Obesity-driven inflammation and cancer risk: A comprehensive review

Obesity is a growing global health challenge, significantly increasing the risk of metabolic diseases and cancer. This review explores the link between obesity-driven inflammation and cancer risk, emphasizing the key biological mechanisms. Chronic low-grade inflammation in obesity, mediated by dysfunctional adipose tissue, promotes a pro-tumorigenic microenvironment through increased secretion of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. These factors contribute to insulin resistance, oxidative stress, and immune cell infiltration, fostering tumorigenesis. Adipokine imbalances, particularly elevated leptin and reduced adiponectin levels, further drive cancer progression by enhancing cell proliferation, angiogenesis, and immune evasion. Additionally, obesity-induced hypoxia, endoplasmic reticulum stress, and gut microbiome dysbiosis amplify systemic inflammation and metabolic dysfunction, further increasing cancer susceptibility. Epidemiological evidence highlights strong associations between obesity and cancers such as breast, colorectal, liver, and pancreatic cancer. Given the rising global prevalence of obesity, addressing inflammation-mediated oncogenesis is crucial. Lifestyle modifications, including weight loss through dietary and physical activity interventions, have demonstrated significant cancer risk reduction. Emerging pharmacological approaches targeting inflammatory pathways and adipokine regulation offer promising therapeutic potential. Understanding the mechanisms linking obesity, inflammation, and cancer provides valuable insights for developing targeted prevention and treatment strategies.