Abstract
Aim The purpose of this study was to investigate the role of PTEN, PAX2 and PINCH protein expressions in endometrial carcinogenesis.MethodsIn this study 27 proliferative endometrium, 24 complex atypical hyperplasia, 10 complex hyperplasia without atypia, 30 simple hyperplasia without atypia, and 89 endometrioid type endometrial adenocarcinoma cases were enrolled. PTEN, PAX2 and PINCH antibodies were applied immunohistochemically to these cases.Results Results of immunohistochemical staining revealed that during progression from normal to malignancy, staining distribution and intensity of both PTEN and PAX2 were found to decrease significantly. Expression of PINCH, on the other hand, was found to be increased distinctly during progression from normal to malignancy which correlated reversely with PAX2 and PTEN expressions. When PTEN, PAX2 and PINCH expressions in endometrioid adenocarcinoma cases were compared with common histopathologic prognostic parameters, a relation between histopathologic grade, angiolymphatic invasion, lymph node metastasis, stage, myometrial invasion and involvement of corpus cervix margin was not detected.Conclusion In conclusion, we suggest that the absence of PTEN and PAX2 expression seem to be associated with the progression of endometrioid carcinomas. Expression of PINCH, on the other hand, was found to be increased distinctly during progression from normal to malignancy. Further studies are necessary to define the biological role of PTEN, PAX2, and PINCH. PTEN, PAX2, and PINCH may have prognostic importance and predictive value for targeted therapies. Those expression profiles of biomarkers might also be expected to identify those patients with endometrial hyperplasia who are at risk of developing carcinoma.
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How to Cite This Article
Esra Karakuş, Özlem Erdem, Çağatay Taşkıran, Anıl Onan, Resul Karakuş. PTEN, PAX2 and PINCH protein expression in normal endometrium, endometrial hyperplasia, and endometrioid adenocarcinomas. J Clin Anal Med 2018;9(2):133-137. doi:10.4328/JCAM.5606
Publication History
- Received:
- 09.12.2017
- Accepted:
- 01.01.2018
- Published Online:
- 05.01.2018
- Printed:
- 01.03.2018