The tumor suppressor PTEN acts as a lipid phosphatase, regulates the phosph
atidylinositol 3-kinase (PI3K)/Akt-signaling pathway, and modulates cell cy
cle progression and cell survival. Somatic mutations of PTEN have been repo
rted in a variety of cancers, especially in endometrial carcinoma. To clari
fy whether and how PTEN and the PI3K/Akt pathway relates to endometrial car
cinoma, we examined the expression of those pathway-related proteins in pat
ients with endometrial carcinoma. Of 103 endometrial carcinomas, 37 (36%) s
howed negative immunohistochemical staining of PTEN, Western blotting revea
led that the expression of PTEN in PTEN-negative cases was significantly lo
wer compared with that in positive cases. In contrast, phospho-Akt level in
negative cases was significantly higher. We found a significant inverse co
rrelation between PTEN and phospho-Akt (r = -0.796), The expression of phos
pho-Bad was greater in negative cases, suggesting that Bad might be a targe
t for Akt. The present study demonstrates the phosphorylation of Akt accomp
anied by the loss of PTEN in clinical specimens of endometrial carcinomas.