Congenital tumours and tumour-like lesions in domestic animals. 3. Horses. A review.

The literature on congenital tumours and tumour-like lesions in horses was reviewed. Included were embryonic tumours and teratomas. Special attention was paid to the ubiquitous adenomatous hyperplasia of the placenta. It appears that temporal teratomas, interstitial hamartomas and placental adenomatous hyperplasia are unique in the horse. Benign teratoma of the undescended testis is far more frequent in the horse than in other species. In horses, as in calves and pigs, congenital skin tumours were of papillomatous, vascular and melanocytic types. The sporadic occurrence of congenital tumours in the horse did not provide an etiologic or pathogenetic clue. The possibility of oncogenic viruses in cases of congenital skin papilloma or malignant lymphoma could neither be proven, nor be excluded. Hereditary tumours were not encountered.

Congenital melanocytic nevi with placental infiltration by melanocytes: a benign condition that mimics metastatic melanoma.

BACKGROUND: Placental metastases from cutaneous malignant melanoma from both the mother and the fetus have been reported. The finding of benign-appearing melanocytes in the placenta in association with congenital melanocytic nevi (CMN) is more exceptional, with only 6 reports in the literature. Clinically, the finding of melanocytes in the placenta in this setting can be alarming and might erroneously lead to the diagnosis of metastatic melanoma. OBSERVATIONS: Herein, we describe 3 additional patients with CMN with placental infiltration by melanocytes with a benign phenotype. In the results of immunoperoxidase stains, the melanocytic cells were positive for S-100 protein and HMB-45 in the 2 lesions available for study. Staining of placental vessels with Ulex europaeus agglutinin I (Vector Laboratories, Burlingame, Calif) failed to show intravascular melanocytes in the 1 lesion available for study. We report for the first time DNA diploidy in 2 lesions available for study, which were analyzed by DNA image cytometry. We describe the first patient with a relatively small, nongiant CMN. CONCLUSIONS: We support the notion of the aberrant migration of melanocytes from the neural crest during fetal development as the most likely explanation of this phenomenon and note the similarity to the association of CMN and leptomeningeal melanocytosis. However, the precise histogenesis of this process remains uncertain. Most importantly, our data provide further evidence for the benign nature of this condition. Awareness of this entity is of vital importance in avoiding overdiagnosis of melanoma in this clinical setting.