Gonadotropin and steroid hormones stimulate proliferation of the rat ovarian surface epithelium

The ovarian surface epithelium (OSE) is a single layer of flattened or cuboidal cells covering the ovary. Ninety percent of all human ovarian malignancies arise from this layer of cells. Incessant ovulation, hyperovulation induced by infertility treatment, and hormone replacement therapy have been s...

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Veröffentlicht in:Journal of cellular physiology 2004-01, Vol.198 (1), p.119-124
Hauptverfasser: Stewart, Sherri L., Querec, Troy D., Gruver, Briana N., O'Hare, Brendan, Babb, James S., Patriotis, Christos
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container_end_page 124
container_issue 1
container_start_page 119
container_title Journal of cellular physiology
container_volume 198
creator Stewart, Sherri L.
Querec, Troy D.
Gruver, Briana N.
O'Hare, Brendan
Babb, James S.
Patriotis, Christos
description The ovarian surface epithelium (OSE) is a single layer of flattened or cuboidal cells covering the ovary. Ninety percent of all human ovarian malignancies arise from this layer of cells. Incessant ovulation, hyperovulation induced by infertility treatment, and hormone replacement therapy have been suggested as risk factors for ovarian cancer. In this study, two groups of rats, with and without surgically induced injury to the ovary, were treated with 17β‐estradiol, pregnant mare's serum gonadotropin (PMSG), human chorionic gonadotropin (hCG), or the combination PMSG/hCG, and the proliferative response of the OSE cells was measured using bromodeoxyuridne (BrdU) and 3H‐thymidine. All hormones, alone or in combination with ovarian surgery, were found to increase significantly the rate of proliferation of the rat OSE. These data demonstrate that hormones associated with infertility treatments and hormone replacement therapy, as well as injury‐ or ovulation‐induced rupture of the ovarian surface, stimulate the rat OSE, and hence could have a role in the development of ovarian cancer via proliferation‐associated mutagenesis, or alternatively, by promoting the rapid selection of OSE cells with accumulated mutations. J. Cell. Physiol. 198: 119–124, 2004. © 2003 Wiley‐Liss, Inc.
doi_str_mv 10.1002/jcp.10401
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Ninety percent of all human ovarian malignancies arise from this layer of cells. Incessant ovulation, hyperovulation induced by infertility treatment, and hormone replacement therapy have been suggested as risk factors for ovarian cancer. In this study, two groups of rats, with and without surgically induced injury to the ovary, were treated with 17β‐estradiol, pregnant mare's serum gonadotropin (PMSG), human chorionic gonadotropin (hCG), or the combination PMSG/hCG, and the proliferative response of the OSE cells was measured using bromodeoxyuridne (BrdU) and 3H‐thymidine. All hormones, alone or in combination with ovarian surgery, were found to increase significantly the rate of proliferation of the rat OSE. These data demonstrate that hormones associated with infertility treatments and hormone replacement therapy, as well as injury‐ or ovulation‐induced rupture of the ovarian surface, stimulate the rat OSE, and hence could have a role in the development of ovarian cancer via proliferation‐associated mutagenesis, or alternatively, by promoting the rapid selection of OSE cells with accumulated mutations. J. Cell. 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subjects Animals
Antimetabolites - metabolism
Bromodeoxyuridine - metabolism
Cell Division - physiology
Chorionic Gonadotropin - pharmacology
Epithelium - anatomy & histology
Epithelium - drug effects
Epithelium - physiology
Female
Gonadotropins, Equine - pharmacology
Humans
Ovary - anatomy & histology
Ovary - drug effects
Ovary - metabolism
Ovary - surgery
Rats
Rats, Sprague-Dawley
Thymidine - chemistry
Thymidine - metabolism
Tritium - chemistry
Tritium - metabolism
title Gonadotropin and steroid hormones stimulate proliferation of the rat ovarian surface epithelium
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