4.5 Review

The obesity-breast cancer link: a multidisciplinary perspective

Journal

CANCER AND METASTASIS REVIEWS
Volume 41, Issue 3, Pages 607-625

Publisher

SPRINGER
DOI: 10.1007/s10555-022-10043-5

Keywords

Obesity; Breast cancer; Diet; Health disparities; Adipose; Immune

Categories

Funding

  1. [R35CA197627]
  2. [BCRF-21-073]
  3. [T32CA057726]

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Obesity plays a significant role in the development and progression of breast cancer through complex metabolic and immune dysregulation. Chronic low-grade inflammation, particularly in white adipose tissue, contributes to immune dysfunction that promotes breast cancer. Understanding the interaction between obesity and breast cancer is crucial for developing effective interventions to mitigate the negative effects of obesity on breast cancer. Dietary interventions have shown promise in offsetting the impact of obesity on breast cancer. The rising rates of obesity worldwide make it urgent to develop safe and equitable interventions to address the burden of obesity on breast cancer.
Obesity, exceptionally prevalent in the USA, promotes the incidence and progression of numerous cancer types including breast cancer. Complex, interacting metabolic and immune dysregulation marks the development of both breast cancer and obesity. Obesity promotes chronic low-grade inflammation, particularly in white adipose tissue, which drives immune dysfunction marked by increased pro-inflammatory cytokine production, alternative macrophage activation, and reduced T cell function. Breast tissue is predominantly composed of white adipose, and developing breast cancer readily and directly interacts with cells and signals from adipose remodeled by obesity. This review discusses the biological mechanisms through which obesity promotes breast cancer, the role of obesity in breast cancer health disparities, and dietary interventions to mitigate the adverse effects of obesity on breast cancer. We detail the intersection of obesity and breast cancer, with an emphasis on the shared and unique patterns of immune dysregulation in these disease processes. We have highlighted key areas of breast cancer biology exacerbated by obesity, including incidence, progression, and therapeutic response. We posit that interception of obesity-driven breast cancer will require interventions that limit protumor signaling from obese adipose tissue and that consider genetic, structural, and social determinants of the obesity-breast cancer link. Finally, we detail the evidence for various dietary interventions to offset obesity effects in clinical and preclinical studies of breast cancer. In light of the strong associations between obesity and breast cancer and the rising rates of obesity in many parts of the world, the development of effective, safe, well-tolerated, and equitable interventions to limit the burden of obesity on breast cancer are urgently needed.

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