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Activation of mammalian target of rapamycin in postmenopausal ovarian endometriosis
  1. T. Yagyu*,
  2. Y. Tsuji,
  3. S. Haruta,
  4. T. Kitanaka,
  5. Y. Yamada,
  6. R. Kawaguchi,
  7. S. Kanayama,
  8. Y. Tanase,
  9. N. Kurita and
  10. H. Kobayashi
  1. *NetForce Co. Ltd., Nakamura, Nagoya, Aichi, Japan
  2. Department of Obstetrics and Gynecology, Nara Medical University, Kashihara, Nara, Japan
  3. Department of Knowledge-Based Information Engineering, Toyohashi University of Technology, Tempaku-cho, Toyohashi, Japan
  1. Address correspondence and reprint requests to: Hiroshi Kobayashi, MD, PhD, Department of Obstetrics and Gynecology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634–8522, Japan. E-mail: hirokoba{at}


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.

  • Akt
  • endometriosis
  • mTOR
  • ovarian cancer

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