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Effects of metformin, buformin, and phenformin on the post-initiation stage of chemically induced mammary carcinogenesis in the rat.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhu, Zongjian Jiang, Weiqin Thompson, Matthew D. Echeverria, Dimas McGinley, John N. Thompson, Henry J.
Description	Author Affiliation: Zhu Z ( Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado.); Jiang W ( Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado.); Thompson MD ( Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland.); Echeverria D ( Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado.); McGinley JN ( Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado.); Thompson HJ ( Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado. henry.thompson@colostate.edu.)
Abstract	Metformin is a widely prescribed drug for the treatment of type II diabetes. Although epidemiologic data have provided a strong rationale for investigating the potential of this biguanide for use in cancer prevention and control, uncertainty exists whether metformin should be expected to have an impact in nondiabetic patients. Furthermore, little attention has been given to the possibility that other biguanides may have anticancer activity. In this study, the effects of clinically relevant doses of metformin (9.3 mmol/kg diet), buformin (7.6 mmol/kg diet), and phenformin (5.0 mmol/kg diet) were compared with rats fed control diet (AIN93-G) during the post-initiation stage of 1-methyl-1-nitrosourea-induced (50 mg/kg body weight) mammary carcinogenesis (n = 30/group). Plasma, liver, skeletal muscle, visceral fat, mammary gland, and mammary carcinoma concentrations of the biguanides were determined. In comparison with the control group, buformin decreased cancer incidence, multiplicity, and burden, whereas metformin and phenformin had no statistically significant effect on the carcinogenic process relative to the control group. Buformin did not alter fasting plasma glucose or insulin. Within mammary carcinomas, evidence was obtained that buformin treatment perturbed signaling pathways related to energy sensing. However, further investigation is needed to determine the relative contributions of host systemic and cell autonomous mechanisms to the anticancer activity of biguanides such as buformin.
File Format	HTM / HTML
ISSN	19406207
e-ISSN	19406215
DOI	10.1158/1940-6207.CAPR-14-0121
Journal	Cancer Prevention Research
Issue Number	6
Volume Number	8
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2015-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Oncology Buformin Pharmacology Cell Transformation, Neoplastic Drug Effects Hypoglycemic Agents Mammary Neoplasms, Experimental Drug Therapy Metformin Phenformin Animals Apoptosis Blotting, Western Carcinogens Toxicity Cell Proliferation Pathology Chemically Induced Rats, Sprague-dawley Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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Effects of Metformin, Buformin, and Phenformin on the Post Initiation Stage of Chemically-Induced Mammary Carcinogenesis in the Rat

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