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Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease

Stein, Stefan, Ott, Marion G, Schultze-Strasser, Stephan, Jauch, Anna, Burwinkel, Barbara, Kinner, Andrea, Schmidt, Manfred, Krämer, Alwin, Schwäble, Joachim, Glimm, Hanno, Koehl, Ulrike, Preiss, Carolin, Ball, Claudia, Martin, Hans, Göhring, Gudrun, Schwarzwaelder, Kerstin, Hofmann, Wolf-Karsten, Karakaya, Kadin, Tchatchou, Sandrine, Yang, Rongxi, Reinecke, Petra, Kühlcke, Klaus, Schlegelberger, Brigitte, Thrasher, Adrian J, Hoelzer, Dieter, Seger, Reinhard, von Kalle, Christof, Grez, Manuel·2010·Nature Medicine
DOI 10.1038/nm.2088
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  1. Cavazzana-Calvo, M. et al. Gene therapy of human severe combined immunodeficiency (SCID)-X1 disease. Science 288, 669–672 (2000). · DOI · Paper page
  2. Aiuti, A. et al. Correction of ADA-SCID by stem cell gene therapy combined with nonmyeloablative conditioning. Science 296, 2410–2413 (2002). · DOI · Paper page
  3. Gaspar, H.B. et al. Gene therapy of X-linked severe combined immunodeficiency by use of a pseudotyped gammaretroviral vector. Lancet 364, 2181–2187 (2004). · DOI
  4. Gaspar, H.B. et al. Successful reconstitution of immunity in ADA-SCID by stem cell gene therapy following cessation of PEG-ADA and use of mild preconditioning. Mol. Ther. 14, 505–513 (2006). · DOI
  5. Aiuti, A. et al. Gene therapy for immunodeficiency due to adenosine deaminase deficiency. N. Engl. J. Med. 360, 447–458 (2009). · DOI
  6. Hacein-Bey-Abina, S. et al. LMO2-associated clonal T cell proliferation in two patients after gene therapy for SCID-X1. Science 302, 415–419 (2003). · DOI · Paper page
  7. Howe, S.J. et al. Insertional mutagenesis combined with acquired somatic mutations causes leukemogenesis following gene therapy of SCID-X1 patients. J. Clin. Invest. 118, 3143–3150 (2008). · DOI · Paper page
  8. Dinauer, M.C. The respiratory burst oxidase and the molecular genetics of chronic granulomatous disease. Crit. Rev. Clin. Lab. Sci. 30, 329–369 (1993). · DOI
  9. Roos, D. The genetic basis of chronic granulomatous disease. Immunol. Rev. 138, 121–157 (1994). · DOI
  10. Segal, A.W. The NADPH oxidase and chronic granulomatous disease. Mol. Med. Today 2, 129–135 (1996). · DOI
  11. Malech, H.L. & Hickstein, D.D. Genetics, biology and clinical management of myeloid cell primary immune deficiencies: chronic granulomatous disease and leukocyte adhesion deficiency. Curr. Opin. Hematol. 14, 29–36 (2007). · DOI · Paper page
  12. Ott, M.G. et al. Correction of X-linked chronic granulomatous disease by gene therapy, augmented by insertional activation of MDS1–EVI1, PRDM16 or SETBP1. Nat. Med. 12, 401–409 (2006). · DOI · Paper page
  13. Fears, S. et al. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family. Proc. Natl. Acad. Sci. USA 93, 1642–1647 (1996). · DOI
  14. Hamaguchi, H. et al. Establishment of a novel human myeloid leukaemia cell line (HNT-34) with t(3;3)(q21;q26), t(9;22)(q34;q11) and the expression of EVI1 gene, P210 and P190 BCR/ABL chimaeric transcripts from a patient with AML after MDS with 3q21q26 syndrome. Br. J. Haematol. 98, 399–407 (1997). · DOI
  15. Claus, R. & Lubbert, M. Epigenetic targets in hematopoietic malignancies. Oncogene 22, 6489–6496 (2003). · DOI
  16. Nolte, F. & Hofmann, W.K. Myelodysplastic syndromes: molecular pathogenesis and genomic changes. Ann. Hematol. 87, 777–795 (2008). · DOI
  17. Christiansen, D.H., Andersen, M.K. & Pedersen-Bjergaard, J. Methylation of p15INK4B is common, is associated with deletion of genes on chromosome arm 7q and predicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia 17, 1813–1819 (2003). · DOI
  18. Khanna, K.K. & Jackson, S.P. DNA double-strand breaks: signaling, repair and the cancer connection. Nat. Genet. 27, 247–254 (2001). · DOI · Paper page
  19. Fernandez-Capetillo, O., Celeste, A. & Nussenzweig, A. Focusing on foci: H2AX and the recruitment of DNA-damage response factors. Cell Cycle 2, 426–427 (2003). · DOI
  20. Kearns, W.G., Yamaguchi, H., Young, N.S. & Liu, J.M. Centrosome amplification and aneuploidy in bone marrow failure patients. Genes Chromosomes Cancer 40, 329–333 (2004). · DOI
  21. Neben, K., Giesecke, C., Schweizer, S., Ho, A.D. & Kramer, A. Centrosome aberrations in acute myeloid leukemia are correlated with cytogenetic risk profile. Blood 101, 289–291 (2003). · DOI
  22. Ganem, N.J., Godinho, S.A. & Pellman, D. A mechanism linking extra centrosomes to chromosomal instability. Nature 460, 278–282 (2009). · DOI
  23. Dinauer, M.C., Curnutte, J.T., Rosen, H. & Orkin, S.H. A missense mutation in the neutrophil cytochrome b heavy chain in cytochrome-positive X-linked chronic granulomatous disease. J. Clin. Invest. 84, 2012–2016 (1989). · DOI
  24. Wang, L., Robbins, P.B., Carbonaro, D.A. & Kohn, D.B. High-resolution analysis of cytosine methylation in the 5′ long terminal repeat of retroviral vectors. Hum. Gene Ther. 9, 2321–2330 (1998). · DOI
  25. Frank, O. et al. Tumor cells escape suicide gene therapy by genetic and epigenetic instability. Blood 104, 3543–3549 (2004). · DOI
  26. Burns, W.R., Zheng, Z., Rosenberg, S.A. & Morgan, R.A. Lack of specific gamma-retroviral vector long terminal repeat promoter silencing in patients receiving genetically engineered lymphocytes and activation upon lymphocyte restimulation. Blood 114, 2888–2899 (2009). · DOI
  27. Metais, J.Y. & Dunbar, C.E. The MDS1–EVI1 gene complex as a retrovirus integration site: impact on behavior of hematopoietic cells and implications for gene therapy. Mol. Ther. 16, 439–449 (2008). · DOI
  28. Du, Y., Jenkins, N.A. & Copeland, N.G. Insertional mutagenesis identifies genes that promote the immortalization of primary bone marrow progenitor cells. Blood 106, 3932–3939 (2005). · DOI
  29. Calmels, B. et al. Recurrent retroviral vector integration at the MDS1–EVI1 locus in non-human primate hematopoietic cells. Blood 106, 2530–2533 (2005). · DOI
  30. Li, Z. et al. Murine leukemia induced by retroviral gene marking. Science 296, 497 (2002). · DOI · Paper page
  31. Modlich, U. et al. Leukemia induction after a single retroviral vector insertion in Evi1 or Prdm16. Leukemia 22, 1519–1528 (2008). · DOI
  32. Buonamici, S. et al. EVI1 induces myelodysplastic syndrome in mice. J. Clin. Invest. 114, 713–719 (2004). · DOI
  33. Du, Y., Spence, S.E., Jenkins, N.A. & Copeland, N.G. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood 106, 2498–2505 (2005). · DOI
  34. Nucifora, G. The EVI1 gene in myeloid leukemia. Leukemia 11, 2022–2031 (1997). · DOI
  35. Dreyfus, F. et al. Expression of the Evi-1 gene in myelodysplastic syndromes. Leukemia 9, 203–205 (1995).
  36. Barjesteh van Waalwijk van Doorn-Khosrovani, S et al. High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients. Blood 101, 837–845 (2003). · DOI
  37. Charrin, C. et al. Structural rearrangements of chromosome 3 in 57 patients with acute myeloid leukemia: clinical, hematological and cytogenetic features. Hematol. J. 3, 21–31 (2002). · DOI
  38. Lin, P., Medeiros, L.J., Yin, C.C. & Abruzzo, L.V. Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet. Cytogenet. 166, 82–85 (2006). · DOI
  39. Stevens-Kroef, M. et al. Translocation t(2;3)(p15–23;q26–27) in myeloid malignancies: report of 21 new cases, clinical, cytogenetic and molecular genetic features. Leukemia 18, 1108–1114 (2004). · DOI
  40. Trubia, M. et al. Characterization of a recurrent translocation t(2;3)(p15–22;q26) occurring in acute myeloid leukaemia. Leukemia 20, 48–54 (2006). · DOI
  41. Laricchia-Robbio, L. & Nucifora, G. Significant increase of self-renewal in hematopoietic cells after forced expression of EVI1. Blood Cells Mol. Dis. 40, 141–147 (2007). · DOI
  42. Perkins, A.S., Mercer, J.A., Jenkins, N.A. & Copeland, N.G. Patterns of Evi-1 expression in embryonic and adult tissues suggest that Evi-1 plays an important regulatory role in mouse development. Development 111, 479–487 (1991). · DOI
  43. Kustikova, O.S. et al. Retroviral vector insertion sites associated with dominant hematopoietic clones mark “stemness” pathways. Blood 109, 1897–1907 (2007). · DOI
  44. Senyuk, V. et al. Repression of RUNX1 activity by EVI1: a new role of EVI1 in leukemogenesis. Cancer Res. 67, 5658–5666 (2007). · DOI
  45. Chi, Y., Senyuk, V., Chakraborty, S. & Nucifora, G. EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity. J. Biol. Chem. 278, 49806–49811 (2003). · DOI
  46. Cattaneo, F. & Nucifora, G. EVI1 recruits the histone methyltransferase SUV39H1 for transcription repression. J. Cell. Biochem. 105, 344–352 (2008). · DOI
  47. Spensberger, D. & Delwel, R. A novel interaction between the proto-oncogene Evi1 and histone methyltransferases, SUV39H1 and G9a. FEBS Lett. 582, 2761–2767 (2008). · DOI
  48. Spensberger, D. 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 47, 6418–6426 (2008). · DOI
  49. Kondo, Y. et al. Downregulation of histone H3 lysine 9 methyltransferase G9a induces centrosome disruption and chromosome instability in cancer cells. PLoS One 3, e2037 (2008). · DOI
  50. Krämer, A., Neben, K. & Ho, A.D. Centrosome replication, genomic instability and cancer. Leukemia 16, 767–775 (2002). · DOI
  51. Zhang, Y. et al. MLL5 contributes to hematopoietic stem cell fitness and homeostasis. Blood 113, 1455–1463 (2009). · DOI
  52. Heuser, M. et al. Loss of MLL5 results in pleiotropic hematopoietic defects, reduced neutrophil immune function, and extreme sensitivity to DNA demethylation. Blood 113, 1432–1443 (2009). · DOI
  53. Madan, V. et al. Impaired function of primitive hematopoietic cells in mice lacking the mixed-lineage-leukemia homolog MLL5. Blood 113, 1444–1454 (2009). · DOI
  54. Sebastian, S. et al. MLL5, a trithorax homolog, indirectly regulates H3K4 methylation, represses cyclin A2 expression, and promotes myogenic differentiation. Proc. Natl. Acad. Sci. USA 106, 4719–4724 (2009). · DOI

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Metadata

Authors
Stein, S., Ott, M. G., Schultze-Strasser, S., Jauch, A., Burwinkel, B., Kinner, A., Schmidt, M., Krämer, A., Schwäble, J., Glimm, H., Koehl, U., Preiss, C., Ball, C., Martin, H., Göhring, G., Schwarzwaelder, K., Hofmann, W.-K., Karakaya, K., Tchatchou, S., Yang, R., Reinecke, P., Kühlcke, K., Schlegelberger, B., Thrasher, A. J., Hoelzer, D., Seger, R., von Kalle, C., & Grez, M.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2010-01-24
Volume
16
Issue
2
Pages
198-204
ISSN
  • 1078-8956
  • 1546-170X
DOI
10.1038/nm.2088
Cited by
716
References
5
Language
en
Licence
www.springer.com/tdm (tdm)

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CoChat. (2026). Citation check: Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease. https://app.cochat.ai/papers/10.1038/nm.2088
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Stein, S., Ott, M. G., Schultze-Strasser, S., Jauch, A., Burwinkel, B., Kinner, A., Schmidt, M., Krämer, A., Schwäble, J., Glimm, H., Koehl, U., Preiss, C., Ball, C., Martin, H., Göhring, G., Schwarzwaelder, K., Hofmann, W.-K., Karakaya, K., Tchatchou, S., . . . Grez, M. (2010). Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease. Nature Medicine. https://doi.org/10.1038/nm.2088