Obesity, Inflammation, and Cancer

Abstract

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.

Obesity and Risk of Cancer: An Introductory Overview

“…Inflammation plays a critical role in tumor progression [54] and may therefore be a critical link to obesity-related cancers [55]. The inflammatory pathway is probably particularly important for colorectal cancer, which is supported by the observation that patients with inflammatory bowel disease have higher colorectal cancer risk and that aspirin use decreases colorectal cancer risk [52].…”

Antioxidant, Enzyme-Inhibitory and Antitumor Activity of the Wild Dietary Plant Muscari comosum (L.) Mill.

“…2 ROS are inevitably produced in biological systems due to oxidative metabolism, and are known to cause various degenerative disorders. 3,4 Plant phenols are defense secondary metabolites produced by plants. They exert a ROS-scavenger activity but also have interesting biological activities related to enzymes inhibition, such as lipases and amylases.…”

Obesity and p16INK4A Downregulation Activate Breast Adipocytes and Promote Their Protumorigenicity

“…Indeed, the master inflammation regulator NF-B was upregulated in all BSAd from obese females, which consequently secreted higher levels of several proinflammatory adipokines such as leptin, IL-6, IL-8, and IL-1␤ than BSAd from lean women. This parallels the fact that obesity is tightly linked to inflammation, which is a hallmark of local fat deposition (30)(31)(32). Moreover, increasing evidence indicates that obesity is associated with a chronic proinflammatory state, and adipose tissue is being considered a major immunologically active endocrine organ (33,34).…”