Retarded growth of murine tumors in vivo by insulin- and glucagon-stimulated immunity and phagocytosis.
Insulin and glucagon injected separately or simultaneously into CBA, C57BL, A, or C3Hf/Bu mice with aplastic carcinoma, fibrosarcoma, melanoma B16, Ehrlich tumor, lymphatic leukemia, or thymoma suppressed tumor growth and prolonged the mouse's mean survival time. Basic mechanistic features of growth retardation by insulin and glucagon were delineated for aplastic carcinoma and fibrosarcoma. In mice bearing these 2 tumors, stimulated plaque-forming capacity and phagocytosis were shown for these hormones. Cyclophosphamide abolished the growth retardation. Insulin- and glucagon-induced tumor suppression appeared mainly mediated by maintenance of high immune reactivity and phagocytosis.
D000818:Animals; D004357:Drug Synergism; D005934:Glucagon / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009374:Neoplasms, Experimental / Q000276:immunology* / Q000473:pathology; D010587:Phagocytosis / Q000187:drug effects*; D011379:Prognosis; D013268:Stimulation, Chemical
D007328:Insulin; D005934:Glucagon