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Estradiol binding and metabolism in human endometrial hyperplasia and adenocarcinoma.
Authors:E Gurpide  S B Gusberg  L Tseng
Affiliation:1. Profamilia, Santo Domingo 10401, Dominican Republic;2. Center for Biomedical Research, Population Council, New York, NY 10065, USA;3. Instituto Chileno de Medicina Reproductiva, Santiago 8320165, Chile;4. Department of Obstetrics/Gynecology, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA;5. Wake Forest University School of Medicine, Winston-Salem, NC 27103, USA;1. Department of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, Saudi Arabia;2. Department of Clinical Laboratory Sciences, College of Applied Medical Science, King Khalid University, Abha, Saudi Arabia;3. Department of Clinical Laboratory Science, College of Applied Medical Science, University of Hail, Hail 2440, Saudi Arabia;4. Molecular Diagnostic and Personalised Therapeutics Unit, University of Hail, Hail 2440, Saudi Arabia;1. University of Medicine and Pharmacy at Ho Chi Minh City, 217 Hong Bang Street, District 5, Ho Chi Minh City, Vietnam;2. IVFMD, My Duc Hospital, 4 Duong Nui Thanh, Phuong 13, Tan Binh, Ho Chi Minh City, Vietnam;3. HOPE Research Center, 4 Nui Thanh Street, Ward 13, Tan Binh District, Ho Chi Minh City, Vietnam;4. Laboratory of Reproductive Biology, The Copenhagen University Hospital and Faculty of Health Science, Copenhagen University, Blegdamsvej 3B, 2200 København, Copenhagen, Denmark;5. The Fertility Clinic, Skive Regional Hospital, Øster Fælled Vej 5, Skive 7800, Denmark;6. Faculty of Health, Aarhus University, Denmark and Faculty of Health, University of Southern Denmark, Nordre Ringgade 1, Aarhus C 8000, Denmark
Abstract:The levels of estradiol receptors (E2R), estimated from the amounts of E2 tightly bound to nuclei after incubation of tissue with excess [3H]-E2, were high in normal proliferative endometrium and postmenopausal hyperplasia. Postmenopausal adenocarcinoma, well- or poorly-differentiated, showed lower levels in untreated patients and higher in patients who had taken Premarin. Significantly lower values were found in normal secretory endometrium and premenopausal adenocarcinoma, likely due to progestational effects. A decline in E2R levels was seen after administration of Provera to postmenopausal patients with endometrial cancer.The E217β dehydrogenase (E2DH) activities, estimated from the rate of conversion of [3H]-E2 to [3H]-estrone under substrate and NAD saturating conditions, were low in all specimens of hyperplastic and neoplastic endometrium from postmenopausal patients. These levels correspond to those of normal proliferative or postmenopausal tissue. Higher levels, typical of normal secretory endometrium, were found in the premenopausal, well-differentiated adenocarcinoma analyzed. Provera treatment of patients with endometrial carcinoma increased the levels of E2DH.The E2R and E2DH levels observed in patients with endometrial cancer can be explained on the basis of the hormonal environment of the tissue at the time of sampling (e.g., relative proportion of E2 and progesterone) without postulating drastically altered binding and metabolism of E2 in abnormal endometrium.
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