{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T11:18:27Z","timestamp":1785842307729,"version":"3.56.0"},"reference-count":26,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,7,17]],"date-time":"2006-07-17T00:00:00Z","timestamp":1153094400000},"content-version":"vor","delay-in-days":3885,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1995,11,27]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We studied 51 cervical carcinomas, among them 25 squamous\u2010cell carcinomas (SCC) and 26 cervical adenocarcinomas (AdCa), and 40 vulvar SCC for the presence of HPV and mutant <jats:italic>p53<\/jats:italic>. HPV was detected by PCR, and <jats:italic>p53<\/jats:italic> alterations by temperature\u2010gradient gel electrophoresis\/direct sequencing and immunohistochemistry. HPV, mostly type 16\/18, was found in 80.4% of the cervical tumors (92.0% of the SCC and 69.2% of the AdCa), but in only 27.5% of vulvar carcinomas. In contrast, <jats:italic>p53<\/jats:italic> mutations were found in 7.8% and 52.5% of cervical and vulvar tumors respectively. Mutant <jats:italic>p53<\/jats:italic> occurred in pre\u2010invasive vulvar lesions, indicating that this oncogenic factor is involved early in carcino\u2010genesis. Further analysis of recurrent\/metastatic lesions of 9 cervical and 14 vulvar tumors also showed remarkable differences: in cervical cancer, HPV was persistent, and <jats:italic>p53<\/jats:italic> mutations absent, whereas in vulvar tumors, HPV was mostly absent or not persistent, and the <jats:italic>p53<\/jats:italic> mutation rate was very high (78.6%). These observations suggest that HPV persistence is an important event for the evolution and maintenance of cervical cancer, whereas for vulvar cancers <jats:italic>p53<\/jats:italic> mutation and not HPV activity is a central oncogenic event. \u00a9 1995 <jats:italic>Wiley\u2010Liss, Inc<\/jats:italic>.<\/jats:p>","DOI":"10.1002\/ijc.2910630507","type":"journal-article","created":{"date-parts":[[2007,2,20]],"date-time":"2007-02-20T01:11:26Z","timestamp":1171933886000},"page":"639-645","source":"Crossref","is-referenced-by-count":74,"title":["Presence and persistence of HPV infection and <i>p53<\/i> mutation in cancer of the cervix uteri and the vulva"],"prefix":"10.1002","volume":"63","author":[{"given":"Karin","family":"Milde\u2010Langosch","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathrin","family":"Albrecht","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simone","family":"Joram","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Horst","family":"Schlechte","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Giessing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"L\u00f6ning","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,7,17]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1006\/gyno.1994.1028"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-71-5-1243"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1992.tb05487.x"},{"key":"e_1_2_1_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90662-M"},{"key":"e_1_2_1_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/jmv.1890360402"},{"key":"e_1_2_1_7_1","first-page":"4855","article-title":"Mutations in the p53 tumor\u2010suppressor gene: clues to cancer etiology and molecular pathogenesis","volume":"54","author":"Greenblatt M. 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