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Endocrine Abstracts (2025) 109 P144 | DOI: 10.1530/endoabs.109.P144

SFEBES2025 Poster Presentations Metabolism, Obesity and Diabetes (68 abstracts)

Diabetes mellitus and endometrial cancer: risks and underlying mechanisms

Zebokhon Koraboeva & Zulaykho Shamansurova


Central Asian University, Tashkent, Uzbekistan


Introduction: Diabetes mellitus (DM), particularly type 2 (T2DM), has become a significant global health issue, with rising rates linked to increased risks of various cancers, including endometrial cancer (EC). Research increasingly suggests a connection between DM and EC, indicating that DM may not only elevate the risk of EC development but also worsen its prognosis. Metformin, an anti-diabetic medication, is under exploration as a potential preventive and therapeutic agent for EC, highlighting the value of treatments targeting glucose metabolism in mitigating EC risks. Studies show that hyperglycemia is an independent risk factor for EC, with individuals with DM twice as likely to develop EC compared to non-diabetics. This heightened risk may stem from high-glucose environments, which promote the growth and invasiveness of EC cells. Although the exact biological mechanisms linking DM to EC are not fully understood, the need for effective prevention and early intervention through glucose regulation is increasingly emphasized as an essential area for future therapeutic developments.

Materials and Methods: Published data over the past two years from sources such as MEDLINE, EMBASE, PubMed, and Research Gate were systematically analyzed to understand the association between DM and EC.

Results: Findings reveal a strong association between EC and T2DM. T2DM significantly raises the risk and mortality rate of EC, with a 4.9% increased risk of EC identified even in early-stage DM patients. Type 1 diabetes is also associated with elevated EC risks, confirming DM as an independent factor for EC mortality. Biological Mechanisms: Insulin resistance and hyperinsulinemia influence endometrial cells, while signaling pathways such as PI3K and MAPK/ERK, facilitated by chronic inflammation markers like TNFα and IL-6, contribute to EC development.

Conclusion: This research advances our understanding of the DM-EC link, proposing antidiabetic therapies as promising options for EC management and inspiring future research directions in this field.

Volume 109

Society for Endocrinology BES 2025

Harrogate, UK
10 Mar 2025 - 12 Mar 2025

Society for Endocrinology 

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