OBJECTIVE

To explore the expression of beta-catenin, Glut-1, PTEN in uterine endometrioid adenocarcinoma and their roles in tumorigenesis.

METHODS

A total of 83 cases of endometrial hyperplasia were selected and reclassified according to EIN diagnostic criteria. Expressions of beta-catenin, Glut-1 and PTEN proteins were investigated by immunohistochemistry in 10 proliferative endometrium, 83 endometrial hyperplasia and 24 endometrioid adenocarcinoma.

RESULTS

(1) 24 EIN (28.9%) lesions were reclassified among 83 previously diagnosed endometrial hyperplasia, of which, 16 of 24 EIN cases (66.7%) had a prior diagnosis of complex atypical hyperplasia. The relation between EIN diagnosis and grade of atypical hyperplasia was not obvious (P > 0.05). (2) Normal (membranous) expression of beta-catenin was present in 10 cases of proliferative endometrium. Abnormal (marked membranous/cytoplasmic, cytoplasmic and/or nuclear or negative) expression rates of beta-catenin in EIN lesions (50%, 12/24) and endometrioid adenocarcinoma (66.7%, 16/24) were significantly higher than that of benign hyperplasia (10.2%, 6/59) respectively (P < 0.01). However, the difference was not significant between EIN lesions and endometrioid adenocarcinomas (P > 0.05). (3) Low level expressions of Glut-1 was present in proliferative endometrium and benign hyperplasia. Overexpression of Glut-1 was present in 58.3% (14/24) of EIN and 70.8% (17/24) of endometrioid adenocarcinoma, respectively, and statistically not significant (P > 0.05). (4) Percentages of loss of PTEN expression showed no difference between EIN lesions (37.5%, 9/24) and proliferative endometrium (2/10), benign hyperplasia (28.8%, 17/59), endometrioid adenocarcinoma (62.5%, 15/24; P > 0.05). However, loss of PTEN expression in endometrioid adenocarcinoma was significantly higher than those in proliferative endometrium and benign hyperplasia (P < 0.05).

CONCLUSIONS

Abnormal expression of beta-catenin and overexpression of Glut-1 may be the early events in tumorigenesis of endometrioid adenocarcinoma. The expression of both markers may be useful in distinguishing a benign hyperplasia from EIN and endometrioid adenocarcinoma. Lack of PTEN expression may be the earliest event in endometrial carcinogenesis. However, it can not be used yet as a diagnostic marker for the EIN lesion.