Novel strategies for reversing platinum resistance

被引:66
作者
Shahzad, Mian M. K. [1 ,2 ]
Lopez-Berestein, Gabriel [3 ,4 ,5 ]
Sood, Anil K. [1 ,4 ,5 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Obstet & Gynecol, Houston, TX 77030 USA
[3] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA
[4] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA
[5] Univ Texas MD Anderson Canc Ctr, Ctr RNA Interference & Noncoding RNA, Houston, TX 77030 USA
关键词
ATP7B; Cisplatin; Chemoresistance; Drug transport; Kinases; MK-0457; Ovarian cancer; siRNA; Tumor stroma; BRCA1; EPITHELIAL OVARIAN-CANCER; ADENOSINE-TRIPHOSPHATASE ATP7B; EXTRACELLULAR-MATRIX PROTEINS; NUCLEOTIDE EXCISION-REPAIR; MEDIATED DRUG-RESISTANCE; INTERFERING RNA DELIVERY; SUPPRESSES TUMOR-GROWTH; TARGETING AURORA KINASE; CELL LUNG-CANCER; IN-VIVO;
D O I
10.1016/j.drup.2009.09.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Platinum-based drugs continue to be the mainstay of therapy for ovarian cancer. Along with adverse effects, chemoresistance (intrinsic or acquired) has become a major limitation in the management of recurrent disease. Even though much is known about the effects of platinum drugs on cancer cells, the mechanisms underlying resistance are poorly understood. In this review, we summarize the current data on chemoresistance and discuss novel strategies to reverse resistance to platinum-based drugs. The most important targets highlighted here include Aurora kinases, PARP, ATP7B, and ERCC1. Furthermore, we discuss the implications of these novel approaches for ovarian cancer treatment. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:148 / 152
页数:5
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