Abstract |
Modification of sister chromatid exchanges and radiation-induced transformation in mouse C3H/10T 1/2 and Syrian hamster embryo cells by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate and two retinoids, the trimethylmethoxyphenyl analog of N-ethyl retinamide and beta-all-trans-retinoic acid, has been studied. 12-O-tetradecanoylphorbol-13-acetate alone enhances, and retinoids alone reduce radiation-induced transformation. When both compounds were present, the retinoids not only reduced the oncogenic effects of radiation but completely eliminated the promoting effects of 12-O-tetradecanoylphorbol-13-acetate. These results were not paralleled by changes in sister chromatid exchange frequencies, indicating that, while sister chromatid exchanges may be useful as indicators of primary carcinogen mutagens, they may have little utility when secondary agents after the response of cells to a primary initiator.
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Authors | R C Miller, C R Geard, R S Osmak, M Rutledge-Freeman, A Ong, H Mason, A Napholz, N Perez, L Harisiadis, C Borek |
Journal | Cancer research
(Cancer Res)
Vol. 41
Issue 2
Pg. 655-9
(Feb 1981)
ISSN: 0008-5472 [Print] United States |
PMID | 7448811
(Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Phorbols
- Tretinoin
- Tetradecanoylphorbol Acetate
- motretinide
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Topics |
- Animals
- Cell Division
(drug effects)
- Cell Survival
(drug effects)
- Cell Transformation, Neoplastic
(drug effects, radiation effects)
- Cells, Cultured
- Cocarcinogenesis
- Cricetinae
- Crossing Over, Genetic
(drug effects)
- Mice
- Phorbols
(pharmacology)
- Sister Chromatid Exchange
(drug effects)
- Tetradecanoylphorbol Acetate
(antagonists & inhibitors, pharmacology)
- Tretinoin
(analogs & derivatives, pharmacology)
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