| Canine nasal carcinomas (CNCs) are aggressive neoplasms with poor prognosis. Treatment approaches include surgical excision and radiation therapy. But, mortality remains high and the etiology of this malignancy is poorly understood. On the other hand, many genetic and environmental factors including inactivation of tumorsuppresser gene p16, a susceptibility locus on human chromosome 4p15.1-q12, and Epstain-Barr virus (a human herpesvirus) have been found to play important roles in the etiology of human nasopharyngeal carcinoma (NPC). Based on the knowledge of NPC, this study was undertaken to determine the roles of these factors of NPC in CNCs. Our results ruled out the involvement of any member of the herpesvirus family and the canine chromosomal region orthologous to human Ch 4p15.1-q12 in the etiology of CNCs. However, frequent loss of p16 expression was observed in the presence of low frequency of loss of heterozygosity (LOH). These result point to the involvement of p16 inactivation, most likely through promoter hypermethylation, as a major contributor to tumorigenesis in CNCs. |
