{Reference Type}: Journal Article
{Title}: Impact of obesity‑associated myeloid‑derived suppressor cells on cancer risk and progression (Review).
{Author}: Jiménez-Cortegana C;Gutiérrez-García C;Sánchez-Jiménez F;Vilariño-García T;Flores-Campos R;Pérez-Pérez A;Garnacho C;Sánchez-León ML;García-Domínguez DJ;Hontecillas-Prieto L;Palazón-Carrión N;De La Cruz-Merino L;Sánchez-Margalet V;
{Journal}: Int J Oncol
{Volume}: 65
{Issue}: 2
{Year}: 2024 Aug
{Factor}: 5.884
{DOI}: 10.3892/ijo.2024.5667
{Abstract}: Obesity is a chronic disease caused by the accumulation of excessive adipose tissue. This disorder is characterized by chronic low‑grade inflammation, which promotes the release of proinflammatory mediators, including cytokines, chemokines and leptin. Simultaneously, chronic inflammation can predispose to cancer development, progression and metastasis. Proinflammatory molecules are involved in the recruitment of specific cell populations in the tumor microenvironment. These cell populations include myeloid‑derived suppressor cells (MDSCs), a heterogeneous, immature myeloid population with immunosuppressive abilities. Obesity‑associated MDSCs have been linked with tumor dissemination, progression and poor clinical outcomes. A comprehensive literature review was conducted to assess the impact of obesity‑associated MDSCs on cancer in both preclinical models and oncological patients with obesity. A secondary objective was to examine the key role that leptin, the most important proinflammatory mediator released by adipocytes, plays in MDSC‑driven immunosuppression Finally, an overview is provided of the different therapeutic approaches available to target MDSCs in the context of obesity‑related cancer.