Consequences of angiogenesis for tumor progression, metastasis and cancer therapy.

作者: Janusz W Rak , Bradley D St Croix , Robert S Kerbel

DOI: 10.1097/00001813-199502000-00001

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摘要: The growth of solid tumors to a clinically relevant size is dependent upon an adequate blood supply. This achieved by the process tumor stroma generation where formation new capillaries central event. Progressive recruitment vessels site and reciprocal support expansion resulting neovasculature are thought result in self-perpetuating loop helping drive tumors. development vasculature also allows 'evacuation route' for metastatically-competent cells, enabling them depart from primary colonize initially unaffected organs. Several molecular cellular mechanisms have been identified which parenchyma may exert its angiogenic effect on host endothelial cells. As this paracrine influence, tumor-associated cells acquire 'immature' phenotype manifested rapid proliferation, migration, release proteases expression cytokines, endothelial-specific tyrosine kinases (e.g. flk-1, tek others) as well numerous other alterations. Consequently network structurally functionally aberrant formed within mass. There evidence that themselves, likewise stromal act reciprocally alter behavior adjacent or cell contact mediated fashion. For example, production interleukin 6(IL-6) differential human melanoma expressing different degrees aggressiveness. In manner derived cytokines could conceivably contribute progression suppressing less aggressive promoting dominance their malignant counterparts 'strategic' perivascular zones. Distinct biological features expressed serve potential prognostic markers disease novel targets therapeutic intervention.

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