Abstract

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.

Links

Publisher Full Text

Authors

Hursting SD, Hursting MJ

Institution

Department of Nutritional Sciences, Dell Pediatric Research Institute, University of Texas at Austin, 1400 Barbara Jordan Blvd, Austin, TX 78723, USA. shursting@austin.utexas.edu

Source

Arteriosclerosis, thrombosis, and vascular biology 32:8 2012 Aug pg 1766-70

MeSH

Adiponectin
Cell Communication
Humans
Inflammation
Insulin
Insulin-Like Growth Factor I
Intercellular Signaling Peptides and Proteins
Leptin
Metabolic Syndrome X
Neoplasms
Obesity
Receptor, IGF Type 1
Receptor, Insulin
Signal Transduction
Vascular Endothelial Growth Factor A

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

22815342