Radiosensitization of tumour cell lines by the polyphenol Gossypol results from depressed double-strand break repair and not from enhanced apoptosis

2007 ◽  
Vol 83 (3) ◽  
pp. 296-303 ◽  
Author(s):  
Ulla Kasten-Pisula ◽  
Sabine Windhorst ◽  
Jochen Dahm-Daphi ◽  
Georg Mayr ◽  
Ekkehard Dikomey
Keyword(s):  
Cell Lines ◽  
Tumour Cell ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Tumour Cell Lines ◽  
Break Repair

scholarly journals Fidelity of DNA double-strand break repair in heterozygous cell lines harbouring BRCA1 missense mutations

Oncogene ◽  
2003 ◽  
Vol 23 (4) ◽  
pp. 914-919 ◽  
Author(s):  
Isabelle Coupier ◽  
Céline Baldeyron ◽  
Alexandra Rousseau ◽  
Véronique Mosseri ◽  
Sabine Pages-Berhouet ◽  
...  
Keyword(s):  
Cell Lines ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Missense Mutations ◽  
Dna Double Strand Break ◽  
Break Repair

scholarly journals Assessing Candidate Gene nsSNPs for Phenotypic Differences in Double-Strand Break Repair Using Radiation-InducedγH2A.X Foci

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Christina A. Markunas ◽  
David M. Umbach ◽  
Zongli Xu ◽  
Jack A. Taylor
Keyword(s):  
Cell Lines ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Screening Criteria ◽  
Phenotypic Differences ◽  
Dna Double Strand Break ◽  
Significant Difference ◽  
Break Repair ◽  
Repair Genes

Nonsynonymous SNPs (nsSNPs) in DNA repair genes may be important determinants of DNA damage and cancer risk. We applied a set of screening criteria to a large number of nsSNPs and selected a subset of SNPs that were likely candidates for phenotypic effects on DNA double-strand break repair (DSBR). In order to induce and follow DSBR, we exposed panels of cell lines to gamma irradiation and followed the formation and disappearance ofγH2A.X foci over time. All panels of cell lines showed significant increases in number, intensity, and area of foci at both the 1-hour and 3-hour time points. Twenty four hours following exposure, the number of foci returned to preexposure levels in all cell lines, whereas the size and intensity of foci remained significantly elevated. We saw no significant difference inγH2A.X foci between controls and any of the panels of cell lines representing the different nsSNPs.

scholarly journals A DNA end-binding factor involved in double-strand break repair and V(D)J recombination.

1994 ◽  
Vol 14 (7) ◽  
pp. 4741-4748 ◽  
Author(s):  
W K Rathmell ◽  
G Chu
Keyword(s):  
Cell Lines ◽  
Mammalian Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
X Rays ◽  
X Ray ◽  
Break Repair ◽  
Group 5 ◽  
Dna Ends

We have identified a nuclear factor that binds to double-stranded DNA ends, independently of the structure of the ends. It had equivalent affinities for DNA ends created by sonication or by restriction enzymes leaving 5', 3', or blunt ends but had no detectable affinity for single-stranded DNA ends. Since X rays induce DNA double-strand breaks, extracts from several complementation groups of X-ray-sensitive mammalian cells were tested for this DNA end-binding (DEB) activity. DEB activity was deficient in three independently derived cell lines from complementation group 5. Furthermore, when the cell lines reverted to X-ray resistance, expression of the DEB factor was restored to normal levels. Previous studies had shown that group 5 cells are defective for both double-strand break repair and V(D)J recombination. The residual V(D)J recombination activity in these cells produces abnormally large deletions at the sites of DNA joining (F. Pergola, M. Z. Zdzienicka, and M. R. Lieber, Mol. Cell. Biol. 13:3464-3471, 1993, and G. Taccioli, G. Rathbun, E. Oltz, T. Stamato, P. Jeggo, and F. Alt, Science 260:207-210, 1993), consistent with deficiency of a factor that protects DNA ends from degradation. Therefore, DEB factor may be involved in a biochemical pathway common to both double-strand break repair and V(D)J recombination.

A DNA end-binding factor involved in double-strand break repair and V(D)J recombination

1994 ◽  
Vol 14 (7) ◽  
pp. 4741-4748
Author(s):  
W K Rathmell ◽  
G Chu
Keyword(s):  
Cell Lines ◽  
Mammalian Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
X Rays ◽  
X Ray ◽  
Break Repair ◽  
Group 5 ◽  
Dna Ends

We have identified a nuclear factor that binds to double-stranded DNA ends, independently of the structure of the ends. It had equivalent affinities for DNA ends created by sonication or by restriction enzymes leaving 5', 3', or blunt ends but had no detectable affinity for single-stranded DNA ends. Since X rays induce DNA double-strand breaks, extracts from several complementation groups of X-ray-sensitive mammalian cells were tested for this DNA end-binding (DEB) activity. DEB activity was deficient in three independently derived cell lines from complementation group 5. Furthermore, when the cell lines reverted to X-ray resistance, expression of the DEB factor was restored to normal levels. Previous studies had shown that group 5 cells are defective for both double-strand break repair and V(D)J recombination. The residual V(D)J recombination activity in these cells produces abnormally large deletions at the sites of DNA joining (F. Pergola, M. Z. Zdzienicka, and M. R. Lieber, Mol. Cell. Biol. 13:3464-3471, 1993, and G. Taccioli, G. Rathbun, E. Oltz, T. Stamato, P. Jeggo, and F. Alt, Science 260:207-210, 1993), consistent with deficiency of a factor that protects DNA ends from degradation. Therefore, DEB factor may be involved in a biochemical pathway common to both double-strand break repair and V(D)J recombination.

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