Abstract
Platelets are thought to be involved in two important steps in the dissemination of cancer: (1) in their interaction with cells released from the primary tumour to form a mixed platelet–tumour cell embolus and (2) in the subsequent attachment or entrapment of this embolus at the vessel wall and the resulting extravasation of the tumour cell and growth of the secondary tumour1. We have recently used the Baumgartner perfusion chamber2 to evaluate the attachment phase of platelet–tumour cell interactions at subendothelial surfaces3. We have found that tumour cells which caused platelet aggregation (Hut 20 line, large cell carcinoma of the lung) were incorporated into mixed platelet–tumour cell thrombi on basement membrane or collagen microfibrils, while those tumour cells that did not cause platelet aggregation (A549 line, epithelial lung carcinoma), were not incorporated in this way. We have now found differences between different donors in the ability of their platelets to aggregate in response to various human tumour cell lines. These different individual susceptibilities seem to be largely independent of the cell line involved and may have implications in the evaluation of mechanisms of human neo-plastic disease.
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Bastida, E., Ordinas, A. & Jamieson, G. Idiosyncratic platelet responses to human tumour cells. Nature 291, 661–662 (1981). https://doi.org/10.1038/291661a0
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DOI: https://doi.org/10.1038/291661a0
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