title: [Tumor-induced platelet aggregation and growth-promoting factors as determinants of probable tumor metastasis].
abstract: Clones isolated from a metastatic variant of mouse colon adenocarcinoma 26; the high metastatic NL-17 and the low metastatic NL-44, induced similar degrees of platelet aggregation in vitro. Heterotypic aggregates of tumor cells and platelets were injected i.v. into mice. The lung colonization potential of NL-17 was dependent upon the extent of tumor cell platelet aggregation. This clearly indicates that the interaction of tumor cells with platelets can lead to enhanced tumor metastasis possibly through more efficient intravascular arrest of the heterotypic aggregates. The interaction of tumor cells with platelets could thus be an important determinant of probable metastasis. NL-44, however, did not form pulmonary metastasis even after the tumor cells had formed heterotypic aggregates with platelets, suggesting that tumor metastasis is dependent on the intrinsic nature of tumor cells. Lung extract enhanced the growth of NL-17 more effectively than that of NL-44. These results suggest that, in addition to the interaction of metastatic cells and platelets, host factors including growth-promoting factors might also have an important role in tumor metastasis.
mesh_terms: D000230:Adenocarcinoma / Q000097:blood / Q000473:pathology*; D000818:Animals; D002460:Cell Line; D002999:Clone Cells; D003110:Colonic Neoplasms / Q000097:blood / Q000473:pathology*; D006133:Growth Substances / Q000502:physiology*; D008175:Lung Neoplasms / Q000473:pathology / Q000556:secondary; D051379:Mice; D009362:Neoplasm Metastasis; D010974:Platelet Aggregation; D014700:Verapamil / Q000494:pharmacology
chemical_list: D006133:Growth Substances; D014700:Verapamil