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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Amabile G,Di Ruscio A,Müller F,Welner RS,Yang H,Ebralidze AK,Zhang H,Levantini E,Qi L,Martinelli G,Brummelkamp T,Le Beau MM,Figueroa ME,Bock C,Tenen DGdoi
10.1038/ncomms8091subject
Has Abstractpub_date
2015-05-22 00:00:00pages
7091issn
2041-1723pii
ncomms8091journal_volume
6pub_type
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