Growth and treatment of B-16 melanoma in hyperglycemic mice
Melanoma B-16 grew slowly in mice with hyperglycemia induced by alloxan, glucagon, or glucose. The mechanism of retarded tumor growth is different and depends on the origin of hyperglycemia. The concentration of immunoreactive insulin in blood of mice with melanoma and in the tumor tissue is increased in nondiabetic as well as in diabetic mice. The chemotherapy of melanoma in diabetic mice is as effective as in nondiabetic mice whereas immunotherapy in diabetic mice is not effective. Combined chemoimmunotherapy of melanoma in diabetic mice is more effective than either therapy alone only when mice are given a daily dose of insulin.
Key wordsMelanoma Hyperglycemia Diabetes mellitus Antitumor therapy
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- 1.Botzenhardt U, Lemmel EM (1978) Kinetics of the reactive cell clones after immunosuppression and induction of tolerance: (1) inhibition of 19S and 7S plaque-forming cells in the primary and secondary immune response to sheep red blood cells by cyclophosphamide and 036.5122 (Asta) Agents Action 5:512–518Google Scholar
- 5.Geran RI, Greenberg NH, Macdonald MM, Schumacher AM, Abbot BJ (1972) Protocols for screening chemical agents and natural products against animal tumors and other biological systems. Cancer Chemother Rep 3:11–13Google Scholar
- 8.Morgan CR, Lazarow A (1963) Immunoassay of insulin: two antibody systems. Plasma insulin levels of normal, subdiabetic, and diabetic rats. Diabetes 12:115–126Google Scholar
- 11.Pavelić K, Hršak I (1978) Effect of immunosuppression on the growth of six murine tumors. Z Krebsforsch 92:147–156Google Scholar
- 15.Sablina II, Zilbere AM, Zidermane AA (1975) The effect of alloxan diabetes on the growth of transplantable tumors. Latv PSR Zinat Akad Vestis 1:53–58Google Scholar
- 18.Weber MJ (1973) Hexose transport in normal and in Rous sarcoma virus-transformed cells. J Biol Chem 24:2978–2983Google Scholar