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Dissecting the role of aberrant DNA methylation in human leukaemia

Author

Listed:
  • Giovanni Amabile

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University)

  • Annalisa Di Ruscio

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University)

  • Fabian Müller

    (Max Plank Institute for Informatics)

  • Robert S. Welner

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University)

  • Henry Yang

    (Cancer Science Institute, National University of Singapore)

  • Alexander K. Ebralidze

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University)

  • Hong Zhang

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University)

  • Elena Levantini

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University
    Institute of Biomedical Technologies, National Research Council (CNR))

  • Lihua Qi

    (Cancer Science Institute, National University of Singapore)

  • Giovanni Martinelli

    (Diagnostic and Specialty Medicine, University of Bologna)

  • Thijn Brummelkamp

    (Netherlands Cancer Institute)

  • Michelle M. Le Beau

    (Section of Hematology/Oncology and the Comprehensive Cancer Center, University of Chicago)

  • Maria E. Figueroa

    (University of Michigan)

  • Christoph Bock

    (Max Plank Institute for Informatics
    CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
    Medical University of Vienna)

  • Daniel G. Tenen

    (Harvard Medical School
    Harvard Stem Cell Institute, Harvard University
    Cancer Science Institute, National University of Singapore)

Abstract

Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the genetic translocation t(9;22)(q34;q11.2) encoding for the BCR-ABL fusion oncogene. However, many molecular mechanisms of the disease progression still remain poorly understood. A growing body of evidence suggests that the epigenetic abnormalities are involved in tyrosine kinase resistance in CML, leading to leukaemic clone escape and disease propagation. Here we show that, by applying cellular reprogramming to primary CML cells, aberrant DNA methylation contributes to the disease evolution. Importantly, using a BCR-ABL inducible murine model, we demonstrate that a single oncogenic lesion triggers DNA methylation changes, which in turn act as a precipitating event in leukaemia progression.

Suggested Citation

  • Giovanni Amabile & Annalisa Di Ruscio & Fabian Müller & Robert S. Welner & Henry Yang & Alexander K. Ebralidze & Hong Zhang & Elena Levantini & Lihua Qi & Giovanni Martinelli & Thijn Brummelkamp & Mic, 2015. "Dissecting the role of aberrant DNA methylation in human leukaemia," Nature Communications, Nature, vol. 6(1), pages 1-10, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8091
    DOI: 10.1038/ncomms8091
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