Obesity and inflammation: new insights into breast cancer development and progression

Am Soc Clin Oncol Educ Book. 2013:33:46-51. doi: 10.14694/EdBook_AM.2013.33.46.

Abstract

The importance of inflammation in promoting carcinogenesis and tumor progression is well recognized. Chronic inflammation caused by a variety of infectious agents can lead to the development of several common malignancies. Similarly, inflammatory bowel disease is a well-known risk factor for colorectal cancer. Much less is known about the link between inflammation and the development of breast cancer. Recent data suggest that obesity causes both in-breast and systemic inflammation that contribute to the development and progression of breast cancer. This observation has potentially important implications in terms of prevention and treatment of breast cancer, especially given the rising worldwide overweight and obesity rates. Inflamed white adipose tissue (WAT) within the breast is associated with elevated levels of proinflammatory mediators, enhanced expression of aromatase (the rate-limiting enzyme for estrogen biosynthesis), and increased estrogen receptor-α (ER-α)-dependent gene expression. Systemic consequences of obesity including altered adipokine levels, elevated circulating estrogen levels, and insulin resistance are also believed to play a role in the pathogenesis of breast cancer. Collectively, these findings suggest a significant role for inflammation in the pathogenesis of breast cancer in obese and overweight patients.

Publication types

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

MeSH terms

  • Adipokines / immunology
  • Adipose Tissue, White / immunology
  • Adipose Tissue, White / metabolism
  • Aromatase / metabolism
  • Breast Neoplasms / immunology*
  • Breast Neoplasms / metabolism
  • Carcinogenesis / immunology
  • Estrogen Receptor alpha / immunology
  • Estrogen Receptor alpha / metabolism*
  • Estrogens / biosynthesis
  • Female
  • Gene Expression Regulation, Neoplastic / immunology*
  • Humans
  • Inflammation / immunology*
  • Insulin Resistance
  • Obesity / immunology*
  • Obesity / metabolism
  • Tumor Microenvironment / immunology

Substances

  • Adipokines
  • Estrogen Receptor alpha
  • Estrogens
  • Aromatase