{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:54:29Z","timestamp":1791849269357,"version":"4.3.4"},"reference-count":28,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2011,3,10]],"date-time":"2011-03-10T00:00:00Z","timestamp":1299715200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Veterinary Dermatology"],"published-print":{"date-parts":[[2011,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Squamous cell carcinomas (SCCs) are common feline skin tumours. While exposure to ultraviolet (UV) light causes some SCCs, a subset develop in UV\u2010protected skin. In cats, papillomaviruses (PVs) cause viral plaques and Bowenoid\n                    <jats:italic>in situ<\/jats:italic>\n                    carcinomas (BISCs). As both may progress to SCC, it was hypothesized that SCCs in UV\u2010protected skin may represent neoplastic transformation of a PV\u2010induced lesion. To investigate this hypothesis, PCR was used to amplify PV DNA from 25 UV\u2010protected and 45 UV\u2010exposed SCCs. Oncogenic human PVs cause neoplasia by mechanisms that also increase p16\n                    <jats:sup>CDKN2A<\/jats:sup>\n                    protein (p16). As increased p16 is present in feline viral plaques and BISCs, immunohistochemistry was used to detect p16 within the SCCs. Papillomaviral DNA was amplified from 76% of UV\u2010protected SCCs, but only 42% of UV\u2010exposed SCCs. Increased p16 was present in 84% of UV\u2010protected SCCs, but only 40% of UV\u2010exposed SCCs. The more frequent detection of PV DNA and increased p16 within UV\u2010protected SCCs supports the hypothesis that some develop from a PV\u2010induced plaque or BISC.\n                    <jats:italic>Felis domesticus<\/jats:italic>\n                    PV\u20102 is thought to cause viral plaques and BISCs. This PV was detected most frequently within the UV\u2010protected SCCs, supporting development from a PV\u2010induced lesion. Increased p16 and PV DNA were less frequent within UV\u2010exposed SCCs, presumably because these developed from actinic keratosis rather than a PV\u2010induced lesion. The results support the hypothesis that some feline cutaneous SCCs are caused by PV infection and suggest that PVs may cause neoplasia by mechanisms that also increase p16.\n                  <\/jats:p>","DOI":"10.1111\/j.1365-3164.2011.00958.x","type":"journal-article","created":{"date-parts":[[2011,3,10]],"date-time":"2011-03-10T05:59:13Z","timestamp":1299736753000},"page":"360-366","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":72,"title":["Papillomaviral DNA and increased p16\n                    <sup>CDKN2A<\/sup>\n                    protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet\u2010protected skin"],"prefix":"10.1111","volume":"22","author":[{"given":"John 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