The topography of and the area covered by tenascin, laminin and type IV collagen (all components of the subendothelial basement membrane), and the microvessel area (an index of angiogenesis), as evaluated with factor VIII, were investigated immunohistochemically in 61 B-cell non-Hodgkin's lymphomas (B-NHL) and 30 benign lymphadenopathies as controls. The three components were located in the microvessels and in a microvessel-bound stromal reticular network, the expression of tenascin being always more extended and finer than the other components. Of the lymphadenopathies, reactive and atypical lymphoid hyperplasias showed vessels and stromal network in the interfollicular zone only, whereas in Castleman's and angioimmunoblastic forms these structures were widely scattered in the tissue, and the area of the three components and that of the microvessels were significantly larger. Of the low-grade B-NHL, follicular subtypes had vessels and stromal network confined to the interfollicular inflammatory zone, but not in tumor follicles, whereas these structures were irregularly distributed throughout the small lymphocytic subtype. The levels of areas in low-grade B-NHL overlapped those of Castleman's and angioimmunoblastic lymphadenopathies. Among the intermediate-grade tumors, the follicular subtype resembled the follicular tumors, and the diffuse subtypes displayed vessels and stromal network throughout the tissue in close association with the neoplastic cells, and with significant increments of both the tenascin and the microvessel areas, but with a significant reduction of both the laminin and the type IV collagen areas. Distribution was similar in high-grade B-NHL, but tenascin and microvessel area variations, on the one hand, and those of laminin and type IV collagen areas were still more apparent than in the intermediate-grade. A high correlation was demonstrated in all groups of tissues between tenascin and microvessel area. In addition, in the diffuse intermediate-grade and high-grade B-NHL highly immature vessels were frequently detected by ultramicroscopy. The results show that tenascin expression and angiogenesis are closely related, and that both increase in function of tumor malignancy. Unlike laminin and type IV collagen, tenascin is associated with highly immature vessels in B-NHL. We suggest that tenascin expression and angiogenesis are governed by the B-NHL-associated inflammatory infiltrate, as well as by the B-NHL cells, particularly in more malignant tumors.