期刊
SEMINARS IN HEMATOLOGY
卷 52, 期 2, 页码 86-96出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.seminhematol.2015.01.003
关键词
-
类别
资金
- American Society of Hematology
- NIH [R01 CA187109]
- Leukemia and Lymphoma Society [6141-14]
- Burroughs Wellcome Translational Scientist Award
- Chemotherapy Foundation
The pathogenesis of diffuse large B-cell lymphoma (DLBCL) is strongly linked to perturbation of epigenetic mechanisms. The germinal center (GC) B cells from which DLBCLs arise are prone to instability in their cytosine methylation patterns. DLBCLs inherit this epigenetic instability and display variable degrees of epigenetic heterogeneity. Greater epigenetic heterogeneity is linked with poor clinical outcome. Somatic mutations of histone-modifying proteins have also emerged as a hallmark of DLBCL. The effect of these somatic mutations may be to disrupt epigenetic switches that control the GC phenotype and lock in certain oncogenic features of GC B cells, resulting in malignant transformation. DNA methyltransferase and histone methyltransferase inhibitors are emerging as viable therapeutic approaches to erase aberrant epigenetic programming, suppress DLBCL growth, and overcome chemotherapy resistance. This review will discuss these recent advances and their therapeutic implications. (C) 2015 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据