Basal lamina redevelopment in tumours metastatic to brain:an immunoperoxidase study using an antibody to type-IV collagen.

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.

Characterization of retraction spaces in basal cell carcinoma using an antibody to type IV collagen.

'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.

The basal lamina in basal cell carcinoma, Bowen's disease, squamous cell carcinoma and keratoacanthoma: an immunoperoxidase study using an antibody to type IV collagen.

The basal lamina in a variety of skin tumours was assessed with an antibody to type IV collagen and the peroxidase-antiperoxidase (PAP) technique. The antibody was raised in rabbits against type IV collagen isolated from human placental tissue. The basal lamina in Bowen's disease was essentially intact while squamous cell and basal cell carcinomas showed focal loss in areas of tumour cell invasion. However, both tumours showed preservation of basal lamina around the majority of projections and nests of tumour within the dermis. Many keratoacanthomas showed extensive loss of the basal lamina. This loss appears associated with advanced keratinization at the base of the lesion and may represent an involutional change possibly secondary to inflammation. It is concluded that epidermal tumour cells following local invasion may cease migration and produce a distinct continuous basal lamina similar to that of the normal dermo-epidermal junction. Loss of basal lamina appears restricted to foci of ongoing tumour invasion.