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Regular Article TA |
a Department of Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Science Park Research Division, Smithville, Texas 78957
b Laboratory of Women's Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709
ABSTRACT
Uterine leiomyomas are responsive to the ovarian steroids, estrogen and progesterone; however, a mechanistic understanding of the role of these hormones in the development of this common gynecologic lesion remains to be elucidated. We have used the Eker rat uterine leiomyoma model to investigate how ovarian hormones regulate or promote the growth of these tumors. Proliferative and apoptotic rates were quantitated in normal uterine tissues and leiomyomas in response to endogenous ovarian steroids. In 2- to 4-mo-old animals, cell proliferation in the normal uterus corresponded with high serum levels of steroid hormones during the estrous cycle, and apoptosis occurred in the rat uterus in all cell types following sharp, cyclical declines in serum hormone levels. It is interesting that the responsiveness of uterine mesenchymal cells changed between 4 and 6 mo of age, with significant decreases in both proliferative and apoptotic rates observed in myometrial and stromal cells of cycling animals. Leiomyomas displayed much higher levels of proliferation than did age-matched myometrium; however, their apoptotic index was significantly decreased in comparison with normal myometrium. This disregulation between proliferative and apoptotic responses, which were tightly regulated during ovarian cycling in the normal myometrium, may contribute to the disruption of tissue homeostasis and underlie neoplastic growth of these tumors.
First decision: 18 February 2000.
1 Supported in part by grants CA72253, ES08263, and CA16672 from the National Institutes of Health; and grant ES07784 from the National Institute of Health Sciences.
2 Correspondence: Cheryl L. Walker, Department of Carcinogenesis, U.T.M.D. Anderson Cancer Center Science Park Research Division, Park Road 1C, Smithville, TX 78957. FAX: 512 237 2475; cwalker{at}odin.mdacc.tmc.edu
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