p53 mutations are found in about 70% of human cancers. In order to evaluate the role of these mutations in response to chemotherapeutic agents, it is important to distinguish between p53 response to DNA-damaging agents in normal and in tumour cells. Here, using normal human fibroblasts (NHFs), we sh
Increased UV-induced SCEs but normal repair of DNA damage in p53-deficient mouse cells
✍ Scribed by Kanji Ishizaki; Yosuke Ejima; Tsukasa Matsunaga; Ryujiro Hara; Ayako Sakamoto; Mituo Ikenaga; Yoji Ikawa; Shin-Ichi Aizawa
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- French
- Weight
- 442 KB
- Volume
- 58
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
UV-induced sister chromatid exchanges (SCEs) in p53deficient mouse cells were studied to obtain more evidence regarding the involvement of p53 protein in the DNA repair pathway as a checkpoint protein. After 5 J/m2 UV irradiation, mutant-type homozygous cells for p53-deficiency showed the same number of SCEs as the heterozygous and wild-type homozygous cells. In the heterozygous and wild-type homozygous cells, no further increase of SCEs was observed after 10 J/mz UV irradiation. In contrast, in mutant-type homozygous cells about twice as many SCEs were induced by 10 J/m2 UV as by 5 J/m2 UV. In mutant-type homozygous cells, fractions of S-phase cells decreased just after 10 J/m2 UV irradiation, but recovered to higher than control levels within a short time, while in heterozygous and wild-type homozygous cells, the decrease in S-phase cells was prolonged by more than 6 hr and no increase above control levels was observed. Although no difference in UV sensitivity and repair of UV-induced DNA damage was found among the 3 genotypes, which were determined by the relative colony-forming ability after UV irradiation
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