Obesity, inflammation, and prostate cancer

Abstract

Obesity and the associated metabolic syndrome produce a complex set of alterations both systemically and locally in tissues that support cancer development and progression. In prostate cancer (PCa), the weight of evidence suggests that obesity is primarily associated with more aggressive disease and increased risk of biochemical failure following prostatectomy or radiation treatment. Inflammation processes and inflammation-associated signaling pathways are upregulated in the obese state, and both human and mouse studies support an important role for inflammation in obesity-driven PCa progression. Inflammation signaling pathways along with other signaling pathways (e.g., growth factor signaling pathways) altered in the obese state represent promising targets for both lifestyle and pharmacologic interventions to prevent or control PCa progression.