Feline oral squamous cell carcinoma: An overview
In four studies comprising 81 cats with oral squamous cell carcinoma, 12 cats (14.8%) had documented metastasis to the ipsilateral submandibular lymph node.3-6 The actual rate of metastasis may have been somewhat higher, as not all cases had cytologic or histologic lymph node evaluation. In eight cats (10%), metastasis was diagnosed at presentation,3-5 while four cats (5%) developed lymph node metastasis after primary tumor treatment.6 Of these four cats, one was euthanized because of the metastasis; the other three were euthanized because of local tumor progression.6 Thoracic radiographs were evaluated in three of the studies, comprising 74 cats, and no evidence of thoracic metastasis was present at initial presentation in any patient.3,5,6 In one cat that had lymph node metastasis, follow-up thoracic radiographs 16 months after treatment showed no evidence of pulmonary metastatic spread.4 These findings are consistent with the belief that feline maxillofacial squamous cell carcinomas have a low metastatic rate and that local disease is usually the cause of death.
ETIOLOGY AND RISK FACTORS
The average age of cats with oral squamous cell carcinoma is 12.5 years, with a range of 3 to 21 years. No significant sex or breed predilection is associated with this tumor. Although several environmental risk factors have been recognized, the cause of feline oral squamous cell carcinoma remains poorly defined. Various potential contributing factors are discussed below.
One clinical study found that cats exposed to household environmental tobacco smoke appear to have an increased risk of developing oral squamous cell carcinoma.7 Cats that had ever lived in a household with a smoker had a nonstatistically significant twofold increase in risk of oral squamous cell carcinoma compared with cats in nonsmoking households. Cats whose owners reported smoking one to 19 cigarettes a day had a statistically significant fourfold increase in the risk of oral squamous cell carcinoma compared with cats in nonsmoking households.7
Another study of p53 expression in oral squamous cell carcinoma determined that cats exposed to any environmental tobacco smoke were four and a half times more likely to overexpress p53 in their tumors than were unexposed cats.8 The p53 protein, the product of a tumor suppressor gene, regulates cell growth and proliferation and prevents unrestrained cell division after chromosomal damage. Abnormal p53 accumulates in the cell, unlike normal, wild-type p53, and can be detected via immunohistochemistry. The absence of functional p53 increases the risk of developing various cancers, and it is suggested that p53 may be a possible site for carcinogen-related mutations within some squamous cell carcinomas.8