Obesity-driven inflammation and cancer risk: role of myeloid derived suppressor cells and alternately activated macrophages

• Type of Material: Article
• Authors: Derick Okwan-Duodu, Emory University; Guillermo Umpierrez, Emory University; Otis W Brawley, Emory University; Roberto Diaz, Emory University
• Language: English
• Date: 2013
• Publisher: e-Century Publishing
• Publication Version: Final Published Version
• Copyright Statement: AJCR Copyright © 2013
• License: Creative Commons Attribution-Noncommercial 3.0 Unported
• Final Published Version (URL): http://www.ajcr.us/AJCR_V3N1.html
• Title of Journal or Parent Work: American Journal of Cancer Research
• ISSN: 2156-6976
• Volume: 3
• Issue: 1
• Start Page: 21
• End Page: 33
• Keywords: alternately activated macrophage; Obesity; inflammation; cancer; myeloid derived suppressor cells
• Research Categories: Health Sciences, Oncology

Abstract

During carcinogenesis, tumors induce dysfunctional development of hematopoietic cells. Myeloid lineage cells, in the form of myeloid derived suppressor cells (MDSCs) and alternatively polarized M2 macrophages, influence almost all types of cancers by regulating diverse facets of immunosuppression, angiogenesis, cell proliferation, growth and metastasis. One-third of Americans are obese, and accumulating evidence suggests that obesity is a risk factor for various cancers. However, the relationship between these immune players and obesity are not well-described. In this review, we evaluate potential mechanisms through which different aspects of obesity, namely insulin resistance, increased estrogen, adiposity and low grade chronic inflammation from adipose tissue macrophages, may coalesce to promote MDSC induction and M2 macrophage polarization, thereby facilitating cancer development. Detailed understanding of the interplay between obesity and myeloid mediated immunosuppression may provide novel avenues for therapeutic targeting, with the goal to reduce the challenge obesity presents towards gains made in cancer outcomes.