Nanotechnology in Cancer Therapy: Targeting the Inhibition of Key DNA Repair Pathways

被引:12
|
作者
Aziz, K. [1 ,2 ]
Nowsheen, S. [3 ,4 ]
Georgakilas, A. G. [1 ,5 ]
机构
[1] E Carolina Univ, Dept Biol, Thomas Harriot Coll Arts & Sci, Greenville, NC 27858 USA
[2] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Dept Radiat Oncol & Mol Radiat Sci, Baltimore, MD 21231 USA
[3] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Sch Med, Dept Radiat Oncol, Nashville, TN 37232 USA
[4] Univ Alabama Birmingham, Hazelrig Salter Radiat Oncol Ctr, Dept Radiat Oncol, Birmingham, AL 35294 USA
[5] Natl Tech Univ Athens, Dept Phys, GR-15773 Zografos, Greece
关键词
Cancer therapy; DNA damage; DNA repair; inhibitors; nanotechnology; base excision repair; double strand break repair; BASE-EXCISION-REPAIR; STRAND-BREAK REPAIR; DEPENDENT PROTEIN-KINASE; BLOOMS-SYNDROME HELICASE; OXIDATIVELY DAMAGED DNA; COCKAYNE-SYNDROME; FANCONI-ANEMIA; POLY(ADP-RIBOSE) POLYMERASE; HOMOLOGOUS RECOMBINATION; ATAXIA-TELANGIECTASIA;
D O I
10.2174/156652410792630599
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Cancer therapy has been changing over the decades as we move away from the administration of broad spectrum cytotoxic drugs and towards the use of therapy targeted for each tumor type. After the induction of DNA damage through chemotherapeutic agents, tumor cells can survive due to their proficient DNA repair pathways, some of which are dysregulated in cancer. Latest improvements in nanotechnology and drug discovery have led to the discovery of some very unique, highly specific and innovative drugs as inhibitors of various DNA repair pathways like base excision repair and double strand break repair. In this review we look at the efficacy and potency of these small chemical molecules to target the processing of DNA damage induced by standard therapeutic agents. Emphasis is given to those drugs currently under clinical trials. We also discuss the future directions of using this nanotechnology to increase the therapeutic ratio in cancer treatment.
引用
收藏
页码:626 / 639
页数:14
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