Tumour-cell-induced platelet aggregation: studies with cloned metastatic and non-metastatic variants.

Blood platelets have been suggested to play an important role in modulating the development of experimental metastases. Tumour cells can induce platelet aggregation in vitro and a number of mechanisms have been proposed to explain the in vivo and in vitro observations. In the present study, we used tumour cells cloned from B16 melanoma and mouse mammary tumour virus (MMTV) carcinoma polyclonal populations to check whether tumour cells with low- and high-metastatic behaviour in vivo had different quantitative and qualitative platelet-aggregating activity in vitro. We found no significant quantitative difference between platelet aggregation induced by the low- and the high-metastatic clones. Indeed both the high and the low metastatic B16 melanoma clones poorly aggregated platelets, while both the high and low metastatic MMTV carcinoma clones efficiently aggregated platelets. Both the B16 melanoma and the MMTV carcinoma parental cell lines, which can be classed as intermediate metastatic, aggregated platelets well. However, based on the results with heparin and creatine phosphate/creatine phosphokinase, it appeared that qualitative differences might exist in the mechanism of platelet aggregation by tumour cells. For the parental lines and highly metastatic clone C1 a thrombin-linked component was more important than an ADP-like component, which was nevertheless present, to promote platelet aggregation. For the low-metastatic clone C2, the ADP-like component appeared to be the most important.