Akademik Veri Yönetim Sistemi
Bratislava Medical Journal, 2026 (SCI-Expanded, Scopus)
Background: Endometriosis is a hormonally responsive inflammatory disease with a recognized association with certain ovarian cancer subtypes. Gonadotropins are widely used in assisted reproductive technologies; however, their direct molecular effects on endometriotic tissue remain insufficiently characterized. Objective: This study aimed to investigate the effects of gonadotropin treatment on molecular markers potentially associated with early carcinogenesis-related processes in endometriotic lesions, using a surgically induced rat model. Methods: Twenty-two female Wistar Albino rats underwent surgical induction of endometriosis via autologous peritoneal implantation. The animals were randomly assigned to two groups: a control group receiving saline and a treatment group receiving gonadotropin (2 IU/kg/day) for 14 days. Following treatment, endometriotic lesions were excised and analyzed histologically and immunohistochemically for phosphatase and tensin homolog (PTEN), tumor protein 53 (TP53), and tumor necrosis factor-alpha (TNF-α) expression. Statistical analyses were performed using the Mann–Whitney U test based on non-parametric data distribution. Results: Histopathological evaluation revealed no significant morphological differences between the groups. However, quantitative immunohistochemical analysis demonstrated that gonadotropin-treated rats exhibited markedly decreased PTEN (p < 0.001) and TP53 (p = 0.001) expression, alongside a significant increase in TNF-α expression (p = 0.035) compared with controls (Table 1, Figs. 5, 6). These alterations reflect early molecular changes involving tumor suppressor gene downregulation and pro-inflammatory cytokine upregulation. Conclusion: These findings suggest that gonadotropin exposure may induce early molecular alterations in endometriotic tissue. Further translational and clinical studies are warranted to validate these findings in human populations.