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Epigenetics and chronic lymphocytic leukemia
Author(s) -
Yu Margaret K.
Publication year - 2006
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.20718
Subject(s) - dna methylation , epigenetics , chronic lymphocytic leukemia , gene silencing , methylation , gene , leukemia , cancer research , biology , myelodysplastic syndromes , decitabine , medicine , genetics , immunology , gene expression , bone marrow
The DNA methylation level in patients with chronic lymphocytic leukemia is generally lower than healthy individuals. Although DNA methylation is globally decreased, regional hypermethylation of gene promoters leads to gene silencing. Many of these genes have tumor suppressor phenotypes. Unlike mutations or deletions, hypermethylation is potentially reversible after inhibition with DNA methylation modulators. Myelodysplastic syndrome has been a model disease in which treatment of patients results in demethylation of specific genes. The story in patients with chronic lymphocytic leukemia is slowly unraveling as epigenetic modifications likely also play an important role. Ongoing clinical trials correlating clinical response to gene expression after treatment with DNA methylation inhibitors will ultimately allow us to better risk stratify and predict the subgroup of patients who will benefit from treatment with this class of drugs. Am. J. Hematol., 2006, © 2006 Wiley‐Liss, Inc.