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首页> 外文期刊>Veterinary Dermatology >Papillomaviral DNA and increased p16CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet-protected skin.
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Papillomaviral DNA and increased p16CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet-protected skin.

机译：在紫外线防护下的猫皮肤鳞状细胞癌中，常存在幼虫病毒DNA和p16 CDKN2A 蛋白增加。

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摘要

Squamous cell carcinomas (SCCs) are common feline skin tumours. While exposure to ultraviolet (UV) light causes some SCCs, a subset develop in UV-protected skin. In cats, papillomaviruses (PVs) cause viral plaques and Bowenoid in situ carcinomas (BISCs). As both may progress to SCC, it was hypothesized that SCCs in UV-protected skin may represent neoplastic transformation of a PV-induced lesion. To investigate this hypothesis, PCR was used to amplify PV DNA from 25 UV-protected and 45 UV-exposed SCCs. Oncogenic human PVs cause neoplasia by mechanisms that also increase p16CDKN2A 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-protected SCCs, but only 42% of UV-exposed SCCs. Increased p16 was present in 84% of UV-protected SCCs, but only 40% of UV-exposed SCCs. The more frequent detection of PV DNA and increased p16 within UV-protected SCCs supports the hypothesis that some develop from a PV-induced plaque or BISC. Felis domesticus PV-2 is thought to cause viral plaques and BISCs. This PV was detected most frequently within the UV-protected SCCs, supporting development from a PV-induced lesion. Increased p16 and PV DNA were less frequent within UV-exposed SCCs, presumably because these developed from actinic keratosis rather than a PV-induced 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.
机译：鳞状细胞癌（SCC）是常见的猫皮肤肿瘤。虽然暴露于紫外线（UV）会导致某些SCC，但在受紫外线保护的皮肤中会形成一个亚群。在猫中，乳头瘤病毒（PVs）会引起病毒斑块和Bowenoid原位癌（BISC）。由于两者都可能发展为SCC，因此有假设认为，受紫外线保护的皮肤中的SCC可能代表PV诱发的病变的赘生性转化。为了研究该假设，PCR用于从25个受紫外线保护的SCC和45个受紫外线暴露的SCC中扩增PV DNA。致癌人类PVs通过增加p16 CDKN2A 蛋白（p16）的机制引起肿瘤。由于猫病毒斑块和BISC中存在p16增加，因此采用免疫组织化学检测了SCC中的p16。从76％的受紫外线保护的SCC中扩增出杆状病毒DNA，但仅从受紫外线照射的SCC中扩增了42％。在受紫外线保护的SCC中，有84％的p16含量增加，但在受紫外线照射的SCC中只有40％。在受紫外线保护的SCC中更频繁地检测PV DNA和增加p16，支持以下假设：一些是由PV诱导的斑块或BISC形成的。 家猫 PV-2被认为会引起病毒斑块和BISC。在受紫外线保护的SCC中最常检测到此PV，从而支持了PV诱发的病变的发展。暴露于紫外线的SCC中p16和PV DNA增加的频率较低，大概是因为它们是由光化性角化病而非PV诱发的病变发展而来的。结果支持以下假设：某些猫科皮肤SCC是由PV感染引起的，并表明PVs可能通过增加p16的机制引起肿瘤。

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