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 and Daniel G. Tenen ()
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Giovanni Amabile: Harvard Medical School
Annalisa Di Ruscio: Harvard Medical School
Fabian Müller: Max Plank Institute for Informatics
Robert S. Welner: Harvard Medical School
Henry Yang: Cancer Science Institute, National University of Singapore
Alexander K. Ebralidze: Harvard Medical School
Hong Zhang: Harvard Medical School
Elena Levantini: Harvard Medical School
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
Daniel G. Tenen: Harvard Medical School

Nature Communications, 2015, vol. 6, issue 1, 1-10

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms8091

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