Growth signals, inflammation, and vascular perturbations: mechanistic links between obesity, metabolic syndrome, and cancer.
Nearly 35% of adults and 20% of children in the United States are obese, defined as a body mass index ≥ 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 progression. This review 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. These interrelated pathways represent possible mechanistic targets for disrupting the obesity-cancer link.
Department of Nutritional Sciences, Dell Pediatric Research Institute, University of Texas at Austin, 1400 Barbara Jordan Blvd, Austin, TX 78723, USA. firstname.lastname@example.org
SourceArteriosclerosis, thrombosis, and vascular biology 32:8 2012 Aug pg 1766-70
Insulin-Like Growth Factor I
Intercellular Signaling Peptides and Proteins
Metabolic Syndrome X
Receptor, IGF Type 1
Vascular Endothelial Growth Factor A
Pub Type(s)Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't