Microenvironmental determinants of cancer progression during obesity: emerging evidence and novel perspectives

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)

Obesity is a global pandemic representing a significant public health threat, with a rising number of affected individuals and numerous associated co-morbidities, including cancer. In obese cancer patients, higher mortality rates are usually observed compared to normal weight/lean individuals. The imbalanced metabolic asset of obese patients fosters tumor growth and its progression by impacting not only on cancer cells, but also affecting their cross-talk with the tumor microenvironment, which represents a relevant and multifaceted player in disease progression. Herein, we deliver a detailed overview of certain peculiar players implicated in the reprogramming of the tumor microenvironment during obesity toward disease evolution. We highlight the key metabolic, molecular and cellular players that co-opt cancer cells and their microenvironment to foster disease progression. We emphasize the role of certain hormones and growth factors-dependent pathways (Insulin/IGF signaling system and VEGF/VEGFR axis) together with inflammatory pathways (RAGE signaling system) in triggering microenvironmental-dependent evolution of neoplastic disease during obesity. Finally, we underline current pitfalls and envisage innovative tools and future directions for better investigating tumor progression in obesity.

Evidence level

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

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