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Summary The expression and the distribution of tenascin as well as the extent of blood vessel formation (angiogenesis) were investigated in 70 invasive human breast carcinomas. Formalin-fixed, paraffin-embedded specimens were stained with monoclonal antibody against tenascin-C (DAKO and Biogenex). Anti-CD31 antibody (Biogenex), an acknowledged marker of stromal angiogenesis, was used to detect endothelial cells. Tenascin immunostaining was positive in the tumours around the persisting normal ducts, around tumour-cell nests, in the neostroma, in some tumour cells, and it was found in or around vascular channels. Tumour vascularity was assessed by quantitative vascular grading (Chalkley point count) and was related to the localization and intensity of tenascin immunoreactivity. 19 tumours (27.1%) were scored as low, 35 (50%) as medium, and 16 (22.9%) as having a high vascular grade. The positive correlation between the vascular grade and the tenascin immunopositivity in tumour stroma was observed. Our results suggest that tenascin expression may be associated with endothelial cell activation and may play an important role in tumour angiogenesis.

Summary The main feature of an atherosclerotic plaque is the formation of a new tissue in the arteries. In this respect atherosclerosis is similar to other conditions where non-neoplastic tissue formation occurs like in embryogenesis, in healing or in repair processes. A progressive intimal thickening occurs in the early phase of human atherosclerotic lesions and also in certain experimental models. Long-standing aortic intimal thickening could be induced by mechanical injury to the inner surface of the aorta with a microsurgical instrument, which causes controlled endothelial denudation. The injury is followed by an arterial remodeling. The latter process is caused by the development of an intimal plaque which consists of two main components: the smooth muscle cell (SMC) and the intercellular matrix. The matrix components are mostly synthetized by the SMC. Two distinct SMC populations could be distinguished by morphological means in the intimal proliferation: the synthetizing type and the proliferating type. Their role will be discussed and their morphological appearance will be compared with SMC present in other lesions.