Introduction/Background The worldwide endometrial cancer (EC) incidence is increasing. EC is tightly linked to obesity. Obesity is also associated with diabetes mellitus (DM) and metabolic syndrome, in part through the low-grade inflammation originating from adipose tissue. A knowledge gap exists how obesity-related low-grade inflammation impacts on immune cell infiltration in EC. We explored the infiltration of a diverse immune cell panel in endometrial biopsies in obese and lean patients with postmenopausal bleeding due to EC or benign pathology.

Methodology A homogenous retrospective cohort was created (n=44) from women attending the gynecology outpatient clinic at Maastricht University Medical Centre (the Netherlands) in 2020. All had endometrial sampling performed. Biopsies were stained for a broad selection of immune cell markers, including macrophages (CD68, CD163), T-cells (CD3, CD8), B-cells (CD20) and NK-cells (CD56). Immune cell infiltration and number were analyzed in epithelium and stroma. Results were stratified for BMI and diagnosis.

Results Overall, a decrease of epithelial immune cell infiltration was seen within the benign samples compared to malignant histology (CD3;148 vs 63 cells/mm2 p=0.003, CD8; 186 vs 57 cells/mm2 p=0.003, CD56; 32 vs9 cells/mm2 p=0.016) and increased immune cell infiltration in the epithelium of lean compared to obese patients (CD163; 7 vs 62 cells/mm² epithelium, p=0.021) was seen. Strikingly, in the subgroup of obese patients with malignancy (n=11), it appeared that diabetes increased immune cell presence (CD56; 26 vs. 1 cells/mm² p=0.034).

Conclusion Most interestingly we show decreased immune cell infiltration in patients with obesity and malignant diagnosis. The differences in immune cell infiltration seen in obese EC patients with and without diabetes suggests a complex interaction where obesity-related low grade inflammation plays a central role. These results needs further studying, including mechanistic studying, in larger cohorts.

Disclosures No disclosures.