgian-Swiss HOVON/SAKK Cooperative Group. J Clin Oncol 2013;31:95–103.
   PubMed Web of Science ®Google Scholar
• De Weer A, Poppe B, Cauwelier B, et al. Screening for EVI1: ectopic expression absent in T-cell acute lymphoblastic leukemia patients and cell lines. Cancer Genet Cytogenet 2006;171:79–80.
   PubMed Web of Science ®Google Scholar
• Liu-Dumlao T, Kantarjian H, Thomas DA, et al. Philadelphia-positive acute lymphoblastic leukemia: current treatment options. Curr Oncol Rep 2012;14:387–394.
   PubMedGoogle Scholar
• Chen W, Kumar AR, Hudson WA, et al. Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells. Cancer Cell 2008;13:432–440.
   PubMed Web of Science ®Google Scholar
• Kreider BL, Orkin SH, Ihle JN. Loss of erythropoietin responsiveness in erythroid progenitors due to expression of the Evi-1 myeloid-transforming gene. Proc Natl Acad Sci USA 1993;90: 6454–6458.
   PubMed Web of Science ®Google Scholar
• Morishita K, Parganas E, Matsugi T, et al. Expression of the Evi-1 zinc finger gene in 32Dc13 myeloid cells blocks granulocytic differentiation in response to granulocyte colony-stimulating factor. Mol Cell Biol 1992;12:183–189.
   PubMed Web of Science ®Google Scholar
• Kustikova OS, Schwarzer A, Stahlhut M, et al. Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells. Leukemia 2013;27:1127–1138.
   PubMed Web of Science ®Google Scholar