Some aspects of blood borne tumour emboli associated with thrombosis.
The ultrastructural morphology of the tumour cycle which has as one of its features the blood-borne tumour embolus associated with thrombosis is illustrated by examples of four phases. (1) The intrinsic vasculature of tumours influences the process of intravasation of tumour cells to form bloodborne emboli. Scanning electron microscopy of melanoma tumours reveals channels containing erythrocytes which are sinusoidal in appearance. (2) The reaction of the circulating blood to the villi and folds of tumour cells is to coat the surface with plasma proteins and platelets. Walker 256 carcinoma cells become encrusted with platelets following agitation with rat platelet rich plasma. (3) Damaged endothelium appears to provide a more secure adhesional site for the tumour embolus. Platelets on a damaged site may provide an active adhesional region for the platelets on the passing embolus. (4) Tumour cells migrate through the endothelial layer from the adherent embolus and can be held up at the level of the basement membrane of the endothelium.
D000818:Animals; D001808:Blood Vessels / Q000648:ultrastructure; D006224:Cricetinae; D004727:Endothelium / Q000648:ultrastructure; D051379:Mice; D008815:Mice, Inbred Strains; D009362:Neoplasm Metastasis / Q000097:blood*; D009369:Neoplasms / Q000097:blood / Q000098:blood supply*; D009374:Neoplasms, Experimental; D009360:Neoplastic Cells, Circulating; D010973:Platelet Adhesiveness; D051381:Rats; D013923:Thromboembolism / Q000209:etiology*