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Metabolic Perturbations Associated with Adipose Tissue Dysfunction and the Obesity–Cancer Link

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Abstract

Nearly 35 % of adults and 20 % of children in the USA are obese, defined as a body mass index (BMI) ≥30 kg/m2. Obesity, which is accompanied by metabolic dysregulation often manifesting in the metabolic syndrome, is an established risk factor for many cancers. Within the growth-promoting, proinflammatory environment of the obese state, crosstalk between adipocytes, macrophages, and epithelial cells occurs via obesity-associated hormones, cytokines, and other mediators that may enhance cancer risk and/or progression. This chapter synthesizes the evidence on key biological mechanisms underlying the obesity–cancer link, with particular emphasis on the relative contributions of increased adiposity per se versus the obesity-associated enhancements in growth factor signaling, inflammation, and vascular integrity processes resulting from adipose tissue dysfunction. These interrelated pathways represent possible mechanistic targets for disrupting the obesity–cancer link.

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Correspondence to Stephen D. Hursting .

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Ford, N.A., DiGiovanni, J., Hursting, S.D. (2013). Metabolic Perturbations Associated with Adipose Tissue Dysfunction and the Obesity–Cancer Link. In: Kolonin, M. (eds) Adipose Tissue and Cancer. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7660-3_1

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