Obesity, energy balance, and cancer: a mechanistic perspective

Cancer Treat Res. 2014;159:21-33. doi: 10.1007/978-3-642-38007-5_2.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adult
  • Animals
  • Energy Metabolism*
  • Humans
  • Metabolic Diseases / complications*
  • Metabolic Diseases / pathology
  • Neoplasms / etiology*
  • Neoplasms / pathology
  • Obesity / complications*
  • Obesity / pathology