On the latency of tumour cells.
The present experiments demonstrate that animals carrying large peripheral intramuscular tumours were free of spontaneous pulmonary metastases. Secondaries in the lung emerged, however, after administration of agents such as trypsin, 10% dextrose or antiserum to alpha-2-macroglobulin (AMG). Such metastases also appeared in animals treated with trypsin after amputation of the tumour-bearing limb. It is believed that the pulmonary vessels of tumour-bearing animals are lined with a layer of tumour-associated AMG. The presence of this peptide on vascular endothelium blocks the transmigration of tumour cells. Tumour emboli may remain dormant, i.e. unattached, in the vascular lumen. Agents inactivating AMG or enhancing vascular permeability (proteases, antisera to AMG or vasodilators) may promote the emergence of a latent tumour cell into an overt state. This is confirmed by the above experiments and by the microscopic appearance of the pulmonary vessels of test animals (shift of tumour cells from the intravascular to the perivascular space). It is suggested that latency is determined by the state of permeability of the vessels harbouring tumour emboli.
D000818:Animals; D002199:Capillary Permeability; D008175:Lung Neoplasms / Q000276:immunology / Q000473:pathology; D009135:Muscular Diseases / Q000276:immunology; D009362:Neoplasm Metastasis; D009374:Neoplasms, Experimental / Q000276:immunology*; D051381:Rats; D014357:Trypsin / Q000494:pharmacology; D000511:alpha-Macroglobulins / Q000276:immunology
D000511:alpha-Macroglobulins; D014357:Trypsin