## Abstract Mutations in the __p53__ tumor suppressor gene have been found in most human tumors. Analyses of the spectrum of __p53__ mutations in certain tumor types have shown a bias for mutations originating from lesions presumed to be in the untranscribed strand of the gene. This implies strand
Double-strand breaks in DNA caused by repair of damage due to ultraviolet light
✍ Scribed by Bradley, Matthews O.
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 1981
- Tongue
- English
- Weight
- 341 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0275-3723
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
DNA DSBs are formed in normal human IMR‐90 cells during repair incubation after 100 and 300 J·m^−2^ of UVL. By contrast, no DSBs are formed after UVL in human XPA cells that are unable to excise pyrimidine dimers. The DSBs are not due to immediate cell death since all the cells excluded trypan blue at the time of assay and because XPA cells, which are much more UVL‐sensitive than IMR‐90, did not form DSBs after UVL. We suggest that these repair‐induced DSBs should be potent lesions that might lead to cytotoxicity, chromosome aberrations, deletion mutations, and perhaps cellular transformation, transformation.
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