| Literature DB >> 25901742 |
Håkon Reikvam1, Tuyen Thi van Hoang, Øystein Bruserud.
Abstract
The recent advances in our understanding of leukemogenesis have clearly demonstrated that human acute myeloid leukemia is a heterogeneous malignancy, and several disease mechanisms should probably be regarded as possible therapeutic targets only for specific subsets of patients and not for acute myeloid leukemia in general. One promising strategy for epigenetic targeting is inhibition of the binding between bromodomain-containing transcription regulators and acetylated lysine residues on histones. This possible approach has been investigated especially for patients with 11q23 and chromosome 8 abnormalities. An alternative target is the histone methyltransferase COT1L. Major challenges for both approaches will be to clarify how these strategies should be combined with each other or with conventional chemotherapy, and whether their use should be limited to certain subsets of patients.Entities:
Keywords: acetylation; acute myeloid leukemia; bromodomain; epigenetic; histone; methyl transferase; methylation; therapy
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Year: 2015 PMID: 25901742 DOI: 10.1586/17474086.2015.1036025
Source DB: PubMed Journal: Expert Rev Hematol ISSN: 1747-4094 Impact factor: 2.929