Background. Endometrial cancer is the most common gynecological malignancy in developed countries. Obesity is a major modifiable risk factor, promoting inflammation, hyperinsulinemia, increased estrogen production, and metabolic disturbances that contribute to carcinogenesis. Aim. This narrative review summarizes current evidence on the pathophysiological mechanisms linking obesity with endometrial cancer and highlights the relevance of molecular classification and lifestyle-related prevention. Material and methods. A narrative analysis of open-access publications (2008–2026) was conducted, focusing on epidemiology, metabolic and hormonal pathways related to obesity, and molecular subtypes of endometrial cancer described by The Cancer Genome Atlas (TCGA). Results. Obesity contributes to endometrial cancer through estrogen excess, insulin resistance, IGF-1 signaling, chronic inflammation, and adipokine imbalance. Four molecular subtypes are recognized: POLE ultramutated, mismatch repair deficient, p53-abnormal, and non-specific profile. Physical activity may reduce cancer risk. Conclusions. Understanding obesity-related molecular pathways in endometrial cancer may improve risk stratification and treatment decisions. Preventive strategies, including weight control and regular physical activity, may reduce disease burden. Key words: endometrial cancer, obesity, molecular classification, TCGA, physical activity.
Pietraszkiewicz et al. (Sun,) studied this question.
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