Document Detail

Varying responses of human cells with discrepant p53 activity to ionizing radiation and heat shock exposure.
MedLine Citation:
PMID:  17227293     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: Both heat shock (HS) and ionizing radiation have an impact on the cell cycle and may induce cell cycle arrest or apoptosis. Mutations of the p53 gene are observed at a high frequency in human tumours and are recognized in about half of all human cancers. Sensitivity to radiation, heat and anticancer agents has been observed in p53(+/+) cells, but not in mutated or p53-deficient cells. Moreover, enhancement of radiosensitivity by HS has been observed in wild-type p53 cells but not in p53-deficient cells. The molecular mechanism of the differential cell response to HS or ionizing radiation is not yet understood. MATERIALS AND METHODS: Differences in cellular response to radiation (200 kV X-ray, 1, 2, 5 Gy) and HS (39 degrees C, 41 degrees C and 43 degrees C for 30 min) on cell cycle progression of cultures of human p53 mutant cells were investigated by flow cytometry. In addition, the effects of stressors used on the expression of several heat shock genes (HSP27, HSP60, HSP70, HSC70, HSP75, HSP78, HSP90) were studied by reverse transcriptase-polymerase chain reaction. RESULTS AND CONCLUSIONS: Yet, with respect to HSP gene expression, different stressors produced similar effects. Combination of HS and radiation treatment significantly induced the transcription of the HSP70 gene above the level induced by each stressor alone. Cell cycle analysis, however, revealed striking differences in prolonged dynamics of cell division in response to each stressor. Thus, p53 status could be a useful indicator in predictive assays for hyperthermia cancer treatment in combination with radiation and/or chemotherapy.
S V Tokalov; S Pieck; H O Gutzeit
Related Documents :
19439913 - P53 regulates mtdna copy number and mitocheckpoint pathway.
1533443 - Inhibition of p53 transactivation required for transformation by adenovirus early 1b pr...
8226753 - Radiation-activated dna-binding protein constitutively present in ataxia telangiectasia...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell proliferation     Volume:  40     ISSN:  0960-7722     ISO Abbreviation:  Cell Prolif.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-01-17     Completed Date:  2007-03-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9105195     Medline TA:  Cell Prolif     Country:  England    
Other Details:
Languages:  eng     Pagination:  24-37     Citation Subset:  IM    
OncoRay-Radiation Research in Oncology, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Fetscherstrasse, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Cycle
Cell Division
Cell Line, Tumor
Cell Proliferation
Heat-Shock Proteins / metabolism*
Heat-Shock Response*
Radiation, Ionizing*
Time Factors
Tumor Suppressor Protein p53 / genetics*
Reg. No./Substance:
0/Heat-Shock Proteins; 0/Tumor Suppressor Protein p53

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

Previous Document:  Progression of astrocytomas and meningiomas: an evaluation in vitro.
Next Document:  Photodynamic therapy combined with a cysteine proteinase inhibitor synergistically decrease VEGF pro...