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The epithelioid cell histiocytoma (ECH) is a polypoidal benign tumor of superficial connective tissue that is often diagnosed as a pyogenic granuloma. ECHs are speculated to originate from dermal dendritic subunits and are composed of 2 primary cell populations, ie, CD34+ primitive fibroblastic dendrocytes and factor XIIIa+ histiocytes. Although dendritic subunits are distributed throughout most collagenous tissues inclusive of oral mucosa, to date, all reported cases of ECH have been cutaneous lesions. ECHs' putative pathogenesis entails activation of CD34+ "sentinel" reserve dendrocytes, followed by an influx of histiocytes and mast cells. Juxtacrine communication increases release of wound healing factors; suggesting a reactive etiologic component. In this current case, the location (ventral tongue) and history (recent increase in size) suggest the possibility that trauma could have initiated the dendritic subunit "wound healing" cascade. Consistent with its benign course, the ECH is managed by local excision, and has an excellent prognosis.

Enhanced hepatocyte growth factor (HGF) receptor (Met) signaling has been suggested to play an important role in the development and progression of various epithelial and nonepithelial tumors. N-terminally truncated forms of the HGF receptor have been shown to be constitutively activated and tumorigenic in animal experiments. In the present study, 102 benign and malignant human musculoskeletal tumors were examined for expression of the HGF receptor by Western blotting and/or immunohistochemistry. A clear predominance of HGF receptor expression was seen in malignant as compared to benign tumors (Western blotting, P < 0.001; immunohistochemistry, P < 0.02). For the first time we show HGF receptor expression in the following four tumor types: dermatofibrosarcoma protuberans, clear cell sarcoma of tendons, malignant primitive neuroectodermal tumor, and benign fibrous histiocytoma. In three cases of sarcoma with high HGF receptor expression by Western blotting, we found indications of a short 85-kd N-terminally truncated HGF receptor that was tyrosine phosphorylated and located in the cytoplasm. Although fragments of this length were seen in 18 of 65 tumors, most were not tyrosine-phosphorylated. Northern blotting revealed only the 7.5-kb full-length HGF receptor transcript, suggesting that the 85-kd fragment is generated by an alternative initiation of translation or by proteolytic cleavage. Southern blotting detected no amplification of the Hgfr/Met gene in the 35 tumors examined, in contrast to our recent report of Hgfr/Met gene amplification in 7, 12-dimethylbenz(a)anthracene (DMBA)-induced rat sarcomas. The present data suggest that the locally aggressive and malignant properties of human mesenchymal tumors maybe related, in part, to high levels of full-length HGF receptors, and in some cases to the occurrence of N-terminally truncated HGF receptors, activated independently of HGF.

Immunocytochemistry was used to examine 18 cases of rat fibrous histiocytic tumours (11 malignant; seven benign). The diagnosis was made by light microscopic criteria and all cases were categorized as pleomorphic-storiform. A selection of polyclonal antibodies to histiocytic, muscle, neural and mesenchymal antigens was used. Fifteen tumours were positive with alpha 1-antitrypsin, four with alpha 1-chymotrypsin, ten with muramidase, five with desmin, 15 with neuron-specific enolase, 14 with S100, one with glial fibrillary acid protein and 12 with vimentin. Many tumours expressed several antigens, highlighting the confusion which has arisen with regard to the histiogenesis of fibrous histiocytic tumours in man, and supporting the concept of differentiation from a primitive mesenchymal common precursor able to differentiate in several directions.