The Role of Angiogenesis in Breast Cancer and Obesity: Unravelling the Connection

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Breast cancer remains one of the leading causes of cancer-related mortality amongst women worldwide, with rising incidence rates paralleling the global obesity epidemic. Obesity has been increasingly recognised as a risk factor for breast cancer, yet the molecular mechanisms underlying the association remain poorly understood. This review explores the role of angiogenesis as the central mechanism linking obesity to breast cancer progression. Angiogenesis is essential for both adipose tissue expansion and tumour growth. It is dysregulated in obesity and breast cancer, resulting in the formation of abnormal vasculature that perpetuates hypoxia and malignancy. Obesity contributes to this process through hypertrophic adipose tissue, altered adipokine profiles and elevated expression of proangiogenic factors, such as VEGF. These changes create a tumour microenvironment conducive to cancer progression, treatment resistance and poor clinical outcomes. Emerging evidence also implicates endothelial cells, pericytes and lipid metabolism in this interaction, suggesting novel therapeutic targets.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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