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Cutancous malignant melanomas in cats, both melanotic and amelanotic, were diagnosed in 57 of 1,530 skin tumors during the period 1991-1995. All melanomas occurred in domestic shorthaircats of ages 3-19 years ( $X = 11.5 years). Postmortem examination was performed on 16 cats. All had metastases in the regional lymph node and several organ systems. The average time of survival after surgical removal of the tumor was 4.5 months. Histologically, five types of melanomas could be distinguished: epithelioid, spindle, mixed, signet-ring, and balloon cell. Whereas all epithelioid, spindle, and mixed epithelioid/spindle cell types showed pigmentation, signet-ring and balloon cell types were often amelanotic. Immunohistochemical examination of the melanomas revealed a positive staining for S-100, vimentin, and neuron-specific enolase. The melanomas were negative for muscle cell markers, except in some of the signet-ring cell melanomas; 13 of 21 tumors showed a weak positive staining for polyclonal desmin. Electron microscopic examination of signet-ring cell melanomas revealed an abundance of intermediate filaments, whereas in some of these tumors a few cells with melanosomes were found. Nonisotopic in situ hybridization for mRNA encoding for tyrosinase verified the melanocytic origin of the amelanotic signet-ring and balloon cell melanomas.

Eight canine tumors originating from specific glandular structures in the anal region, as well as metastatic tumor tissue of two of these cases (case Nos. 7, 8), were immunohistochemically analyzed using various monoclonal antibodies (MoAbs) directed against human keratin types, vimentin, neurofilament proteins, and α-smooth muscle actin. These tumors also were stained for the broad-spectrum neuroendocrine markers neuron-specific enolase (NSE) and synaptophysin. In histologically normal canine anal structures, α-smooth muscle actin and NSE antibodies stained basally localized (probably myoepithelial) cells in the anal glands and the anal sac glands. NSE staining also was present in a limited number of luminal cells in both anal glands and anal sac glands. Synaptophysin labeling was not observed in any of these glandular structures. Histologically, the tumors were differentiated into well- and moderately differentiated perianal gland tumors ( n = 5) and carcinomas without perianal gland differentiation (n = 3), corresponding to the so-called apocrine carcinomas of the anal region. Immunohistochemically, the perianal gland tumors could be differentiated from the carcinomas by marked differences in staining pattern with the various keratin MoAbs, particularly MoAbs directed against human keratin types 7 and 18. The keratin-staining characteristics of the carcinomas suggest a glandular luminal cell origin. Metastases of the carcinomas showed loss of some keratin-staining characteristics as compared with the primary tumor. Staining for NSE was only observed in solitary cells and small cell clusters in the carcinomas and their metastases, whereas the α-smooth muscle actin antibody did not react with the carcinoma cells. None of the tumors stained for neurofilament proteins or synaptophysin. An unequivocal neuroendocrine nature of the carcinomas could not be substantiated by our immunohistochemical study, although the presence of a population of neuroendocrine cells within these neoplasms seems likely. Because the immunohistochemical features of the carcinomas with respect to various keratin MoAbs and NSE are similar to those of the anal glands and the anal sac glands, both these glands might be considered as site of origin of these carcinomas.

Within a 6-month-period, solitary or multiple tumors were observed in 25 young pigs in their first weeks of life in a swine breeding farm. The herd comprised approximately 100 animals, and affected pigs were observed in several litters. The number of affected littermates varied from one to three. Five animals, all from different litters and with a total of 11 tumors, were studied. Histologically the tumors were classified as undifferentiated sarcomas. Electron microscopic examination of the tumors ( n = 3) revealed myogenic differentiation, characterized by the presence of numerous cytoplasmic filaments with longitudinal densities and cytoplasmic dense bodies. Immunohistochemically, all 11 tumors were labeled by vimentin and desmin antibodies. Two tumors from which frozen material was available were additionally labeled by a titin antibody but did not show immunoreactivity with antibodies directed against myosin and α-sarcomeric actin. The tumors were finally diagnosed as undifferentiated rhabdomyosarcomas. The high incidence of these tumors within a short period of time in multiple young animals in different litters indicates a common causative event. The clinical history suggests a genetic cause.

Ten malignant canine mammary gland tumours and five metastases from three of these tumours were studied immunohistochemically with monoclonal antibodies (MoAbs) directed against different human keratin types (K), alpha-smooth muscle actin, vimentin, and desmin. In all tumours the neoplastic epithelium was rather homogeneously labelled with the keratin MoAbs RCK 102 (K 5 and 8) and CAM 5.2 (K 8). The adenocarcinomas (n = 5), the solid carcinomas (n = 2), and the carcinosarcoma (n = 1) showed heterogeneous labelling with the MoAbs specific for luminal cell antigens in the normal canine mammary gland, i.e., K 18, K 7 and K 19 MoAbs. These cells were also immunoreactive with K 4 and K 10 MoAbs. The spindle cell carcinomas (n = 2), however, did not react with these MoAbs. All tumours except one adenocarcinoma were characterized by the absence of immunoreactive labelling with the alpha-smooth muscle actin MoAb. In the solid carcinomas this was associated with the absence of labelling with one or both basal cell specific keratin MoAbs, i.e., 8.7 (K 14 and 17) and RCK 107 (K 14), respectively. In contrast, the other malignant tumours showed marked labelling of neoplastic epithelium with these MoAbs. Another remarkable finding was the labelling of a limited to moderate number of neoplastic epithelial cells with the vimentin MoAb. The presence of such labelling patterns in canine mammary gland tumours may be indicative of malignancy. Metastatic tumour tissues had a labelling pattern largely similar to that of the primary tumour, although also loss of reactivity for some keratin MoAbs was seen.

Duct ectasias (n = 2) and different types of benign canine mammary tumours (n = 19) were studied immunohistochemically with monoclonal antibodies (MoAbs) directed against various human keratin types (K), alpha-smooth muscle actin, vimentin, and desmin. In the duct ectasias and in most tumours the epithelial structures revealed an inner and outer cell layer. The inner cell layer was characterized by labelling with K 7, 8, 18, 19 and mostly also with K 4 and/or K 10 MoAbs. The outer cell layer was almost invariably labelled by K 14, K 14 and 17, and a-smooth muscle actin MoAbs. The labelling patterns of both duct ectasias and tumours corresponded largely to the patterns observed in normal mammary gland tissue, although a more distinct heterogeneity was seen. Tumours histomorphologically assumed to be of a myoepithelial origin did not show immunohistochemical features of myoepithelial cells. The myoepithelial nature of the vast majority of spindle-shaped cells present in the adenomas of the complex type and in the fibroadenomas of the benign mixed type could not be confirmed immunohistochemically. These cells, however, unequivocally expressed vimentin, suggesting proliferation of stromal cells in these tumours, which in the fibroadenomas of the benign mixed type may show metaplasia to bone or cartilage. In the duct ectasias and in some tumours, a fraction of elongated stromal cells, probably representing myofibroblasts, was labelled with the alpha-smooth muscle actin MoAb.

One hundred and thirty nine canine perineal tumours were histologically evaluated. The vast majority (134 tumours = 96.4 Yo) appeared to originate from the characteristic glandular structures of this region. They were classified as well differentiated perianal gland tumours (58.3 Yo). as moderately or poorly differentiated perianal gland tumours (21.6 %) and as carcinomas without perianal gland differentiation (16.5 Yo). Only 5 tumours (3.6 Yo) appeared to originate from non-characteristic perineal structures. A prominent male predominance was found with respect to the perianal gland tumours, whereas the carcinomas showed a distinct female predisposition. Tumours showing perianal gland differentiation almost invariably will have a benign behaviour. The carcinomas lacking any perianal gland differentiation often show a distinct malignant behaviour with metastases to regional lymph nodes and internal organs. These malignant neoplasms showed morphological and clinical features comparable to canine anal sac gland adenocarcinomas and carcinoids in man and animals. Se evaluaron histológicamente ciento treinta y nueve tumores perineales caninos. La gran mayoría (134 tumores = 96,4 Yo) parecían originarse en las estructuras glandulares características de esta región. Se clasificaron como tumores de glándulas perianales bien diferenciados (58,3 Yo). como tumores de glándulas perianales moderadamente o mal diferenciados (21,6%) y como carcinomas sin diferenciación de glándulas perianales (16,5 Yo). Sólo 5 tumores (3,6 Yo) parecían originarse en estructuras perineales no características. Se encontró un predominio masculino prominente con respecto a los tumores de glándulas perianales, mientras que los carcinomas mostraron una clara predisposición femenina. Los tumores que muestran una diferenciación de las glándulas perianales tienen casi siempre un comportamiento benigno. Los carcinomas que carecen de diferenciación de las glándulas perianales suelen mostrar un comportamiento claramente maligno con metástasis a los ganglios linfáticos regionales y a los órganos internos. Estas neoplasias malignas presentan características morfológicas y clínicas comparables a los adenocarcinomas de las glándulas del saco anal canino y a los carcinoides en el hombre y en los animales. Universidad Nacional, Costa Rica Escuela de Medicina Veterinaria