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Anticoagulants and experimental metastases-evaluation of antimetastatic effects in different model systems

  • Original Papers
  • Experimental Oncology
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Summary

Intravenous tumor cell injection and spontaneously metastasising transplantable tumors have been used as models for haematogenous tumor spread. To evaluate the validity of these two experimental approaches for the study of blood coagulability and metastases, the effect of anticoagulants on “secondary” tumor growth was investigated in both models and the results were compared. The B16 melanoma and the Lewis lung carcinoma in C57BL mice were employed throughout the study, and anticoagulation was rendered through the use of phenprocoumon, heparin and ancrod. All anticoagulants were capable of reducing lung colonies after i.v. tumor cell injection, whereas only phenprocoumon significantly diminished the formation of spontaneous metastases. A review of the current literature on anticoagulants and tumor dissemination and the observations described lead to the following conclusions: (1) Results from studies with i.v. introduced tumor cells cannot be extrapolated to spontaneously metastasising tumors. (2) Spontaneously metastasising tumors represent the preferable model for the study of antimetastatic effects of anticoagulants. (3) Little evidence exists to support the concept of the pathogenetic role of fibrin formation in the establishment of spontaneous metastases from blood-borne tumor cells. (4) Coumarin derivatives are potent antimetastatic drugs, their mode of action appears to be independent of their anticoagulant activity.

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This study was performed in a programme of the EORTC Metastasis Project Group. Parts of the experiments were carried out at the “West German Cancer Centre”, University of Essen, FRG. Dr. P. Hilgard was supported by a grant from the “Deutsche Forschungsgemeinschaft”, Bonn-Bad Godesberg, FRG (Hi 213/3-4)

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Maat, B., Hilgard, P. Anticoagulants and experimental metastases-evaluation of antimetastatic effects in different model systems. J Cancer Res Clin Oncol 101, 275–283 (1981). https://doi.org/10.1007/BF00410113

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  • DOI: https://doi.org/10.1007/BF00410113

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