EXPRESSION OF TENASCIN IS RELATED TO HISTOLOGIC MALIGNANCY AND ANGIOGENESIS IN B-CELL NON-HODGKINS-LYMPHOMAS

The topography of and the area covered by tenascin, laminin and type I V collagen (all components of the subendothelial basement membrane), a nd 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 control s. The three components were located in the microvessels and in a micr ovessel-bound stromal reticular network, the expression of tenascin be ing always more extended and finer than the other components. Of the l ymphadenopathies, reactive and atypical lymphoid hyperplasias showed v essels and stromal network in the interfollicular zone only, whereas i n Castleman's and angioimmunoblastic forms these structures were widel y scattered in the tissue, and the area of the three components and th at of the microvessels were significantly larger. Of the low-grade B-N HL, follicular subtypes had vessels and stromal network confined to th e interfollicular inflammatory zone, but not in tumor follicles, where as 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 fo llicular tumors, and the diffuse subtypes displayed vessels and stroma l network throughout the tissue in close association with the neoplast ic cells, and with significant increments of both the tenascin and the microvessel areas, but with a significant reduction of both the lamin in and the type IV collagen areas. Distribution was similar in high-gr ade B-NHL, but tenascin and microvessel area variations, on the one ha nd, and those of laminin and type IV collagen areas were still more ap parent than in the intermediate-grade. A high correlation was demonstr ated in all groups of tissues between tenascin and microvessel area. I n addition, in the diffuse intermediate-grade and high-grade B-NHL hig hly immature vessels were frequently detected by ultramicroscopy. The results show that tenascin expression and angiogenesis are closely rel ated, and that both increase in function of tumor malignancy. Unlike l aminin and type IV collagen, tenascin is associated with highly immatu re vessels in B-NHL. We suggest that tenascin expression and angiogene sis are governed by the B-NHL-associated inflammatory infiltrate, as w ell as by the B-NHL cells, particularly in more malignant tumors.