Mechanisms of Resistance to Histone Deacetylase Inhibitors

被引：81

作者：

Lee, Ju-Hee ^{[1
]}

Choy, Megan L. ^{[1
]}

Marks, Paul A. ^{[1
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Dept Cell Biol, Sloan Kettering Inst, New York, NY 10021 USA

来源：

HISTONE DEACETYLASE INHIBITORS AS CANCER THERAPEUTICS | 2012年 / 116卷

关键词：

PHASE-II TRIAL; SUBEROYLANILIDE HYDROXAMIC ACID; T-CELL LYMPHOMA; ACUTE MYELOID-LEUKEMIA; TRANS-RETINOIC ACID; NF-KAPPA-B; REFRACTORY SOLID TUMORS; CONTROLS CHONDROCYTE HYPERTROPHY; ENDOPLASMIC-RETICULUM STRESS; CHRONIC LYMPHOCYTIC-LEUKEMIA;

D O I：

10.1016/B978-0-12-394387-3.00002-1

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Histone deacetylase (HDAC) inhibitors are a new class of anticancer agents. HDAC inhibitors induce acetylation of histones and nonhistone proteins which are involved in regulation of gene expression and in various cellular pathways including cell growth arrest, differentiation, DNA damage and repair, redox signaling, and apoptosis (Marks, 2010). The U.S. Food and Drug Administration has approved two HDAC inhibitors, vorinostat and romidepsin, for the treatment of cutaneous T-cell lymphoma (Duvic gl Vu, 2007; Grant et al., 2010; Marks & Breslow, 2007). Over 20 chemically different HDAC inhibitors are in clinical trials for hematological malignancies and solid tumors. This review considers the mechanisms of resistance to HDAC inhibitors that have been identified which account for the selective effects of these agents in inducing cancer but not normal cell death. These mechanisms, such as functioning Chk1, high levels of thioredoxin, or the prosurvival BCL-2, may also contribute to resistance of cancer cells to HDAC inhibitors.

引用

页码：39 / 86

页数：48

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