Abstract

Obesity drives a state of chronic, low-grade inflammation that reshapes tissue physiology and systemic 
immunity, accelerates carcinogenesis, and blunts responses to therapy. Adipocyte hypertrophy, hypoxia, and 
lipotoxicity trigger cytokine and chemokine cascades, recruit and polarize myeloid cells, and distort stromal 
architecture, yielding a tumor microenvironment that is immunosuppressed, fibrotic, and metabolically hostile. 
Nanotechnology offers a toolkit to precisely modulate this inflammatory circuitry while minimizing off-target 
toxicity. Liposomal and polymeric carriers, biomimetic vesicles, and inorganic or hybrid platforms can 
concentrate anti-inflammatory drugs, nucleic acids, and immune agonists in adipose depots and tumors, program 
release to match local pH/ROS/enzymatic cues, and bias delivery toward myeloid or stromal targets. This 
review synthesizes mechanistic links between obesity-induced inflammation and cancer, surveys 
nanotherapeutic strategies that dampen pathologic signaling or re-educate immune and stromal compartments, 
and outlines translational guidance for dosing, safety, and manufacturing in high-BMI populations. A unifying 
theme is context-aware engineering that aligns carrier physicochemistry and ligands with the altered vascular, 
immune, and metabolic landscapes of obesity to convert a systemic liability into a therapeutic entry point.