The basal lamina in a variety of metastatic tumours in brain was assessed with an antibody to type-IV collagen and the indirect immunoperoxidase technique. The antibody was raised in rabbits against type-IV collagen isolated from human placental tissue. Basal lamina redevelopment was demonstrated around individual melanoma cells, between melanoma cells and cerebral parenchyma, and at the tumour-stroma interface in both metastatic melanoma and metastatic carcinoma. At the periphery of metastatic carcinomatous deposits, no basal lamina was observed between tumour cells and the adjacent cerebral parenchyma. Basal lamina staining other than that of cerebral vessels was absent in deposits of poorly differentiated tumours which were unaccompanied by the development of a tumour stroma. It is concluded that metastatic tumours retain the ability to produce basal lamina and, in the case of metastatic epithelial tumours, the redevelopment of basal lamina is dependent on interaction with mesenchymal tissue. The stromal dependency of basal lamina formation by metastatic epithelial tumours suggests the reactivation of a control mechanism acting in normal tissue. Although basal lamina formation in metastatic melanoma can occur in the absence of mesenchymal tissue, there may be some interaction between tumour cells and stroma in the redevelopment of basal lamina at the tumour-stroma interface.

'Retraction spaces' observed in 18 of 30 basal cell carcinomas were readily classified into two distinct types using the PAP immunoperoxidase technique and an antibody to human type IV collagen, raised in rabbits. In processing artefacts, true retraction spaces were observed between the epithelial cells and the basal lamina, while in areas of stromal mucinous change, accumulation of mucinous material resulted in clear spaces separating the normal stroma from the overlying basal lamina.

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