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Photosensitized reactions and carcinogenesis
National Cancer Institute Monograph
|December 1, 1978
Summary
This study on mice reveals that while DNA cross-link formation from 8-methoxypsoralen (8-MOP) plus UV light is not strain-dependent, skin cancer susceptibility is. Tumor promotion events are strain-dependent, influenced by UV wavelength and timing.
Area of Science:
- Dermatology
- Photobiology
- Carcinogenesis
Background:
- DNA interstrand cross-links are induced by 8-methoxypsoralen (8-MOP) and UV radiation (UVR).
- These cross-links are implicated in skin carcinogenesis.
- Understanding the factors influencing UVR-induced DNA damage and subsequent tumor development is crucial.
Purpose of the Study:
- To investigate the role of DNA interstrand cross-links in skin carcinogenesis.
- To examine strain-dependent differences in tumor susceptibility following 8-MOP plus UVR exposure.
- To explore the interaction between UV wavelengths and psoralen photoadducts in tumorigenesis.
Main Methods:
- Two strains of hairless mice (SKH:hairless-1 and HRS/J/An1) were used.
- Mice received topical 8-MOP and were exposed to UV light (300-400 nm, 320-400 nm, or predominantly 365 nm).
- Tumor incidence was assessed, with and without TPA administration, and the timing of exposures was varied.
Main Results:
- No strain dependency was observed for DNA cross-link production.
- Significant strain-dependent differences in tumor susceptibility were noted.
- Tumorigenic effect varied with UV wavelength spectrum (300-400 nm being most effective) and the time interval between 8-MOP and UV exposure.
Conclusions:
- Skin carcinogenesis following 8-MOP plus UVR is influenced by mouse strain.
- Tumor promotion events are strain-dependent.
- The interplay between UV wavelength, psoralen photoadducts, and timing is critical in determining tumorigenic outcomes.