Abstract. A retrospective study was performed to characterize 64 cases of anal sac gland carcinoma (ASGC) in cats. All ASGCs diagnosed between 1995 and 2007 at a private diagnostic laboratory in the UK were reviewed. Apocrine gland origin was confirmed in a subset of these tumors by immunohistochemistry and the use of the glandular cytokeratin antibody (CAM 5.2). Associated clinical, gross, and histologic features were compared with those of canine ASGC. Anal sac gland carcinoma accounted for 0.5% of all feline skin neoplasms. Thirty-nine of the cats with ASGC were female, with a female : male ratio of 1.56. Fifty-two (81.1%) of the 64 tumors were in Domestic Shorthair cats, 5 (7.8%) in Siamese, 3 (4.8%) in Domestic Longhair, 2 (3.1%) in Burmese, and 1 (1.6%) each in a Birman and a Persian cat. Significant differences in prevalence of ASGC among breeds were not detected. Cats ranged in age from 6 to 17 years (median and mean age, 12 years). More than three quarters of the affected cats for which postsurgical outcome was known were euthanatized or died as a direct consequence of the neoplasm, with a median survival of 3 months. Survival rates at 1 and 2 years were 19 and 0%, respectively.

Since axonal injury (AI) is an important component of many veterinary neurologic disorders, we assessed the relative ability of a panel of antibodies (amyloid precursor protein, 3 subunits of neurofilament protein, protein gene product 9.5, ubiquitin, and synaptophysin) to detect axonal swellings or spheroids. Abundant axonal spheroids found in necrotic internal capsule foci produced in 4 sheep by chronic Clostridium perfringens type D epsilon neurotoxicity provided a model system in which to evaluate this important diagnostic tool. There was heterogeneous labeling of subsets of spheroids by the respective antibodies, suggesting that, in order to detect the complete spectrum of AI in diagnostic cases, a range of antibodies should be used, not only when spheroids are plentiful but also when they are few in number or incompletely developed. The application of insufficient markers in the latter cases can potentially lead to the contribution of AI to lesion pathogenesis being underappreciated.

Uterine lymphoma is rare in the dog, in other animal species, and in humans. The lymphoma in the two female dogs presented as a primary tumour of uterine tissue and was classified as diffuse centroblastic B cell lymphoma. Terminally, the uterine lymphoma metastasized to various organs in one of the dogs, despite chemotherapy. This case study describes a very rare form of canine lymphoma and suggests to include lymphoma in the differential diagnoses in bitches with uterine masses.

Mast cell tumours (MCT) have been documented in numerous species and mutations within the KIT proto‐oncogene are implicated in the neoplastic biology of mast cells in humans, dogs and cats. This study determined high KIT gene nucleotide and Kit amino acid sequence homology between several species known to suffer mast cell neoplasia and especially high sequence conservation between the cheetah (Acinonyx jubatus) and domestic cat (Felis catus) KIT sequences. As a result, we hypothesised that KIT mutations would exist in the neoplastic DNA of four cheetahs diagnosed with MCT from a recent case series. PCR and Sanger sequencing identified conservative exon 6 KIT mutations in two of the four cheetahs. The mutations were different between the two cheetahs. Only wild‐type DNA in exons 6, 8, 9 and 11 of KIT was observed in the MCTs of the remaining two cheetahs. Twenty cutaneous MCTs from domestic cats were collected for KIT mutation comparison. Twelve tumours possessed a mutation within KIT exons 6, 8 or 9 (60%, 95% CI 38.5%‐81.5%). No mutations were detected in exon 11. There was no significant association between domestic feline MCT KIT mutation status and tumour histological grade (traditional schematic, P = .934; Sabattini 2‐tier schematic, P = .762) or mitotic index (P = .750). KIT mRNA and Kit protein sequences are conserved across species but the role of KIT in feline MCT pathogenesis is not completely understood.