DNA Methylation in Chronic Myeloid Leukemia
Elisa Leo* and Giovanni Martinelli
Istituto di Ematologia “L. e A. Seràgnoli”, DIMES, Università di Bologna, via Massarenti 9, Bologna, Italy
- Corresponding Author:
- Elisa Leo, PhD
Istituto di Ematologia “L. e A. Seràgnoli” – DIMES – Università di Bologna
via Massarenti 9, 40138 Bologna – Italy
E-mail: [email protected]
Received date: June 10, 2014; Accepted date: July 10, 2014; Published date: July 20, 2014
Citation: Leo E and Martinelli G (2014) DNA Methylation in Chronic Myeloid Leukemia. J Mol Genet Med 08:118. doi: 10.4172/1747-0862.1000118
Copyright: © 2014 Leo E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
Despite the high efficiency of tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia, 20-25% of patients develop drug resistance resulting in therapy failure. Besides mutations of the BCR-ABL1 kinase domain, the abnormal epigenetic regulation of the expression of critical genes for cell proliferation and survival has a central role in the disease pathogenesis and progression towards the drug resistant phenotype. Such epigenetic changes have the potential to be modulated by specific drugs including demethylating agents and histone deacetylase inhibitors. Here the current knowledge on the BCR-ABL1-associated methylation status is reviewed.