ArticleTurkish journal of obstetrics and gynecology2026
Differential expression of c-kit, E-cadherin, and beta-catenin in endometriosis and normal endometrial tissue.
Article in Turkish journal of obstetrics and gynecology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: C-kit, E-cadherin and beta-catenin adhesion molecules and proto-oncogenes are thought to be associated with molecular mechanisms related to the invasion, implantation and persistence of ectopic endometrial cells. Comparing the expression levels of these molecules in endometriomas, other types of endometriosis, and normal endometrial tissue may provide further insight into the mechanisms driving endometriosis development. The present study sought to examine the molecular pathophysiological roles of these molecules by determining their expression profiles in different types of endometriosis and in the healthy endometrium. Materials and Methods: Retrospective data from 180 cases were analyzed, comprising 60 endometriomas, 60 cases of other types of endometriosis (superficial and deep), and 60 normal proliferative endometrial tissue samples. Immunohistochemical staining for c-kit, E-cadherin, and beta-catenin was performed. The expression levels of E-cadherin and beta-catenin were quantified using the H-score method. Results: C-kit positivity was found in 9% of endometriomas and 10% of other endometriosis tissues, but was absent in normal endometrium. Beta-catenin H-scores were significantly lower in endometriosis tissues compared with normal endometrial tissues (p<0.001). E-cadherin levels showed no significant difference between the groups. A post-hoc power analysis confirmed that the study was adequately powered to detect group differences in E-cadherin, indicating that the non-significant finding likely reflects a true absence of a difference. Conclusion: Increased c-kit expression, along with reduced beta-catenin expression in endometriosis samples, suggests that these molecules contribute to endometriosis pathogenesis. However, because no significant difference was found in E-cadherin expression, a definitive conclusion cannot be made regarding the involvement of E-cadherin in endometriosis development.
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