Evaluation of feline oral squamous cell carcinomas for p16CDKN2A protein immunoreactivity and the presence of papillomaviral DNA

Felis catus papillomavirus types 1 and 4 are rarely present in neoplastic and inflammatory oral lesions of cats

“…Further evidence that FcaPV-1 caused the epithelial hyperplasia included the histological evidence of PV-induced cytopathy within the lesion and the previous observation that FcaPV-1 can cause the epithelial hyperplasia that characterizes a feline oral papilloma (Munday et al, 2015). However, while p16 can be used to suggest a PV etiology, other causes of loss of retinoblastoma protein can also increase p16 immunostaining and increased p16 has previously been observed in 2 of 30 feline OSCCs in the absence of any detectable PV DNA (Munday et al, 2011c).…”

“…While it is unknown what causes feline OSCCs, around a quarter of human OSCCs are caused by human papillomaviruses (PVs) (Gillison, 2007). Three previous studies have used consensus PCR primers to detect PV DNA within 1 of 20 (Munday et al, 2009), 2 of 30 (O'Neill et al, 2011), and 0 of 30 (Munday et al, 2011c) feline OSCCs. However, only human PV types were detected in these previous studies and, as PVs are almost always highly species and location specific (Sundberg et al, 2000), the significance of these results is difficult to determine.…”

A Naturally Occurring Feline Model of Head and Neck Squamous Cell Carcinoma

“…However, the clinical response and molecular properties of HPV-positive and HPV-negative tumors differ greatly, with HPV-negative HNSCCs having a worse overall survival [38]. In FOSCC, increased p16 immunoreactivity or papillomavirus DNA has been identified in only a small percentage of tissue samples, suggesting a potential role for PV-associated oncogenesis in a subset of FOSCC [39–41]. This suggests that FOSCCs are more similar to HPV-negative HNSCC, with no detectable papillomavirus DNA present in the majority of FOSCC [39–41].…”

“…In FOSCC, increased p16 immunoreactivity or papillomavirus DNA has been identified in only a small percentage of tissue samples, suggesting a potential role for PV-associated oncogenesis in a subset of FOSCC [39–41]. This suggests that FOSCCs are more similar to HPV-negative HNSCC, with no detectable papillomavirus DNA present in the majority of FOSCC [39–41]. Alternatively, it has been suggested by the “hit-and-run” mechanism of HPV-mediated carcinogenesis in HNSCC that perhaps HPV infection is an early initiating oncogenic event, but not necessary later for tumor progression, and thus HPV DNA may no longer be detectable [38].…”

Equine ocular squamous cell carcinoma: a case report

“…Abnormal RB expression results in an accumulation of p16CD-KN2A protein (p16), which can be detected using immunohistochemistry. While the presence of p16 has not previously been investigated in horse SCC lesions, recent studies of skin and oral samples revealed that p16 immunoreactivity is rarely present within feline-negative PV SCCs (Munday et al 2011b), while there was an intense cytoplasmic and nuclear immunoreactivity in oral Papillomas associated with Felis catus Papillomavirus Type 1 (Munday et al 2015).…”