Targeting DNA repair and the cell cycle in glioblastoma

被引：37

作者：

Alexander, Brian M. ^{[1
]}

Pinnell, Nancy ^{[1
]}

Wen, Patrick Y. ^{[2
]}

D'Andrea, Alan ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Dept Radiat Oncol, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Dept Neurol, Boston, MA 02115 USA

来源：

JOURNAL OF NEURO-ONCOLOGY | 2012年 / 107卷 / 03期

关键词：

DNA repair; Cell cycle; Glioblastoma; PHASE-I TRIAL; TEMOZOLOMIDE PLUS O-6-BENZYLGUANINE; STRAND BREAK REPAIR; APURINIC/APYRIMIDINIC ENDONUCLEASE ACTIVITY; NUCLEOTIDE EXCISION-REPAIR; DEPENDENT KINASE INHIBITOR; FACTOR RECEPTOR COMMON; ADP-RIBOSE POLYMERASE; POLY(ADP-RIBOSE) POLYMERASE; MISMATCH-REPAIR;

D O I：

10.1007/s11060-011-0765-4

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Glioblastoma is a disease with poor outcomes despite standard therapy. Specific targeting of the DNA damage response is a strategy that is becoming increasingly employed in oncology and has intriguing potential for improving outcomes in glioblastoma. DNA damage targeting has implications for improving current therapy as well as the potential to leverage inherent differences in glioblastoma cells to widen the therapeutic window.

引用

页码：463 / 477

页数：15

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