Dissecting the role of aberrant DNA methylation in human leukaemia

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, Michelle M. Le Beau, Maria E. Figueroa, Christoph Bock, Daniel G. Tenen

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


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.

Original languageEnglish (US)
Article number7091
JournalNature communications
StatePublished - May 22 2015
Externally publishedYes

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)


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