{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T02:02:58Z","timestamp":1791338578701,"version":"4.3.1"},"reference-count":40,"publisher":"National Academy of Sciences","issue":"17","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2001,8,14]]},"abstract":"<jats:p>\n                    Epidemiological studies have suggested an association between\n exposure to solar UV radiation and the incidence of lymphoid\n malignancies, which has increased substantially worldwide during the\n last two decades. Findings from animal studies have raised the question\n of whether UV radiation might influence the development of lymphoid\n malignancies by means of its immunosuppressive effect. In this study,\n we examined the effect of UV irradiation on the development of lymphoid\n malignancies in mice with no or only one functional copy of\n                    <jats:italic>p53<\/jats:italic>\n                    . Mice that lack both copies of\n                    <jats:italic>p53<\/jats:italic>\n                    spontaneously develop high frequency of lymphoid malignancies in the\n thymus and spleen.\n                    <jats:italic>p53<\/jats:italic>\n                    heterozygous mice with only one\n copy of the wild-type allele also develop lymphoid malignancies, but\n with a much lower frequency and a long latent period. In our study\n using mice of the C57BL\/6 background, only one of the unirradiated\n mice lacking one copy of\n                    <jats:italic>p53<\/jats:italic>\n                    (\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    ) spontaneously developed a lymphoid\n tumor (6%), whereas 88% of UV-irradiated\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice developed lymphoid tumors in\n the spleen or liver. None of the control or UV-irradiated\n                    <jats:italic>p53<\/jats:italic>\n                    wild-type mice developed lymphoid tumors during the\n 60-week observation period. Both UV-irradiated and unirradiated mice\n lacking both copies of\n                    <jats:italic>p53<\/jats:italic>\n                    (\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) rapidly developed thymic\n lymphomas and\/or lymphoid tumors in spleen or liver. All of the\n lymphoid tumors tested were of T cell type. The immune responses of the\n mice to contact sensitization were identical and were suppressed to the\n same extent by UV irradiation regardless of the genotype. These results\n indicate that differences in immune reactivity do not account for the\n different effects of UV radiation on lymphoid malignancies and, in\n addition, that p53 is not required for generation of T cell-mediated\n immunity. Interestingly, whereas\n                    <jats:italic>p53<\/jats:italic>\n                    mutations or loss\n of heterozygosity did not account for the accelerated development of\n lymphoid tumors in UV-irradiated\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice, deletions in the\n                    <jats:italic>p16<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>INK4a<\/jats:italic>\n                    <\/jats:sup>\n                    gene\n were quite common. These data provide the experimental evidence that UV\n irradiation induces lymphoid neoplasms in genetically susceptible mice\n and support the hypothesis that extensive sunlight exposure contributes\n to the induction of lymphoma in humans.\n                  <\/jats:p>","DOI":"10.1073\/pnas.171066498","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:37:36Z","timestamp":1027679856000},"page":"9790-9795","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":27,"title":["UV irradiation augments lymphoid malignancies in mice with one functional copy of wild-type\n                    <i>p53<\/i>"],"prefix":"10.1073","volume":"98","author":[{"given":"Weidong","family":"Jiang","sequence":"first","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Honnavara N.","family":"Ananthaswamy","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. Konrad","family":"Muller","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allal","family":"Ouhtit","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana","family":"Bolshakov","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen E.","family":"Ullrich","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adel K.","family":"El-Naggar","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret L.","family":"Kripke","sequence":"additional","affiliation":[{"name":"Departments of Immunology and Pathology, University\r of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and\r Department of Pathology, University of Tasmania, Hobart,\r Tasmania 7000, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2001,7,31]]},"reference":[{"key":"e_1_3_3_1_2","first-page":"5432","volume":"52","author":"Devesa S S","year":"1992","unstructured":"S S Devesa, F Fears Cancer Res 52,Suppl., 5432\u20135440 (1992).","journal-title":"Cancer 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