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The Obesity-Cancer Link: Lessons Learned from a Fatless Mouse

¹ Division of Nutritional Sciences, University of Texas, Austin, Texas; ² Department of Carcinogenesis, University of Texas-M. D. Anderson Cancer Center, Smithville, Texas; and ³ Laboratory of Human Carcinogenesis and ⁴ Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland

Requests for reprints: Charles R. Vinson, Gene Regulation Section, National Cancer Institute, Room 2D24, Building 37, Bethesda, MD 20892. Phone: 301-496-8753; Fax: 301-494-8419; E-mail: vinsonc{at}mail.nih.gov.

Current dogma suggests that the positive correlation between obesity and cancer is driven by white adipose tissue that accompanies obesity, possibly through excess secretion of adipokines. Recent studies in fatless A-Zip/F1 mice, which have undetectable adipokine levels but display accelerated tumor formation, suggest that adipokines are not required for the enhanced tumor development. The A-Zip/F-1 mice are also diabetic and display elevated circulating levels of other factors frequently associated with obesity (insulin, insulin-like growth factor-1, and proinflammatory cytokines) and activation of several signaling pathways associated with carcinogenesis. In view of this information, the risk factors underlying the obesity-cancer link need to be revisited. We postulate that the pathways associated with insulin resistance and inflammation, rather than adipocyte-derived factors, may represent key prevention and therapeutic targets for disrupting the obesity-cancer link. [Cancer Res 2007;67(6):2391–3]

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