[HTML][HTML] Dissecting the role of aberrant DNA methylation in human leukaemia
Nature communications, 2015•nature.com
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 …
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 …
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.
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