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Aims: Ductal carcinoma in situ (DCIS) is a pre-invasive form of mammary carcinoma with no microscopic evidence of cancer cell invasion through the basement membrane. However, for initiation of invasion, tumour cells have to acquire and focus proteolytic activity on to the cell surface in order to infiltrate the surrounding extracellular matrix. The receptor (uPA-R or CD87) for the serine protease urokinase-type plasminogen activator (uPA) plays a central role in invasion and metastasis. This study was performed to determine and localize m-RNA and protein of uPA-R in ductal carcinoma in situ of the breast., Methods and Results: We analysed uPA-R mRNA and protein expression by in-situ hybridization and immunohistochemistry, respectively, in 50 formalin-fixed, paraffin-embedded specimens of DCIS. Three different antibodies were used to stain cell-associated uPA-R; chicken polyclonal antibody (pAb) HU277 and monoclonal antibodies (mAb) IID7 and 3936. In all cases, myoepithelial and stromal cells reacted with either antibody. Especially, reaction of macrophage-like cells with mAb 3936 resulted in a well-marked and bright staining. Applying mAb IID7, in 46 of the 50 breast specimens tumour cells showed a positive immunoreaction. Likewise pAb HU277 stained tumour cells in 40 of the 50 cases, whereas mAb 3936 reacted with only 24 of the 50 tissue sections. Endothelial cells were marked by both mAb IID7 and pAb HU277 (46/50 and 35/50, respectively); mAb 3936 did not label at all. All of the cell types stained by mAb IID7 and pAb HU277 also displayed reactivity with uPA-R mRNA-specific antisense oligonucleotides in in-situ hybridization., Conclusions: Our results reveal the presence of the tumour invasion-related receptor for the protease uPA not only in invasive ductal breast carcinoma but also in different types of DCIS.

Sinus histiocytosis with massive lymphadenopathy (SHML) is a disorder of unknown origin which is only infrequently associated with lymphoid neoplasms. We report the first two cases of Hodgkin's disease with simultaneous SHML-like changes in the same lymph node.

Twenty hamartomas of the spleen were studied by histological, immuno- and enzyme-histochemical methods. In all cases nodules of varying size resembling proliferation of splenic red pulp structures were present that exhibited considerable morphological variation with regard to plasmacytosis, extramedullary haematopoiesis and phagocytic activity of macrophages. Splenic red pulp structures could be identified by immuno- and enzyme-histochemical markers reacting with sinus endothelium, including Factor VIII related antigen, proteinase inhibitors and non-specific esterases. In conjunction with the absence of organized lymphoid tissue and of dendritic reticulum cells these studies allow the differentiation of splenic hamartomas from haemangiomas that may possess a deceptively similar morphological appearance.

Lymphocyte subpopulations and macrophages in 16 spleens from patients with Hodgkin's disease were analysed immunohistochemically using monoclonal antibodies of the Leu and the Ki M series. In non-involved splenic tissue there is an increase of T-lymphocytes with an increased T-helper/T-suppressor cell ratio, while Ki M-1, -2, -3 and -5-positive, i.e. phenotypically different macrophages, are reduced. These results indicate that involvement of the spleen in Hodgkin's disease is accompanied by changes with respect not only to lymphocyte subpopulations but also to cells of the mononuclear phagocyte system. The immunodeficiency associated with Hodgkin's disease is probably not solely due to lymphocyte dysfunction, since the disease may lead, at least in the spleen, to alterations in macrophages and accessory cells and this may contribute to the impairment of cell-mediated immunity.