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Introduction/Background* Endometrial cancer is the most common gynecological cancer diagnosis in developed countries. Personalized treatments for these cancers depend on identification of prognostic and predictive biomarkers that allow stratification of patients. The aldo-keto reductase (AKR) superfamily is getting attention in cancer research, because of AKR’s involvements in important biochemical processes. The enzyme AKR1C3 has many functions, which include production of prostaglandins, androgens, estrogens, and metabolism of different chemotherapeutics. AKR1C3 is thus implicated in the pathophysiology of different cancers. Methodology In our study, we evaluated the immunohistochemical (IHC) staining of AKR1C3 in 123 paraffin-embedded samples of endometrial cancer and statistically examined possible correlations between expression of AKR1C3 and clinicopathological data (survival, stage of disease, lymphovascular invasion, menopausal status, parous status, smoking, use of hormone replacement therapy). Result(s)* In endometrioid endometrial carcinoma, high AKR1C3 IHC expression correlated with better overall survival (p = 0.008) and with disease-free survival (p = 0.027). Significantly higher percentages of positive epithelial cells were seen for adjacent nonneoplastic endometrium compared to endometrioid endometrial cancer (p = 1 × 10−4). Conclusion* These results demonstrate the potential use of AKR1C3 as an independent prognostic biomarker in endometrioid endometrial cancer. Clinically, this might mean that levels of AKR1C3 in endometrioid endometrial cancer could be determined preoperatively on diagnostic tissue samples to allow prediction of the cancer behavior and stratification of the patients for more personalized treatments. Disclosures Conflicts of Interest The authors declare no conflict of interest. Study was supported by the grants J3-2535 to T.L.R. from the Slovenian Research Agency. Ethical Issues The study was approved by the National Medical Ethics Committee of the Republic of Slovenia (0120-701/2017-6). |
