Anticoagulants and experimental metastases - evaluation of antimetastatic effects in different model systems
article
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 modles 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. Chemicals/CAS: ancrod, 9046-56-4; heparin, 37187-54-5, 8057-48-5, 8065-01-8, 9005-48-5; phenprocoumon, 435-97-2; Anticoagulants
Topics
ancrodcoumarin derivativeheparinphenprocoumonanimal experimentblood clottingcancer graftintraperitoneal drug administrationlewis carcinomamelanomametastasisrespiratory systemsubcutaneous drug administrationAnimalAnticoagulantsDisease Models, AnimalMaleMiceMice, Inbred C57BLNeoplasm MetastasisNeoplasms, Experimental
TNO Identifier
229129
ISSN
01715216
Source
Journal of Cancer Research and Clinical Oncology, 101(3), pp. 275-283.
Pages
275-283
Files
To receive the publication files, please send an e-mail request to TNO Repository.