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Papillomaviral DNA and increased p16 CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet‐protected skin
Author(s) -
Munday John S.,
Gibson Isobel,
French Adrienne F.
Publication year - 2011
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/j.1365-3164.2011.00958.x
Subject(s) - cdkn2a , lesion , carcinogenesis , pathology , immunohistochemistry , biology , dna damage , cancer research , dna , medicine , cancer , genetics
Abstract 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 p16 CDKN2A 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.