DNA damage response and repair: insights into strategies for radiation sensitization of gliomas

Future Oncol. 2011 Nov;7(11):1335-46. doi: 10.2217/fon.11.111.


The incorporation of radiotherapy into multimodality treatment plans has led to significant improvements in glioma patient survival. However, local recurrence from glioma resistance to ionizing radiation remains a therapeutic challenge. The tumoricidal effect of radiation therapy is largely attributed to the induction of dsDNA breaks (DSBs). In the past decade, there have been tremendous strides in understanding the molecular mechanisms underlying DSB repair. The identification of gene products required for DSB repair has provided novel therapeutic targets. Recent studies revealed that many US FDA-approved cancer agents inhibit DSB repair by interacting with repair proteins. This article will aim to provide discussion of DSB repair mechanisms to provide molecular targets for radiation sensitization of gliomas and a discussion of FDA-approved cancer therapies that modulate DSB repair to highlight opportunities for combination therapy with radiotherapy for glioma therapy.

Publication types

  • Research Support, American Recovery and Reinvestment Act
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Cell Survival / radiation effects
  • Combined Modality Therapy
  • DNA Breaks, Double-Stranded*
  • DNA Repair / drug effects*
  • Glioblastoma / drug therapy*
  • Glioblastoma / mortality
  • Glioblastoma / radiotherapy*
  • Humans
  • Neoplasm Recurrence, Local / radiotherapy
  • Radiation Tolerance
  • Radiation-Sensitizing Agents / therapeutic use*


  • Antineoplastic Agents
  • Radiation-Sensitizing Agents