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Department of Biochemistry and The University of Rochester Cancer Center, The University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642
The R3230AC mammary adenocarcinoma was not dependent on insulin; tumor growth was equal to or greater in diabetic rats than in intact animals. However, tumor growth was reduced when daily doses of insulin were administered. Treatment with estrogen inhibited growth of the R3230AC carcinoma, either in diabetic rats or in intact animals simultaneously treated with insulin. The effects of insulin plus estrogen treatment appeared to be additive in causing inhibition of tumor growth. Tumors from diabetic rats showed few metabolic alterations as reflected by little or no changes in the activities of selected glycolytic enzymes, pyruvate kinase, phosphofructokinase, and hexokinase, nor any striking changes in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, representing the pentose phosphate pathway. A modest reduction in the ratio of utilization of [1-14C]glucose:[6-14C]glucose was seen in vitro by tumors from diabetic rats. It was concluded that insulin, along with estrogen and prolactin, should be considered as a hormonal factor that influences growth of this automonous, hormone-responsive adenocarcinoma.
1 Supported by USPHS Grants CA 12836 and CA 16660, and a grant from the Monroe County Cancer and Leukemia Association.
2 Submitted in partial fulfillment of the requirements for the Ph.D. degree. Present address: Department of Biochemistry, Case Western Reserve University, School of Medicine, Cleveland, Ohio.
3 To whom requests for reprints should be addressed.
Received 10/18/74. Accepted 11/21/74.
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