The Merkel cell: who coined the eponym?
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Among 32 neuroendocrine carcinomas of the skin, 11 were from patients with previous or concomitant squamous carcinoma. The medical records and pathologic material for these 11 cases were reviewed, and the diagnosis of neuroendocrine carcinoma was confirmed in each instance by electron microscopy. In two cases, the squamous and neuroendocrine carcinomas were admixed, but each preserved its identity and transition between the two was not identified. Despite the lack of evidence for origin from a single cell, the observations nevertheless indicate a common carcinogenetic influence for squamous and neuroendocrine carcinomas of the skin.
Twenty-one examples of neuroendocrine carcinoma of the skin were examined by the unlabeled antibody enzyme method for several neural hormones and peptides, carcinoembryonic antigen, S-100 protein, neuron-specific enolase, and three intermediate filaments: neurofilament, glial fibrillary acidic protein, and cytokeratin. Vasoactive intestinal polypeptide from two sources reacted with the neoplastic cells of four (18%) and seven (32%) of the cases, and pancreatic polypeptide reacted with scattered cells of one case. Neuron-specific enolase reactivity occurred in 50% of the cases. Neurofilament (70, 150, 200 kilodaltons) was strongly positive in 40% of the tumors whereas neurofilament (200 kilodaltons) was negative. Two monoclonal anticytokeratin antibodies of 54 kilodaltons and 44-54 kilodaltons reacted in 77% and 64% of the cases, respectively, in a distribution similar to the neurofilament. Sections reacted with antisera against cytokeratins of higher molecular weight were negative. The demonstration of vasoactive intestinal polypeptide, pancreatic polypeptide, neurofilament, and neuron-specific enolase is evidence of the neuroendocrine nature of this neoplasm.
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Nine cutaneous neuro-endocrine tumours have been immunostained with monoclonal antibodies to low molecular weight cytokeratin (CAM 5.2) and neurofilament. Polyclonal antisera to neurone-specific enolase, calcitonin and laminin were also used. All nine cases showed paranuclear, dot-like positive staining with CAM 5.2 and diffuse cytoplasmic staining for neurone-specific enolase. Neurofilament and calcitonin immunoreactivity could not be demonstrated. All tumours were negative for laminin immunoreactivity. The limitations of staining for neurone-specific enolase are discussed and the value of CAM 5.2 in the differential diagnosis of cutaneous neuro-endocrine tumours is emphasized. The histogenetic implications of the absence of laminin staining are considered.
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