This report describes a monoclonal antibody designated G 250, subclass IgGl, that recognizes an antigen preferentially expressed on cell membranes of renal-cell carcinoma cells (RCC) and not expressed in normal proximal tubular epithelium. G 250 antibody reacted with 46 of 47 primary RCC, with 7 of 8 RCC metastases and with a few other malignant tumors. The staining pattern of G 250 differs from that of other RCC-related antibodies described. Preliminary experiments show that this antibody can be used to visualize RCC xenografts in nude mice by immunoscintigraphy.

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Summary Expression of HLA antigens and 132-microglobulin was studied by immunoperoxidase staining of frozen sections of 9 mucinous and 10 nonmucinous colorectal adenocarcinomas, 1 cloacogenic carcinoma, 12 colorectal adenomas and 4 samples of normal colorectal mucosa using monoclonal antibodies (MAbs). Staining results were related to histopathological features. HLA Class I antigens were strongly expressed in morphologically normal colorectal epithelium, in all adenomas tested and in all non-mucinous carcinomas. In contrast, expression of HLA class I antigens by the majority of tumour cells was present in only 2 of the 9 mucinous carcinomas, whereas 2 of these mucinous carcinomas were completely negative. In the mucinous carcinomas a striking scarcity of mononuclear inflammatory infiltrate, especially around the mucus accumulations, was observed. HLA class II antigen expression was not detected in normal epithelium and was only focally present in 1 of the 12 adenomas. In 6 out of the 20 carcinomas tested between 20% and 90% of the tumour cells were stained by MAbs against HLA class II antigens. Apart from the low expression of HLA class I antigens in mucinous carcinomas no relationship was found between expression of HLA antigens and histological features of the tumours. The relative poor prognosis of mucinous colorectal carcinoma as reported in the literature may be associated with low expression of HLA class I antigens and scant mononuclear inflammatory infiltrate, which may be a reflection of a weak immune response to the tumour cells.

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A patient with diffuse cutaneous mastocytosis, present since birth, developed several cutaneous mastocytomas without any symptoms after puberty. Although the histological picture of the tumours, showing nuclear atypia, mitotic figures and varying metachromasia of the granules, raises suspicion of systemic involvement, this has not appeared so far. The absence of symptoms could be due to the synthesis of an abnormal secretory product by the mast cells, which is supported by the absence of oedema and dilated blood vessels in the presence of extensive degranulation and by the unusual ultrastructural picture of the mast cell granules, i.e. little electron density with the almost complete absence of lamellar and crystalline structures.