Mice With Genetically Determined High Susceptibility to Ultraviolet (UV)-Induced Immunosuppression Show Enhanced UV Carcinogenesis
To assess the premise that genetically determined differences in susceptibility to UV-induced immunosuppression are reflected in UV carcinogenesis, we investigated UV skin cancer induction in two strains of reciprocal F1 hybrid mice CB6F1 males with high susceptibility to UV immunosuppression and a...
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Published in | Journal of investigative dermatology Vol. 121; no. 5; pp. 1175 - 1181 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Danvers, MA
Elsevier Inc
01.11.2003
Nature Publishing Elsevier Limited |
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Abstract | To assess the premise that genetically determined differences in susceptibility to UV-induced immunosuppression are reflected in UV carcinogenesis, we investigated UV skin cancer induction in two strains of reciprocal F1 hybrid mice CB6F1 males with high susceptibility to UV immunosuppression and a BALB/c X-chromosome and B6CF1 males with low susceptibility to UV immunosuppression and a C57BL/6 X-chromosome. Four experimental groups comprising both strains treated three times weekly with two UV regimens (daily doses incremented from 2.25 to 6 or 4.5 to 12 kJ per m2) were monitored for skin tumor development. Survival without a skin tumor differed over the four groups (p< 0.0001) and differed according to UV regimen within each strain (p<0.0005). Differences between strains were significant for the higher dose (p=0.03) but not for the lower dose (p=0.19) of UV, suggesting a dose–strain interaction. Comparing the higher UV dose regimen to the lower UV dose regimen within a strain at three reference points, tumor-free survival was reduced significantly more (p<0.05) in the CB6F1 mice than in the B6CF1 mice. Histologic assessment of all tumors revealed fibrosarcomas, squamous carcinomas, and mixed tumors. Immunohistochemistry of the mixed tumors for vimentin, keratin, and E-cadherin confirmed the presence of squamous and fibrosarcomatous elements. The enhanced susceptibility to UV carcinogenesis of CB6F1 males treated with the higher UV pro-tocol was attributable to a significantly enhanced proportion (p<0.005) of mixed tumors. Analysis of the data by comparing the proportion of animals tumor free at three reference time points confirmed a dose–strain interaction only in the development of mixed tumors, putatively the malignantly advanced carcinomas (p<0.03). A dose–strain interaction was also observed for systemic UV immunosuppression of contact hypersensitivity (p<0.025). These findings support the concept that genetic differences in susceptibility to UV-induced immunosuppression may be a risk factor for skin cancer. |
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AbstractList | To assess the premise that genetically determined differences in susceptibility to UV-induced immunosuppression are reflected in UV carcinogenesis, we investigated UV skin cancer induction in two strains of reciprocal F1 hybrid mice CB6F1 males with high susceptibility to UV immunosuppression and a BALB/c X-chromosome and B6CF1 males with low susceptibility to UV immunosuppression and a C57BL/6 X-chromosome. Four experimental groups comprising both strains treated three times weekly with two UV regimens (daily doses incremented from 2.25 to 6 or 4.5 to 12 kJ per m2) were monitored for skin tumor development. Survival without a skin tumor differed over the four groups (p < 0.0001) and differed according to UV regimen within each strain (p < 0.0005). Differences between strains were significant for the higher dose (p = 0.03) but not for the lower dose (p = 0.19) of UV, suggesting a dose-strain interaction. Comparing the higher UV dose regimen to the lower UV dose regimen within a strain at three reference points, tumor-free survival was reduced significantly more (p < 0.05) in the CB6F1 mice than in the B6CF1 mice. Histologic assessment of all tumors revealed fibrosarcomas, squamous carcinomas, and mixed tumors. Immunohistochemistry of the mixed tumors for vimentin, keratin, and E-cadherin confirmed the presence of squamous and fibrosarcomatous elements. The enhanced susceptibility to UV carcinogenesis of CB6F1 males treated with the higher UV protocol was attributable to a significantly enhanced proportion (p < 0.005) of mixed tumors. Analysis of the data by comparing the proportion of animals tumor free at three reference time points confirmed a dose-strain interaction only in the development of mixed tumors, putatively the malignantly advanced carcinomas (p < 0.03). A dose-strain interaction was also observed for systemic UV immunosuppression of contact hypersensitivity (p < 0.025). These findings support the concept that genetic differences in susceptibility to UV-induced immunosuppression may be a risk factor for skin cancer. To assess the premise that genetically determined differences in susceptibility to UV-induced immunosuppression are reflected in UV carcinogenesis, we investigated UV skin cancer induction in two strains of reciprocal F1 hybrid mice CB6F1 males with high susceptibility to UV immunosuppression and a BALB/c X-chromosome and B6CF1 males with low susceptibility to UV immunosuppression and a C57BL/6 X-chromosome. Four experimental groups comprising both strains treated three times weekly with two UV regimens (daily doses incremented from 2.25 to 6 or 4.5 to 12 kJ per m2) were monitored for skin tumor development. Survival without a skin tumor differed over the four groups (p< 0.0001) and differed according to UV regimen within each strain (p<0.0005). Differences between strains were significant for the higher dose (p=0.03) but not for the lower dose (p=0.19) of UV, suggesting a dose–strain interaction. Comparing the higher UV dose regimen to the lower UV dose regimen within a strain at three reference points, tumor-free survival was reduced significantly more (p<0.05) in the CB6F1 mice than in the B6CF1 mice. Histologic assessment of all tumors revealed fibrosarcomas, squamous carcinomas, and mixed tumors. Immunohistochemistry of the mixed tumors for vimentin, keratin, and E-cadherin confirmed the presence of squamous and fibrosarcomatous elements. The enhanced susceptibility to UV carcinogenesis of CB6F1 males treated with the higher UV pro-tocol was attributable to a significantly enhanced proportion (p<0.005) of mixed tumors. Analysis of the data by comparing the proportion of animals tumor free at three reference time points confirmed a dose–strain interaction only in the development of mixed tumors, putatively the malignantly advanced carcinomas (p<0.03). A dose–strain interaction was also observed for systemic UV immunosuppression of contact hypersensitivity (p<0.025). These findings support the concept that genetic differences in susceptibility to UV-induced immunosuppression may be a risk factor for skin cancer. |
Author | Noonan, Frances P. De Fabo, Edward C. Kusewitt, Donna F. Johnson, Tracy M. Konrad Muller, H. Fears, Thomas R. |
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Keywords | ultraviolet radiation skin cancer immunosuppression risk factor Vertebrata Immunosuppression Ultraviolet radiation Mammalia skin cancer/risk factor/ultraviolet radiation/immunosuppression Mouse Dermatology Animal Rodentia Genetics Carcinogenesis |
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contributor: fullname: Nishigori – volume: 34 start-page: 187 year: 1972 ident: 10.1046/j.1523-1747.2003.12560.x_bb0040 article-title: Regression models and life-tables publication-title: J R Stat Soc B contributor: fullname: Cox – year: 1981 ident: 10.1046/j.1523-1747.2003.12560.x_bb0115 contributor: fullname: Miller – volume: 1 start-page: 251 year: 2000 ident: 10.1046/j.1523-1747.2003.12560.x_bb0035 article-title: Genetic control of susceptibility to UV-induced immunosuppression by interacting quantitative trait loci publication-title: Genes Immunity doi: 10.1038/sj.gene.6363667 contributor: fullname: Clemens – volume: 57 start-page: 579 year: 1970 ident: 10.1046/j.1523-1747.2003.12560.x_bb0025 article-title: A generalized Kruskal–Wallis test for comparing K samples subject to unequal patterns of censorship publication-title: Biometrical doi: 10.1093/biomet/57.3.579 contributor: fullname: Breslow |
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Snippet | To assess the premise that genetically determined differences in susceptibility to UV-induced immunosuppression are reflected in UV carcinogenesis, we... |
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SubjectTerms | Animals Biological and medical sciences Dermatology Dose-Response Relationship, Radiation Female Genetic Predisposition to Disease Immune Tolerance - radiation effects Immunohistochemistry immunosuppression Male Medical sciences Mice Mice, Inbred BALB C Mice, Inbred C57BL Neoplasms, Radiation-Induced - etiology Neoplasms, Radiation-Induced - immunology risk factor skin cancer Species Specificity Survival Analysis ultraviolet radiation Ultraviolet Rays - adverse effects |
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Title | Mice With Genetically Determined High Susceptibility to Ultraviolet (UV)-Induced Immunosuppression Show Enhanced UV Carcinogenesis |
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