Next Article in Journal
Pathogen and Host Response Dynamics in a Mouse Model of Borrelia hermsii Relapsing Fever
Previous Article in Journal
Cat Mammary Tumors: Genetic Models for the Human Counterpart

p16, pRb, and p53 in Feline Oral Squamous Cell Carcinoma

Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA
Author to whom correspondence should be addressed.
Academic Editor: Jaime F. Modiano
Vet. Sci. 2016, 3(3), 18;
Received: 9 June 2016 / Revised: 9 August 2016 / Accepted: 15 August 2016 / Published: 18 August 2016
Feline oral squamous cell carcinoma (FOSCC) is a highly aggressive head and neck cancer in cats, but the molecular pathogenesis of this cancer is still uncertain. In this study, p16, p53, and pRb proteins were detected and quantified by immunohistochemistry in forty-three FOSCC primary tumors and three FOSCC xenografts. p16 mRNA levels were also measured in three FOSCC cell lines (SCCF1, F2, and F3), which were consistent with their p16 immunoreactivity. Feline SCCF1 cells had very high levels of p16 protein and mRNA (55-fold greater) compared to SCCF2 and F3. A partial feline p16 cDNA sequence was amplified and sequenced. The average age of cats with FOSCC with high p16 immunoreactivity was significantly lower than the average age in the low p16 group. Eighteen of 43 (42%) FOSCCs had low p16 intensity, while 6/43 (14%) had high p16 immunoreactivity. Feline papillomavirus L1 (major capsid) DNA was not detected in the SCC cell lines or the FOSCCs with high p16 immunostaining. Five of 6 (83%) of the high p16 FOSCC had low p53, but only 1/6 (17%) had low pRb immunoreactivity. In summary, the staining pattern of p16, p53, and pRb in FOSCC was different from human head and neck squamous cell carcinoma and feline cutaneous squamous cell carcinoma. The majority of FOSCCs have low p16 immunostaining intensity, therefore, inactivation of CDKN2A is suspected to play a role in the pathogenesis of FOSCC. A subset of FOSCCs had increased p16 protein, which supports an alternate pathogenesis of cancer in these cats. View Full-Text
Keywords: feline; oral; squamous cell carcinoma; p16; p53; pRb; immunohistochemistry feline; oral; squamous cell carcinoma; p16; p53; pRb; immunohistochemistry
Show Figures

Graphical abstract

MDPI and ACS Style

Supsavhad, W.; Dirksen, W.P.; Hildreth, B.E.; Rosol, T.J. p16, pRb, and p53 in Feline Oral Squamous Cell Carcinoma. Vet. Sci. 2016, 3, 18.

AMA Style

Supsavhad W, Dirksen WP, Hildreth BE, Rosol TJ. p16, pRb, and p53 in Feline Oral Squamous Cell Carcinoma. Veterinary Sciences. 2016; 3(3):18.

Chicago/Turabian Style

Supsavhad, Wachiraphan, Wessel P. Dirksen, Blake E. Hildreth, and Thomas J. Rosol. 2016. "p16, pRb, and p53 in Feline Oral Squamous Cell Carcinoma" Veterinary Sciences 3, no. 3: 18.

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop