Document Detail


Receptor signaling as a regulatory mechanism of DNA repair.
MedLine Citation:
PMID:  19615770     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Radiotherapy plays a crucial role in the treatment of many malignancies; however, locoregional disease progression remains a critical problem. This has stimulated laboratory research into understanding the basis for tumor cell resistance to radiation and the development of strategies for overcoming such resistance. We know that some cell signaling pathways that respond to normal growth factors are abnormally activated in human cancer and that these pathways also invoke cell survival mechanisms that lead to resistance to radiation. For example, abnormal activation of the epidermal growth factor receptor (EGFR) promotes unregulated growth and is believed to contribute to clinical radiation resistance. Molecular blockade of EGFR signaling is an attractive strategy for enhancing the cytotoxic effects of radiotherapy and, as shown in numerous reports, the radiosensitizing effects of EGFR antagonists correlate with a suppression of the ability of the cells to repair radiation-induced DNA double strand breaks (DSBs). The molecular connection between the EGFR and its governance of DNA repair capacity appears to be mediated by one or more signaling pathways downstream of this receptor. The purpose of this review is to highlight what is currently known regarding EGFR signaling and the processes responsible for repairing radiation-induced DNA lesions that would explain the radiosensitizing effects of EGFR antagonists.
Authors:
Raymond E Meyn; Anapama Munshi; John V Haymach; Luka Milas; K Kian Ang
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2009-07-15
Journal Detail:
Title:  Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology     Volume:  92     ISSN:  1879-0887     ISO Abbreviation:  Radiother Oncol     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-15     Completed Date:  2010-01-12     Revised Date:  2010-09-07    
Medline Journal Info:
Nlm Unique ID:  8407192     Medline TA:  Radiother Oncol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  316-22     Citation Subset:  IM    
Affiliation:
Department of Experimental Radiation Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA. rmeyn@mdanderson.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line, Tumor / radiation effects
DNA Breaks, Double-Stranded / radiation effects
DNA Damage / radiation effects
DNA Repair / physiology*,  radiation effects
Humans
Neoplasms / genetics,  radiotherapy
Radiation Injuries / prevention & control
Radiation Tolerance
Radiobiology*
Receptor, Epidermal Growth Factor / metabolism,  radiation effects*
Signal Transduction / radiation effects*
Grant Support
ID/Acronym/Agency:
P01 CA006294-440033/CA/NCI NIH HHS; P01 CA06294/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
EC 2.7.10.1/Receptor, Epidermal Growth Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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