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Life sciences · Journal article
Frontiers in Oncology · October 12, 2026
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Obesity increases the risk and progression of at least 13 types of cancer. Although the epidemiologic links between excess adiposity and these cancers are well documented, the biological mechanisms linking obesity to carcinogenesis and tumor progression remain incompletely understood. White adipose tissue in obesity is a source of inflammatory and immunosuppressive signals that act systemically, driving metabolic, inflammatory, and immune dysfunction whose consequences differ across tumor types. As adipose tissue expands and adipocytes enlarge, the blood supply becomes inadequate, leading to hypoxia, fibrosis, lipolytic stress, macrophage recruitment, and chronic low-grade inflammation. These obesity-induced perturbations generate endocrine, cytokine, lipid, and metabolic signals that act systemically, within the tumor microenvironment (TME), and/or cell-intrinsically to activate oncogenic and tumor-promoting pathways. The same signals reshape innate and adaptive immunity, promoting tumor-permissive macrophage states and myeloid-derived suppressor cell expansion, while the effector arms weaken as antigen presentation, natural killer cell and T cell function all decline. This review synthesizes current evidence linking obesity-associated inflammation and immune dysregulation to cancer initiation, progression, and treatment responses across multiple obesity-related cancers. Emphasis is placed on adipose tissue inflammation, myeloid cell biology, T cell immunometabolism, endocrine-inflammatory crosstalk, and the relationship between obesity and immunotherapy. Finally, we discuss translational opportunities for preventing or intercepting obesity-related cancers, including weight loss achieved through lifestyle, surgical, or pharmacologic approaches, with an emphasis on GLP-1 receptor agonists given their substantial efficacy, rapid clinical uptake, and potential to reshape obesity-related cancer prevention and survivorship strategies. Defining the metabolic, immune, and inflammatory phenotypes that drive obesity-associated cancer risk and progression will be essential for developing more precise, mechanism-based strategies for prevention, treatment, and survivorship care.