A review study led by Maria D. Sanchez-Pino, PhD, an assistant research professor in the departments of Interdisciplinary Oncology and Genetics at LSU Health New Orleans' School of Medicine and Stanley S. Scott Cancer Center, advances knowledge about the connection between obesity-associated inflammation and cancer. The researchers suggest that inflammatory cells with immunosuppressive properties may act as a critical biological link between obesity and cancer risk, progression, and metastasis. The paper is published in the June 2021 issue of Obesity, available here.

Despite evidence showing that obesity increases the risk of cancer progression, efforts are needed to identify the causal relationship between immunosuppressive cells and the response of immunotherapy in patients with obesity.

The function of myeloid cells is shaped by the metabolic microenvironment. Along with macrophages, myeloid cells with immunosuppressive properties called Myeloid-derived suppressor cells (MDSCs) are generated in obesity. One of the major factors associated with the metabolic inflammation of obesity is the expansion of MDSCs. In cancer patients, MDSCs are associated with poor survival and resistance to immunotherapy.

Although there is tremendous cross-talk between inflammation and metabolic/endocrine disturbances that promote tumor growth in obesity, the biological and molecular mechanisms are not completely understood. The researchers reviewed the literature and explain that altered metabolic factors such as lipids, insulin, and leptin in obesity contribute to the activation of immunosuppressive and cancer developing capabilities of myeloid cells.

"Deciphering the molecular mechanisms by which obesity-associated metabolic factors activate or enhance the function of Myeloid-derived Suppressor Cells and immunosuppressive macrophages will allow us to identify biomarkers for prognosis and therapeutic responses," notes Dr. Sanchez-Pino. "It will also lead to the discovery of potential targets for pharmacological therapies that may disrupt the pathophysiologic inflammatory link between obesity and cancer."