{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T20:22:19Z","timestamp":1791145339256,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,7,10]],"date-time":"2012-07-10T00:00:00Z","timestamp":1341878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Brm is an <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>ase subunit of the <jats:styled-content style=\"fixed-case\">SWI<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">SNF<\/jats:styled-content> chromatin\u2013remodelling complex. Previously, we identified a novel hotspot mutation in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm in human skin cancer, which is caused by exposure to ultraviolet radiation (<jats:styled-content style=\"fixed-case\">UVR<\/jats:styled-content>). As <jats:styled-content style=\"fixed-case\">SWI<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">SNF<\/jats:styled-content> is involved in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair, we investigated whether <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212 mice had enhanced photocarcinogenesis. P53+\/\u2212 and <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212p53+\/\u2212 mice were also examined as the p53 tumor suppressor gene is mutated early during human skin carcinogenesis. Mice were exposed to a low\u2010dose irradiation protocol that caused few skin tumors in wild\u2010type mice. <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212 mice with both p53 alleles intact had an increased incidence of skin and ocular tumors compared to <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm+\/+p53+\/+ controls. <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm loss in p53+\/\u2212 mice did not further enhance skin or ocular cancer incidence beyond the increased photocarcinogenesis in p53+\/\u2212 mice. However, the skin tumors that arose early in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212 p53+\/\u2212 mice had a higher growth rate. <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212 did not prevent <jats:styled-content style=\"fixed-case\">UVR<\/jats:styled-content>\u2010induced apoptotic sunburn cell formation, which is a protective response. Unexpectedly, <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm\u2212\/\u2212 inhibited <jats:styled-content style=\"fixed-case\">UVR<\/jats:styled-content>\u2010induced immunosuppression, which would be predicted to reduce rather than enhance photocarcinogenesis. In conclusion, the absence of <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm increased skin and ocular photocarcinogenesis. Even when one allele of p53 is lost, <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>rm has additional tumor suppressing capability.<\/jats:p>","DOI":"10.1111\/j.1600-0625.2012.01522.x","type":"journal-article","created":{"date-parts":[[2012,5,2]],"date-time":"2012-05-02T06:31:34Z","timestamp":1335940294000},"page":"599-604","source":"Crossref","is-referenced-by-count":18,"title":["The absence of <scp>B<\/scp>rm exacerbates photocarcinogenesis"],"prefix":"10.1111","volume":"21","author":[{"given":"Gary M.","family":"Halliday","sequence":"first","affiliation":[{"name":"Discipline of Dermatology Bosch Institute Sydney Medical School University of Sydney Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Zhou","sequence":"additional","affiliation":[{"name":"Discipline of Dermatology Bosch Institute Sydney Medical School University of Sydney Sydney NSW Australia"},{"name":"Dermatology Department Hebei General Hospital Shijiazhuang Hebei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul W.","family":"Sou","sequence":"additional","affiliation":[{"name":"Discipline of Dermatology Bosch Institute Sydney Medical School University of Sydney Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao X. 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