Obesityand Gynaecological Cancers, with a Focus on Morbid Obesity: Risk Stratification, Early Diagnosis and Management.

Authors

Magdalena Bizoń, Karolina Piotrowska-Lis, Anna Sztokinier, Justyna Domienik-Karłowicz, Maciej Olszewski, Anna Rulkiewicz

Published in

Diagnostics (Basel, Switzerland). Volume 16. Issue 14. Jul 22, 2026. Epub Jul 22, 2026.

Abstract

Obesity is a chronic, relapsing disease and a significant oncological risk factor. The correlation is most pronounced and consistent for endometrial cancer. Conversely, evidence linking obesity to ovarian cancer is less robust and varies by histotype, while the association with cervical cancer is influenced by factors related to screening, diagnosis, treatment, and survival. This review examines obesity, particularly class III (morbid) obesity, in relation to the risk of gynaecological cancer, diagnostic approaches, and management strategies. A structured narrative review of PubMed/MEDLINE, Cochrane Library, Scopus and Web of Science Core Collection was conducted for literature published between January 2000 and December 2025. Eligible evidence included systematic reviews, meta-analyses, cohort and case-control studies, mechanistic studies and clinical guidance relevant to obesity and endometrial, ovarian or cervical cancer. Title/abstract screening and full-text selection were conducted using predefined criteria for conceptual relevance and clinical applicability. Excess adiposity contributes to endometrial carcinogenesis through hormonal dysregulation, insulin resistance and hyperinsulinaemia, adipokine imbalance, chronic inflammation, and oxidative stress. In ovarian cancer, associations are generally weaker but appear more relevant for selected histological subtypes and cumulative adiposity exposure. In cervical cancer, obesity should not be interpreted as replacing HPV-driven pathogenesis; rather, it may affect screening adequacy, treatment selection, perioperative risk, and disease-specific survival in morbidly obese patients. Current evidence does not support morbid obesity as an independent driver of all gynaecological cancers. It supports obesity as a major modifiable risk factor and clinical modifier, particularly for endometrial cancer, and highlights the need for pragmatic risk stratification based on BMI class, adiposity distribution, metabolic comorbidity, functional status and cancer-site-specific pathways. Biomarker evidence remains hypothesis-generating, and obesity-integrated oncological pathways require prospective validation in patients with a BMI ≥ 40 kg/m².

PMID:
42510158
Bibliographic data and abstract were imported from PubMed on 28 Jul 2026.

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