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406


EQUINE VETERINARY EDUCATION / AE / AUGUST 2019


a)


c)


b)


d)


Fig 3: Immunohistochemical staining of neoplastic cells; 400 3 magnification. a) Strong cytoplasmic immunoreactivity of neoplastic cells for vimentin. b) Strong cytoplasmic immunoreactivity of neoplastic cells for S-100. c) Negative staining of neoplastic cells for melan-A. d) Weak immunoreactivity of neoplastic cells for cytokeratin, compared to strong immunoreactivity of surrounding normal epithelial cells for cytokeratin.


the equine melanocytic tumours evaluated, nor in normal melanocytes of equine skin (Ramos-Vara et al. 2014). The neoplastic cells in our biopsy were negative for melan-A, as were the melanocytes at the periphery of the specimen, which served as an internal control. The last IHC marker evaluated in our case was


Fig 4: At recheck 11 weeks after surgery and 1 week after finishing mitomycin C therapy, there is mild fibrosis of the dorsal


and lateral cornea. The medial periocular skin shows early depigmentation.


2004). Various studies have shown positive S100 immunoreactivity in 87.5% of feline melanocytic neoplasms (Ramos-Vara et al. 2002), 76% of canine oral melanocytic neoplasms (Ramos-Vara et al. 2000) and 83% of canine amelanotic melanocytic neoplasms (Sandusky et al. 1985). Tumours of neuronal and neuroectodermal origin, such as neurofibromas, schwannomas and malignant peripheral nerve sheath tumours, will also stain positive for S100 (de Wit et al. 2004). Carcinomas will generally not express vimentin or S100 (Desnoyers et al. 1990). Neoplastic cells were negative for melan-A, a


cytoplasmic protein of melanosomal differentiation. While melan-A is generally considered a highly sensitive and specific marker for human and canine pigmented melanocytic neoplasms (Choi and Kusewitt 2003; Smedley et al. 2011), it appears to be a less sensitive marker of melanocytic neoplasia in horses. In one study, the monoclonal antibody to melan-A did not react with any of


© 2017 EVJ Ltd


cytokeratin. Keratins are intermediate filaments found in epithelial cells, and IHC for cytokeratin is commonly used to identify carcinomas (Desnoyers et al. 1990). Neoplastic cells in our case had weak cytoplasmic immunoreactivity for cytokeratin, while surrounding normal epithelial cells had strong immunoreactivity. This difference in staining intensity between the neoplastic cells and epithelial cells suggests that the neoplasm was not epithelial in origin, and the weakly positive cytokeratin immunoreactivity could simply be nonspecific staining. Additionally, anomalous expression of keratins and other intermediate filaments is a well-reported phenomenon in some human melanocytic neoplasms (Romano et al. 2015), which may also explain the cytokeratin expression. Based on the neoplastic cell distribution and other IHC markers in this case, melanocytic neoplasia was considered the most appropriate diagnosis. Melanocytes are not normally found in the cornea, thus


primary corneal melanocytic neoplasia is an infrequent diagnosis. The lack of melanocytic tumours in other areas of the body in our case (prior or following surgery) makes the possibility that the corneal malignant melanoma was a metastasis from a primary neoplasia less likely, although complete staging was not performed. In humans, corneal melanocytic neoplasms are most commonly a result of contiguous spread from a conjunctival melanocytic neoplasm, but there are rare reports of pigmented and nonpigmented melanocytic tumours isolated to the cornea (Uc


akhan-G€ und€ uz et al. 2012). In veterinary medicine,


corneal melanocytic neoplasms are more commonly seen as extensions from limbal tumours, and this is most frequently diagnosed in dogs (Donaldson, Sansom, Scase, Adams and Mellersh 2006). There is only one report of a dog with a primary corneal melanocytoma, which was completely


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