Abstract
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.
Highlights
Feline oral squamous cell carcinoma (FOSCC) is one of the most common cancers in cats [1]
The immunohistochemical staining patterns for p16, Rb, and p53 have been described for FOSCC
The immunohistochemistry patterns of p16, p53, and phosphorylated retinoblastoma (pRb) in FOSCC were different from human HNSCC and feline cutaneous SCC
Summary
Feline oral squamous cell carcinoma (FOSCC) is one of the most common cancers in cats [1]. Pathogenesis of this cancer is not well-understood and few treatment options are available with limited success. FOSCC and human head and neck cancer (HNSCC) have a high degree of biological similarity including location of tumors and bone-invasive behavior [3] HNSCC can be classified in two major categories; human papillomavirus (HPV)-induced and non-viral-associated HNSCC [6] A favorable prognosis as well as good treatment response was commonly reported in patients with the HPV HNSCC, while most patients with non-viral-associated HNSCC have a poor prognosis. Inactivation or mutation of tumor suppressor genes, especially CDKN2A and TP53, were reported in more than 60% of non-viral associated HNSCC patients [6] Inactivation or mutation of tumor suppressor genes, especially CDKN2A and TP53, were reported in more than 60% of non-viral associated HNSCC patients [6] (pp. 9–22)
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