Contribution of the tumor and obese microenvironment to triple negative breast cancer

Cancer Lett. 2021 Jul 1:509:115-120. doi: 10.1016/j.canlet.2021.03.024. Epub 2021 Mar 30.

Abstract

The growing burden of obesity and incidence of the aggressive triple negative breast cancer (TNBC) is a challenge, especially amongst vulnerable populations with unmet medical needs and higher mortality from breast cancer. While some mechanisms linking obesity and TNBC have been identified, the complex nature of pathogenesis, in both obesity as well as TNBC poses a real challenge in establishing a causative role of obesity in risk of TNBC. In this review article, we discuss pathological mechanisms identified in the tumor microenvironment (TME) as well as the obese microenvironment (OME), such as inflammation, insulin resistance and survival pathways that contribute to the development and progression of TNBC. Insights into the cross-talk between TME and OME, and their contribution to TNBC development and progression, may pave the way for personalized therapies against TNBC progression, relapse and metastasis.

Keywords: Immunotherapy; Obese microenvironment; Obesity; Triple negative breast cancer; Tumor microenvironment.

Publication types

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

MeSH terms

  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology
  • Animals
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Disease Progression
  • Energy Metabolism
  • Female
  • Humans
  • Incidence
  • Inflammation Mediators / metabolism
  • Insulin Resistance
  • Obesity / epidemiology
  • Obesity / metabolism*
  • Obesity / pathology
  • Obesity / therapy
  • Risk Factors
  • Signal Transduction
  • Triple Negative Breast Neoplasms / epidemiology
  • Triple Negative Breast Neoplasms / metabolism*
  • Triple Negative Breast Neoplasms / pathology
  • Triple Negative Breast Neoplasms / therapy
  • Tumor Microenvironment*

Substances

  • Inflammation Mediators