Canine and feline nasal tumors - Veterinary Medicine
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Canine and feline nasal tumors
Detecting this mainly localized disease process early is difficult but important to improve an animal's prognosis. New advances in radiation technology may also help improve the outcome of dogs and cats with these neoplasms.


VETERINARY MEDICINE


ETIOLOGY AND RISK FACTORS

Environmental carcinogens

Urban environments, with consequential nasal filtering of pollutants and exposure to environmental tobacco smoke, have been suggested to increase the risk of nasal tumor development.17,19 Although biologically reasonable, this possible influence still remains debatable since there are too few studies to draw definitive conclusions.

p53 expression

Known as the "guardian of the genome," the p53 gene produces p53 protein, which is essential for two key cellular processes—apoptosis and cell cycle regulation. The loss of p53 gene function within a cell predisposes it to genomic instability and predilection for acquiring gene mutations, which may lead to malignant transformation. Mutations in the p53 gene are frequently identified in a variety of tumor histopathologies, and evidence suggests that a mutated p53 gene may increase the risk of developing nasal tumors in dogs. Wild type (nonmutated) p53 protein has a short half-life and, thus, is typically not identified in a large proportion of normal cells. However, mutant p53 protein has an extended half-life secondary to protein conformational changes, and its accumulation and identification within the nucleus of malignant cells suggests that p53 protein may be involved in malignant transformation. In one study, the accumulation of p53 protein in the nucleus by immunohistochemistry was detected in 11 of 19 nasal adenocarcinomas, which suggests that p53 gene and protein mutation may participate in nasal tumorigenesis.20

COX-2 expression

Inflammatory eicosanoids, including prostaglandins and thromboxanes, participate in many physiologic and pathologic processes. Two enzymes, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), are responsible for the production of eicosanoids. COX-2 activity is induced by inflammatory stimuli and has been associated with tumorigenesis. Three studies evaluating COX-2 expression in canine nasal tumors found that 71% to 87% of nasal carcinomas are COX-2 positive,12,21,22 suggesting that COX-2 activity may participate in nasal tumorigenesis through suppression of apoptosis, promotion of angiogenesis and tumor invasion, and stimulation of cell proliferation.12

BIOLOGIC BEHAVIOR

Nasal tumors are characterized by rapid and progressive local tissue invasion but a low metastatic rate. Humane euthanasia of dogs and cats with nasal tumors is usually the result of local tumor progression rather than the development of metastatic disease. Varying between histopathologic types and investigational studies, the metastatic rate reported for nasal tumors in dogs ranges from 0% to 28% from the time of presentation to death.1,3,4,11,16,18,23

One recent study reported a metastatic rate of 8%, with identified metastases limited to the local lymph nodes, agreeing with other historical studies reporting a low incidence of pulmonary metastases in dogs.16,18 Although the incidence of regional and distant metastases for nasal tumors is relatively low, the histopathologic type may influence metastatic behavior. In one study based on histologic findings at necropsy, dogs with nasal carcinomas had a higher rate of metastases than dogs with nasal sarcomas had, suggesting a more aggressive metastatic phenotype for these epithelial-type tumors.3

Even within epithelial-type tumors, carcinomas may be subcategorized as being less or more aggressive. Dogs with aggressive carcinomas, such as anaplastic carcinoma or squamous cell carcinoma, generally have shorter survival times than dogs with less aggressive carcinomas, including adenocarcinoma and well-differentiated carcinoma. The median survival time of dogs with aggressive carcinomas and less aggressive carcinomas has been reported to be 7.2 and 11.9 months, respectively, compared with 24.1 months for dogs with sarcomas.6

CLINICAL SIGNS


Figure 1. A mixed-breed dog with nasal carcinoma with direct extension of disease through the caudal nasal sinuses and into overlaying soft tissue. (Image courtesy of Louis-Philippe de Lorimier, DVM, DACVIM [oncology].)
The most common clinical signs seen in animals with nasal tumors include epistaxis, facial asymmetry, nonhemorrhagic nasal discharge, and sneezing. Physical examination findings may include stertorous breathing, enlarged mandibular lymph nodes, neurologic signs, decreased retropulsion of the eyes, exophthalmos, ocular discharge resulting from nasolacrimal duct obstruction, and overt facial deformation (Figure 1).

Although a facial deformity is highly suggestive of a cancerous process, other differential diagnoses should include fungal or bacterial rhinitis, a foreign body, trauma, developmental abnormalities, and dental pathology. Systemic clinical signs including inappetence, lethargy, and weight loss may also be reported.13,16,23,24

Epistaxis is a common clinical sign in dogs and cats with nasal tumors. Most dogs (about 85%) with nasal neoplasia will manifest with frank hemorrhagic or serosanguinous nasal discharge, which correlates with a poorer prognosis.13,18,25 Although common in dogs with nasal cancer, epistaxis is not pathognomonic and is frequently observed in dogs with nonneoplastic rhinitis.18,25,26 In one retrospective study with 35 dogs presenting for evaluation of epistaxis, the underlying cause of nasal hemorrhage in 19 dogs (54%) was secondary to neoplasia.27


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Source: VETERINARY MEDICINE,
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