Abstract |
Using elegant targeting techniques such as IMRT, radiation oncology has improved the therapeutic ratio of prostate cancer radiotherapy through increased physical precision (e.g. increased local control through dose-escalation without increased normal tissue toxicity). The therapeutic ratio might be further improved by the addition of " biologic precision and escalation" pertaining to the use of molecular inhibitors of DNA damage sensing and repair. Indeed, proteins involved in the ATM-p53 damage signaling axis and the homologous (HR) and non-homologous end-joining (NHEJ) pathways of DNA double-strand break (DNA- dsb) rejoining pathways may be attractive candidates to elucidate cancer risk, prognosis, prediction of response and to develop sensitizers towards oxic and hypoxic prostate tumor cells. This review highlights DNA- dsb in prostate cancer research in terms of novel molecular inhibitors, the role of the microenvironment in DNA- dsb repair and potential DNA- dsb biomarkers for clinical trials.
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Authors | Robert G Bristow, Hilmi Ozcelik, Farid Jalali, Norman Chan, Danny Vesprini |
Journal | Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
(Radiother Oncol)
Vol. 83
Issue 3
Pg. 220-30
(Jun 2007)
ISSN: 0167-8140 [Print] Ireland |
PMID | 17531338
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
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Topics |
- Biomarkers
(metabolism)
- DNA Repair
(radiation effects)
- Humans
- Male
- Prostatic Neoplasms
(genetics, radiotherapy)
- Recombination, Genetic
(radiation effects)
- Risk Factors
- Sequence Homology
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