The Role of Histone Deacetylase Inhibitors in the Treatment of Patients With Cutaneous T-Cell Lymphoma

被引:24
作者
Hymes, Kenneth B. [1 ]
机构
[1] NYU, Langone Med Ctr, Inst Canc, Dept Med Hematol, New York, NY 10016 USA
关键词
Belinostat; Disease burden; Epigenetics; Panobinostat; Romidepsin; Vorinostat; SUBEROYLANILIDE HYDROXAMIC ACID; CHROMOBACTERIUM-VIOLACEUM NO-968; I CLINICAL-TRIAL; MYCOSIS-FUNGOIDES; PHASE-I; DEPSIPEPTIDE FR901228; SEZARY-SYNDROME; VORINOSTAT; CANCER; SAHA;
D O I
10.3816/CLML.2010.n.014
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The term epigenetics refers to modifications in gene activity that occur without directly affecting the DNA sequence, and irregularities in cellular epigenetics have been implicated in the development of a number of malignancies. As such, there is considerable interest in the anticancer effects of agents that can modify cellular epigenetics. Histone deacetylase (HDAC) inhibitors represent a class of anticancer agents that have shown promise in the treatment of both solid and hematologic malignancies. Although there are a number of HDAC inhibitors in advanced stages of clinical development, vorinostat, and more recently, romidepsin, are currently the only HDAC inhibitors approved for use. Vorinostat was approved in the United States in 2006 for the treatment of cutaneous manifestations of T-cell lymphoma in patients with progressive, persistent, or recurrent disease on or following 2 systemic therapies. Romidepsin was approved in the United States in 2009 for the treatment of cutaneous T-cell lymphoma (CTCL) in patients who have received >= 1 prior systemic therapy. This review aims to assess the clinical progress that vorinostat and other HDAC inhibitors have made in symptom relief and treatment of patients with CTCL and to provide practical advice for the management of associated toxicities.
引用
收藏
页码:98 / 109
页数:12
相关论文
共 80 条
[1]   Belinostat (PXD101) in patients with recurrent or refractory peripheral or cutaneous T-Cell lymphoma: Results of a phase II study [J].
Advani, Ranjana ;
Hymes, K. ;
Pohlman, B. ;
Jacobsen, E. ;
McDonnell, J. ;
Belt, R. ;
Lerner, A. ;
Kim, Y. ;
Mundis, R. ;
Mansfield, T. ;
Buhl-Jensen, P. ;
Ooi, C. E. ;
Duvic, M. ;
Foss, F. .
BLOOD, 2007, 110 (11) :1012A-1012A
[2]  
[Anonymous], National Comprehensive Cancer Network Compendium
[3]   Histone deacetylase inhibitors: From chromatin remodeling to experimental cancer therapeutics [J].
Arts, J ;
de Schepper, S ;
Van Emelen, K .
CURRENT MEDICINAL CHEMISTRY, 2003, 10 (22) :2343-2350
[4]  
Bates S, 2008, BLOOD, V112, P556
[5]  
BUNN PA, 1979, CANCER TREAT REP, V63, P725
[6]  
Butler LM, 2000, CANCER RES, V60, P5165
[7]   Depsipeptide (FR901228): A novel therapeutic agent with selective, in vitro activity against human B-cell chronic lymphocytic leukemia cells [J].
Byrd, JC ;
Shinn, C ;
Ravi, R ;
Willis, CR ;
Waselenko, JK ;
Flinn, IW ;
Dawson, NA ;
Grever, MR .
BLOOD, 1999, 94 (04) :1401-1408
[8]  
CAMPASMOYA C, 2007, DRUGS TODAY BARC, V45, P787
[9]   Aggresome induction by proteasome inhibitor bortezomib and α-tubulin hyperacetylation by tubulin deacetylase (TDAC) inhibitor LBH589 are synergistic in myeloma cells [J].
Catley, Laurence ;
Weisberg, Ellen ;
Kiziltepe, Tanyel ;
Tai, Yu-Tzu ;
Hideshima, Teru ;
Neri, Paola ;
Tassone, Pierfrancesco ;
Atadja, Peter ;
Chauhan, Dharminder ;
Munshi, Nikhil C. ;
Anderson, Kenneth C. .
BLOOD, 2006, 108 (10) :3441-3449
[10]   Report of an international workshop to standardize response criteria for non-Hodgkin's lymphomas [J].
Cheson, BD ;
Horning, SJ ;
Coiffier, B ;
Shipp, MA ;
Fisher, RI ;
Connors, JM ;
Lister, TA ;
Vose, J ;
Grillo-López, A ;
Hagenbeek, A ;
Cabanillas, F ;
Klippensten, D ;
Hiddemann, W ;
Castellino, R ;
Harris, NL ;
Armitage, JO ;
Carter, W ;
Hoppe, R ;
Canellos, GP .
JOURNAL OF CLINICAL ONCOLOGY, 1999, 17 (04) :1244-1253