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Anticoagulants and Tumor Cell Lodgment¹

Departments of Surgery and Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

There is evidence that the coagulation mechanism plays a role in the development of metastases and that anticoagulants, by interfering with the adherence of tumor cells to vascular endothelium, may impair secondary tumor growth. The present study, employing ⁵¹Cr-labeled tumor cells in rats and rabbits, provided quantitative information relative to the effect of heparin, fibrinolysin, and the antifibrinolytic agent -aminocaproic acid (EACA) on deposition and organ retention of such cells. It was observed: (a) that adequate continuous heparinization failed to promote the residence of tumor cells in the blood stream or to affect the lodgment of tumor cells in lung, liver, kidney, and spleen of rats from 1 hr to 7 days following the jugular vein injection of Walker tumor cells; (b) that the intraportal inoculation of Walker tumor cells resulted in similar retention of tumor cells in livers of heparinized and unheparinized rats; (c) that findings similar to those in the rat were noted following the jugular vein injection of V2 carcinoma cells in heparinized and fibrinolysin-treated rabbits; and (d) that EACA failed to affect the organ retention of tumor cells in the rabbit.

It is concluded that anticoagulants do not influence metastases by preventing tumor cell lodgment and/or by promoting their residence within blood vessels. Other mechanisms to explain their effects on secondary tumor growth must be sought.

¹ Supported by American Cancer Society Grant P-142 and USPHS Grants CA-05949 and CA-06670.

Received 7/ 6/66. Accepted 9/30/66.

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				M. Hejna, M. Raderer, and C. C. Zielinski Inhibition of Metastases by Anticoagulants J Natl Cancer Inst, January 6, 1999; 91(1): 22 - 36. [Abstract] [Full Text] [PDF]