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Fibrinogen Deposition without Thrombin Generation in Primary Human Breast Cancer Tissue¹

Departments of Medicine [V. C., L. R. Z.] and Pathology [V. A. M.], Dartmouth Medical School, Hanover, New Hampshire; Veterans Administration Medical Center, White River Junction, Vermont 05001 [V. C., L. R. Z., S. M. R.]; Department of Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131 [W. K.]; and Plasma Protein-Coagulation Laboratory, New York Blood Center, New York, New York 10021 [B. J. K.]

The occurrence and distribution of components of coagulation pathways in situ were determined using immunohistochemical techniques applied to 10 cases of primary carcinoma of the breast, normal breast tissue obtained from two patients undergoing reductive mammoplasty, and three patients with benign breast tumors. Tumor cells stained for factor X and thrombomodulin but not for tissue factor, factor V, factor VII, or factor XIII. Rare nonneoplastic duct epithelial cells stained for thrombomodulin, but these tissues did not otherwise stain for any of these antigens. Macrophages within the tumor stroma stained for tissue factor, factor VII, and factor XIII but not for factor V or factor X. These features of macrophages were the same in malignant and nonmalignant breast tissue. Fibrinogen was present in abundance throughout the connective tissue in breast cancer but not in nonmalignant tissues. By contrast, no staining was observed using fibrin-specific antibodies. These results suggest that an intact coagulation pathway does not exist in breast cancer tissue and that thrombin capable of transforming fibrinogen to fibrin is not generated in significant amounts in this tumor type. While fibrin is not a feature of the connective tissue stroma in breast cancer, it is conceivable that the abundant fibrinogen present in the tumor connective tissue (and factor XIII present in connective tissue macrophages) might contribute to the structural integrity of breast tumor tissues.

¹ Supported in part by the Veterans Affairs Medical Research Service; research grants from the National Institutes of Health HL35246 (W. K.), HL21465 (B. J. K.), and BRSG S07RR05392 (L. R. Z.); and Blood Systems, Inc. (W. K.).

² V. C. is a Visiting Scientist, Dartmouth Medical School and recipient of a fellowship from the Italian National Research Council-NATO. Permanent address: Instituto di Semeiotica Medica, Università di Perugia, Via E. dal Pozzo, 06100 Perugia, Italy.

³ To whom requests for reprints should be addressed, at the VA Medical and Regional Office Center, White River Junction, VT 05001.

Received 8/13/90. Accepted 9/24/90.

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