PT  - JOURNAL ARTICLE
AU  - Yagyu, T.
AU  - Tsuji, Y.
AU  - Haruta, S.
AU  - Kitanaka, T.
AU  - Yamada, Y.
AU  - Kawaguchi, R.
AU  - Kanayama, S.
AU  - Tanase, Y.
AU  - Kurita, N.
AU  - Kobayashi, H.
TI  - Activation of mammalian target of rapamycin in postmenopausal ovarian endometriosis
AID  - 10.1136/ijgc-00009577-200607000-00008
DP  - 2006 Jul 01
TA  - International Journal of Gynecologic Cancer
PG  - 1545--1551
VI  - 16
IP  - 4
4099  - http://ijgc.bmj.com/content/16/4/1545.short
4100  - http://ijgc.bmj.com/content/16/4/1545.full
SO  - Int J Gynecol Cancer2006 Jul 01; 16
AB  - The purpose of this study was to determine whether Akt and mammalian target of rapamycin (mTOR), downstream targets of phosphatidylinositol 3-kinase, are activated in endometriosis and ovarian cancer specimens. We measured total and phosphorylated levels of Akt and mTOR from 17 frozen ovarian cancers and 15 benign endometriosis specimens (nine from premenopausal women and six from postmenopausal women) by quantitation of signals from western blots using antibodies against these proteins. Elevated phospho-Akt was detected in ovarian cancer versus endometriosis specimens from premenopausal women and endometriosis specimens from postmenopausal women (2.3 ± 0.45 versus 0.10 ± 0.06 and 0.17 ± 0.11; P < 0.05) when the western blot signal of activated kinase was normalized to total kinase levels. Elevated phospho-mTOR was detected in ovarian cancer and postmenopausal endometriosis versus premenopausal endometriosis (0.52 ± 0.19 and 0.46 ± 0.29 versus 0.13 ± 0.08; P < 0.05). Expression of total kinases (normalized to β-actin) was higher in carcinoma versus endometriosis specimens. Elevation of the active mTOR was specifically detected in postmenopausal endometriosis.