Case Description—A 7-year-old Persian cat was evaluated for recurrence of multiple cystic periocular masses. A number of cyst-like lesions had been resected from the left eyelids 18 months earlier, with lesions recurring within 6 months after surgery. The cat had blepharospasm and signs of discomfort following rupture of the largest cyst the day prior to examination. Previous histologic examination of the cysts had revealed apocrine hidrocystomas.
Clinical Findings—Multiple pigmented nodules were seen around the skin of the upper and lower left eyelids. The nodules were brownish to black, round, soft, and fluid-filled. Signs of pain were not evident during palpation of the nodules.
Treatment and Outcome—The largest cyst on the upper eyelid was removed by means of a V-shaped full-thickness excision. Histologic and immunohistochemical examination of the excised tissue confirmed the diagnosis of apocrine hidrocystoma. The remaining periocular cysts were surgically debrided and then treated topically with 20% trichloroacetic acid. All lesions healed rapidly without any signs of discomfort. During a recheck examination 12 months later, the upper and lower left eyelids appeared morphologically normal, and there was no evidence of recurrence.
Clinical Relevance—Findings suggested that chemical ablation with trichloroacetic acid may be a useful treatment for apocrine hidrocystomas in cats.
Objective—To investigate the antitumor effect of the chicken anemia virus (CAV) VP3 gene in canine mammary tumor (CMT) cells.
Sample Populations—Established primary canine cell lines that originated from epithelial cells of resected CMTs and nonneoplastic mammary gland epithelial (MGE) cells.
Procedures—Expression vectors and lentiviral vectors encoding the VP3 gene from a Taiwan-Ilan isolate of CAV were used to deliver the VP3 gene into CMT cells and nonneoplastic MGE cells. Ectopic gene expression and the pro-apoptotic effect of the VP3 gene on CMT and nonneoplastic MGE cells by either transfection or viral infection were evaluated via immunofluorescence microscopy, western blot analysis, and terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling analysis.
Results—Overexpression of the enhanced green fluorescent protein–VP3 fusion protein was detected predominantly in the nuclei of CMT cells. In contrast, the VP3 protein was localized to the cytoplasm of nonneoplastic MGE cells. Among the fusion protein–expressing CMT cells, most underwent characteristic changes of apoptosis, whereas apoptosis was not detected in fusion protein–expressing, nonneoplastic MGE cells. Induction of apoptosis by VP3 gene overexpression in CMT cells was associated with the caspase-9–, but not the caspase-8–, mediated apoptosis pathway.
Conclusions and Clinical Relevance—These data indicate that the VP3 gene of the CAV induces apoptosis in malignant CMT cells, but not in nonneoplastic canine MGE cells. On the basis of such tumor cell–specific killing, the VP3 gene may be a promising agent for the treatment of malignant mammary gland tumors in dogs.