Obesity, Inflammation, and Cancer

Tuo Deng, Christopher J. Lyon, Stephen Bergin, Michael A. Caligiuri, Willa A. Hsueh

Research output: Contribution to journalArticlepeer-review

560 Scopus citations


Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including cancer, and is increasingly recognized as a growing cause of preventable cancer risk. Chronic inflammation, a well-known mediator of cancer, is a central characteristic of obesity, leading to many of its complications, and obesity-induced inflammation confers additional cancer risk beyond obesity itself. Multiple mechanisms facilitate this strong association between cancer and obesity. Adipose tissue is an important endocrine organ, secreting several hormones, including leptin and adiponectin, and chemokines that can regulate tumor behavior, inflammation, and the tumor microenvironment. Excessive adipose expansion during obesity causes adipose dysfunction and inflammation to increase systemic levels of proinflammatory factors. Cells from adipose tissue, such as cancer-associated adipocytes and adipose-derived stem cells, enter the cancer microenvironment to enhance protumoral effects. Dysregulated metabolism that stems from obesity, including insulin resistance, hyperglycemia, and dyslipidemia, can further impact tumor growth and development. This review describes how adipose tissue becomes inflamed in obesity, summarizes ways these mechanisms impact cancer development, and discusses their role in four adipose-associated cancers that demonstrate elevated incidence or mortality in obesity.

Original languageEnglish (US)
Pages (from-to)421-449
Number of pages29
JournalAnnual Review of Pathology: Mechanisms of Disease
StatePublished - May 23 2016


  • Adipokine
  • Adipose tissue
  • Body mass index
  • Cancer risk
  • Cytokine
  • Metabolic dysregulation
  • Weight loss

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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