Expression of N-cadherin supports the diagnosis of malignant mesothelioma and use of appropriate antibodies would be a useful addition to a diagnostic antibody panel. Focal staining for E-cadherin does not exclude mesothelioma. Signalling pathways mediated via met and erbB-2 may play a role in the growth and spread of malignant mesotheliomas.

Paraffin sections from 29 lung carcinomas (28 primary and 1 metastatic) and 9 pleural malignant mesotheliomas were immunostained with antisera to human hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, met. For HGF/SF, immunoreactivity was demonstrated in all 9 mesotheliomas, 9 of 12 adenocarcinomas, and 7 of 10 squamous cell carcinomas. None of seven cases of small cell anaplastic carcinoma was positive. The adenocarcinomas frequently showed enhanced luminal staining, suggesting possible secretion of HGF/SF, and this pattern of staining was also seen occasionally in bronchial epithelium adjacent to the tumour. Stromal fibroblasts also showed immunoreactivity for HGF/SF in 6/8 cases of mesothelioma but in only 3/12 adenocarcinomas, 1/10 squamous cell carcinomas, and 1/4 small cell anaplastic carcinomas. All tumours stained for met, usually strongly. The staining was mainly cytoplasmic in nature, but some plasma membrane staining was usually evident. Adenocarcinomas showed strong luminal membrane staining, as did adjacent, histologically normal bronchial epithelium. This study demonstrates the presence of HGF/SF and met in most of the tumour types described, particularly mesotheliomas, and suggests that the HGF/SF/met signalling system may play a role in the development of these tumours, either by autocrine or by paracrine mechanisms.

Summary Pleural effusion samples were obtained from 55 patients with malignant disease, including patients with primary lung cancers and those with a variety of other tumours metastatic to the pleura. The effusions were assayed for the presence of hepatocyte growth factor/scatter factor (HGF/SF), by both ELISA and bioassay. The presence of malignant cells in the effusions was also assessed. Detectable amounts of the factor, as judged by both criteria, were found in over 90% of all the effusions, including those from patients with a wide variety of carcinomas and also lymphomas. A wide range of HGF/SF levels were found for all tumour classes, some effusions containing high levels above 4 ng ml-. It is concluded that tumours within the pleura and adjacent lung tissue are usually exposed to biologically significant levels of HGF/SF.

Immunohistochemical studies to localise collagen IV, laminin, fibronectin and tenascin were undertaken in 59 bladder biopsies. These were non-neoplastic or contained foci of flat dysplasia or of transitional cell neoplasia. Collagen IV and laminin were reliably demonstrated in basement membranes but focal loss of reactivity for collagen IV was found in the urothelial basement membrane in some cases of inflammation, dysplasia, and non-invasive papillary transitional cell tumour. Basement membranes were rarely demonstrated around invasive transitional cell carcinomas. Fibronectin and tenascin were found in the sub-urothelial lamina propria and in some urothelial basement membranes. The stroma of invasive tumours reacted strongly for both. Increased numbers of sub-urothelial capillaries were present in association with some cases of cystitis, flat dysplasia or non-invasive transitional cell neoplasia suggesting an angiogenic stimulus in these circumstances. Immunohistochemical staining of basement membrane components is unlikely to be of value in the routine histopathological assessment of transitional cell neoplasms of the bladder.

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