title: Obesity, energy balance, and cancer: a mechanistic perspective.
abstract: Nearly 36 % of adults and 20 % of children in the USA are obese, defined as a body mass index (BMI) ≥30 kg/m(2). 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, cross talk between macrophages, adipocytes, 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 obesity-associated enhancements in growth factor signaling, inflammation, and vascular integrity processes, as well as obesity-dependent microenvironmental perturbations, including the epithelial-to-mesenchymal transition. These interrelated pathways represent possible mechanistic targets for disrupting the obesity-cancer link.
authors.affiliation: Department of Nutritional Sciences, Dell Pediatric Research Institute, University of Texas at Austin, 1400 Barbara Jordan Blvd, Austin, TX, 78723, United States, shursting@austin.utexas.edu.
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Hursting
mesh_terms: D000328:Adult; D000818:Animals; D004734:Energy Metabolism; D006801:Humans; D008659:Metabolic Diseases / Q000150:complications* / Q000473:pathology; D009369:Neoplasms / Q000209:etiology* / Q000473:pathology; D009765:Obesity / Q000150:complications* / Q000473:pathology