Elisa Leo and Giovanni Martinelli
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.
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