Endocrine Abstracts

Introduction: Diabetes mellitus (DM) has emerged as a significant global health concern, contributing to increased mortality and complications, thereby adversely affecting overall quality of life. The incrising incidence of DM, particularly type-2 DM (T2DM), correlates with rising rates of various cancers, suggesting a potential direct link between DM and cancer. Mounting evidence suggests DM as a potential contributor to the heightened incidence of endometrial cancer (EC) and underlines its association with poor prognosis. Early intervention with metformin is anticipated to serve as an effective adjuvant alternative for EC, thereby offering new avenues for preventive and therapeutic strategies targeting glucose metabolism. Epidemiological studies affirm hyperglycemia as an independent risk factor for EC development. Patients with DM face a doubled risk of progressing to EC, possibly due to the conducive environment for the growth and invasiveness of EC cells in high-glucose settings. However, the etiological relationship between DM and EC remains unclear, and the precise biological mechanisms linking the two are not well understood. As existing treatments fail to prevent or delay EC progression, exploring early and effective prevention through glucose metabolism interventions holds promise for innovative targeted therapeutic interventions in EC, carrying substantial medical and social value.

Materials and Methods: A comparative analysis was conducted through a systematic search over the past two years, combining and analyzing published data from MEDLINE, EMBASE, PubMed, and Research Gate.

Results: Most epidemiological studies indicate a strong association between EC and T2DM. Analysis of T2DM’s impact on cancer risk and mortality reveals a significant increase in both morbidity and mortality for EC. Early-stage DM, aside from T2DM patients, shows a 4.9% increased risk of EC. T1DM is also linked to an elevated risk of EC. Additionally, DM emerges as an independent risk factor for EC mortality. Biological Mechanisms: Increasing evidence suggests that insulin resistance (IR) and hyperinsulinemia, mediated by insulin and insulin-like growth factors, influence endometrial cells and signaling pathways, such as PI3K, MAPK/ERK, and VEGFR, promoting angiogenesis and EC occurrence. Chronic inflammation factors like TNFα, IL-6, and COX-2 contribute to carcinogenesis.

Conclusion: This study enhances the understanding of the complex relationship between DM and EC, offering a global perspective on the effects of DM on EC through various mechanisms. It emphasizes the clinical application of antidiabetic medications for EC, providing valuable insights for future research and therapeutic strategies.