Background & objective: A new candidate tumor suppressor gene, called phosphatase and tension homology deleted on chromosome ten (PTEN), was the first gene that was found to be phospholipase tumor suppressor gene. Loss of PTEN function by mutation or other mechanisms is closely related to tumorigenesis and progression of multiple carcinomas. This study was designed to investigate the expression of PTEN in carcinogenesis and development of endometrium carcinoma.
Methods: The expression of PTEN were detected by reverse transcription polymerase chain reaction (RT-PCR) for 24 cases with endometrial carcinoma, 10 cases with endometrial atypical hyperplasia, 10 cases with endometrial hyperplasia,and 10 cases with normal endometrium and by SP immunohistochemical methods for 73 cases with endometrial carcinoma, 25 cases with endometrial atypical hyperplasia, 71 cases with endometrial hyperplasia,and 31 cases with normal endometrium. The results were compared with clinical parameters (histological classification, differentiation, depth of myometrium invasion, and clinical stage).
Results: PTEN expression levels of both RNA and protein in patients with endometrial carcinoma and endometrial atypical hyperplasia were significantly lower than those in patients with endometrial hyperplasia and normal endometrium. mRNA relative values were 0.35+/-0.13, 0.46+/-0.11, 2.32+/-0.32, and 2.45+/-0.51, respectively. Loss of PTEN expression rates were 66.67% (38/57), 76.00% (19/25), 5.63% (4/71), and 0 (0/31), respectively. Loss of PTEN expression in patients with endometrial carcinoma was significantly related to histological classification (P< 0.0001) and differentiation (P=0.0349). It was not related to depth of myometrium invasion and clinical stage(P >0.05).
Conclusion: Loss of PTEN expression is an early event in endometrial tumorigenesis. Detection of PTEN protein may be a diagnostic biomarker for the earliest endometrial precancers and adenocarcinoma.