The Role of Obesity in Breast Cancer Pathogenesis

Research has shown that obesity increases the risk for type 2 diabetes mellitus (Type 2 DM) by promoting insulin resistance, increases serum estrogen levels by the upregulation of aromatase, and promotes the release of reactive oxygen species (ROS) by macrophages. Increased circulating glucose has been shown to activate mammalian target of rapamycin (mTOR), a significant signaling pathway in breast cancer pathogenesis. Estrogen plays an instrumental role in estrogen-receptor-positive breast cancers. The role of ROS in breast cancer warrants continued investigation, in relation to both pathogenesis and treatment of breast cancer. We aim to review the role of obesity in breast cancer pathogenesis and novel therapies mediating obesity-associated breast cancer development. We explore the association between body mass index (BMI) and breast cancer incidence and the mechanisms by which oxidative stress modulates breast cancer pathogenesis. We discuss the role of glutathione, a ubiquitous antioxidant, in breast cancer therapy. Lastly, we review breast cancer therapies targeting mTOR signaling, leptin signaling, blood sugar reduction, and novel immunotherapy targets.

Automated summary

Research has identified that obesity increases the chances of developing Type 2 diabetes by causing insulin resistance, elevating estrogen levels, and promoting the release of reactive oxygen species. Additionally, high glucose levels activate the mTOR signaling pathway, contributing to the pathogenesis of breast cancer. This article reviews the role of obesity in breast cancer development and correlates it with body mass index (BMI) and oxidative stress. It also explores the potential use of antioxidants and therapies targeting various signaling pathways in treating breast cancer.