A rare case of carcinoma characterized by extensive chondroid elements at a site of primary esophageal and metastatic lesion is reported. The patient was a 67-year-old man complaining of dysphagia due to an ulcerative lesion at the lower middle esophagus. He underwent irradiation treatment prior to surgery. Histologically, the tumor consisted of both carcinomatous and chondroid elements and had invaded deeply into the esophageal wall. The carcinomatous cells had gradually become chondroid cells embedded within an extensive extracellular matrix. In addition, the metastatic lesion showed findings similar to those of the primary lesion. Immunohistochemistry revealed that both carcinomatous and chondroid elements were immunostained with cytokeratin and epithelial membrane antigen, suggesting an epithelial nature to the chondroid cells. Conversely, only chondroid cells were positively stained for S-100 protein. Furthermore, bone morphogenetic proteins (BMP) were positive for chondroid cells and their surrounding carcinomatous cells. Given the apparent transition between carcinomatous and chondroid cells based on microscopy and immunohistochemical findings in the present case, we concluded that the chondroid cells were derived from carcinomatous cells. In addition, our findings suggest that BMP produced by carcinomatous cells lead to chondroid differentiation of the carcinoma cells.
Primary malignant fibrous histiocytoma of the gastrointestinal tract is extremely rare. To date, only 10 cases of primary malignant fibrous histiocytoma arising in the small intestine have been reported in the English literature. We describe here the genetic alterations and morphologic features of a primary malignant fibrous histiocytoma arising in the jejunum. Immunohistochemically, the tumor cells expressed vimentin, CD68 and alpha-1-antitrypsin, but were negative for other markers. Ultrastructurally, they showed features of fibroblasts and histiocytes. Immunohistochemical overexpression of p53 and MDM2 was observed. Mutation analysis of the p53 gene detected a missense mutation in codon 158 of exon 5. Our results suggest that p53 gene mutations and MDM2 overexpression may play an important role in the tumorigenesis. To our knowledge, the present report is the first genetic study of this rare lesion.
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