Obesity, Energy Balance, and Cancer: A Mechanistic Perspective

摘要

Nearly 36 % 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, proinfiammatory environment of the obese state, cross talk between macro-phages, 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.