Molecular fingerprinting of radiation resistant tumors: can we apprehend and rehabilitate the suspects?

BMC Cancer. 2009 Jul 9;9:225. doi: 10.1186/1471-2407-9-225.

Abstract

Radiation therapy continues to be one of the more popular treatment options for localized prostate cancer. One major obstacle to radiation therapy is that there is a limit to the amount of radiation that can be safely delivered to the target organ. Emerging evidence suggests that therapeutic agents targeting specific molecules might be combined with radiation therapy for more effective treatment of tumors. Recent studies suggest that modulation of these molecules by a variety of mechanisms (e.g., gene therapy, antisense oligonucleotides, small interfering RNA) may enhance the efficacy of radiation therapy by modifying the activity of key cell proliferation and survival pathways such as those controlled by Bcl-2, p53, Akt/PTEN and cyclooxygenase-2. In this article, we summarize the findings of recent investigations of radiosensitizing agents in the treatment of prostate cancer.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Proliferation
  • Cell Survival
  • Cyclooxygenase 2 / metabolism
  • Gene Expression Profiling / methods
  • Humans
  • Male
  • Mice
  • Neoplasm Transplantation
  • Oligonucleotides, Antisense / metabolism
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / radiotherapy*
  • RNA, Small Interfering / metabolism
  • Radiation-Sensitizing Agents / pharmacology*
  • Radiotherapy / methods
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Oligonucleotides, Antisense
  • RNA, Small Interfering
  • Radiation-Sensitizing Agents
  • Tumor Suppressor Protein p53
  • Cyclooxygenase 2