Targeting DNA Damage Response and Repair as a Therapeutic Strategy for Ovarian Cancer

被引：21

作者：

Konstantinopoulos, Panagiotis A. ^{[1
]}

Matulonis, Ursula A. ^{[2
]}

机构：

[1] Harvard Med Sch, Dana Farber Canc Inst, Gynecol Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA

[2] Harvard Med Sch, Dana Farber Canc Inst, Div Gynecol Oncol, 450 Brookline Ave, Boston, MA 02215 USA

来源：

HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA | 2018年 / 32卷 / 06期

关键词：

Ovarian cancer; PARP-inhibitors; Homologous recombination deficiency; DNA repair deficiency; Platinum agents; BRCA2; MUTATIONS; PARP INHIBITOR; SOMATIC MUTATIONS; WOMEN; COMBINATION; CARCINOMA; OLAPARIB; ASSOCIATION; HYPERMETHYLATION; GEMCITABINE;

D O I：

10.1016/j.hoc.2018.07.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Large-scale genomic studies have demonstrated that ovarian cancer is characterized by frequent genetic and epigenetic alterations of gene members of the homologous recombination repair pathway. Homologous recombination repair deficiency induces genomic instability and hyperdependence on alternative DNA repair mechanisms, and is associated with enhanced sensitivity to double-strand break-inducing agents such as platinum analogues and poly(adenosine diphosphate)-ribose polymerase inhibitors. The authors review the DNA repair pathway alterations that are present in ovarian cancer, and discuss current and emerging therapeutic approaches that target the DNA damage response and repair focusing on chemotherapy and poly(adenosine diphosphate)-ribose polymerase inhibitors.

引用

页码：997 / +

页数：15

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