Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00691 (EE2)
 7,802 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol and testosterone levels in the peripheral and ovarian circulation of patients with endometrial cancer and of postmenopausal women were studied. These levels proved to be the same in the two groups. The ovaries of neither group secreted estradiol. The testosterone level in the ovarian circulation of all examined women was four times higher than that in the peripheral circulation, thus indicating the ovarian origin of testosterone.
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PMID:Estradiol and testosterone levels in the peripheral and ovarian circulations in patients with endometrial cancer. 49 50

The menopause is centered on the ovary and its in-built obsolescence. The events of the menopause start when the active ovary begins to fail and end when the ovary lapses into inactivity. The duration of these events is variable. Stimulated by the pituitary, 1 follicle develops each month as a hormone-producing organ. The life span of the follicle is then 28 days. Follicles continue to develop unt il none respond to the stimulus of the pituitary. The 32-week fetus has about 7 million primordial follicles. At birth, the number has dropped to 2 million. By puberty only 300,000 3008000 remain. During adult life about 400 follicles will have provided the ova and the hormones. The last few capable of funtion may have poor endocrine function. Ovarian activity is controlled by a "biological clock" in the hypothalamus. This controls the pituitary by a gonadotropin-releasing h ormone. In response the pituitary secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH). The creation of the corpus luteum follows in the ovary and secretes progesterone while estrogen secretion continues. A cyclic drop in pituitary gonadotropin secretions causes the corpus luteum to degenerate. The ovary makes estrogen from cholesterol, converting it to pregnenolone, then to progesterone which is androstenedione to andnostenedione and on to estradiol. Estradiol is the estrogen secreted by the ovary, but it can be changed in the liver t o estrone and estriol. The pathways of the steroid hormone synthesis are the same in the adrenal cortex. When estrogen deficiency occurs in the menopause LH levels increase. Later the FSH is raised and remains high for the rest of life. This raised FSH and low estrogen levels appear to cause the characteristic hot flashes. Abrupt deprivation of estrogen causes more symptoms than a slow decline of function. Estrogen therapy may relieve these symptoms. Prevalence of coronary thrombosis rises sharply in the postmenopausal years. Estrogen-containing pills increase the incidence of venous thrombosis. Estrogen therapy reverses the atrophy of the genital tract. Cycles of treatment imitate the normal action of the functioning ovary but usually are not large enough to promote menstruation. Endometrial cancer appears to be increased by estrogen therapy. It may be that the addition of progesterone would protect against this from of cancer. The adjustment of tissues to an altered hormonal environment and the unrelated changes of aging make complicated problem.
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PMID:The menopause: the events of the menopause. 95 89

The aim of this study was to overtake the mechanism of the control system in endometrial cancer cell line in vitro. Ishikawa cell (IK cell) and HEC-1 cell (HEC cell) derived from endometrial cancers were cultured with serum free medium (SFM-101). IK cell possessed Estrogen receptor (ER), Progesterone receptor (PR), Epidermal growth factor (EGF) and its receptor (EGFR). HEC cell had PR, EGF, and EGFR, however HEC cell did not keep ER. EGF stimulated the growth of IK cell, but the growth of HEC cell was not stimulated by EGF. S phase cells were increased by EGF in IK cell, but were not increased by EGF in HEC cell. The growth of IK cell was stimulated significantly by EGF and Estradiol-17 beta (E2) +EGF than control. However, E2+EGF did not stimulate the growth of IK cell than EGF significantly. Danazol (D) and D+EGF inhibited the growth of IK cell significantly than control. S phase cells were decreased by the treatment of D and D+EGF. From our results, EGF stimulated the growth of ER positive endometrial cancer cell, but EGF did not stimulate ER negative endometrial cancer cell. E2+EGF and EGF stimulated the growth of IK cell as a same. However, D inhibited the growth of IK cell that was stimulated by EGF.
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PMID:[Cell cycle analysis of endometrial cancer cells in vitro treated with growth factor and steroid hormone]. 130

While antiestrogens are useful agents in the treatment of breast cancer, the usefulness of these agents in the treatment of endometrial cancer remains controversial. There is some concern that the currently available antiestrogens may have partial agonist activity in uterine tissue. To better understand the mechanisms by which estrogens and antiestrogens modulate growth of endometrial adenocarcinoma cells, we have compared the effects of 17-beta estradiol and three antiestrogens, 4-hydroxytamoxifen (OH-TAM), ICI 164384, and LY 117018 on proliferation and transforming growth factor (TGF) mRNA accumulation in two human endometrial adenocarcinoma cell lines. In HEC-50 cells, neither estradiol nor anti-estrogens had any effect on cell proliferation or TGF mRNA abundance under estrogen-depleted culture conditions [basal medium containing 1% twice charcoal-treated fetal bovine serum (ctFBS)] or in the presence of estrogen (basal medium containing 5% fetal bovine serum). At very high concentrations, both estradiol and OH-TAM caused a small decrease in HEC-50 cell proliferation in medium containing 5% serum. In contrast, the antiestrogens had different effects on Ishikawa cells, depending upon the culture conditions. In medium containing 5% fetal bovine serum, the antiestrogens inhibited cell proliferation and significantly decreased TGF-alpha mRNA abundance and TGF-alpha secretion. OH-TAM was more potent than the other antiestrogens. Under these culture conditions, estradiol had no effect on cell proliferation or TGF-alpha mRNA levels but increased TGF-alpha secretion. In medium supplemented with 1% ctFBS, estradiol increased cell proliferation and TGF-alpha mRNA (2.72-fold, P less than 0.005) and TGF-alpha secretion (700 +/- 156 versus 250 +/- 23 pg/10(6) cells/24 h, P less than 0.05), whereas OH-TAM, which also stimulated cell proliferation, reduced TGF-alpha mRNA abundance (P less than 0.05) but had no significant effect on TGF-alpha secretion. Under these conditions, ICI 164384 and LY 117018 had no effect on either cell proliferation or TGF-alpha expression. Estradiol treatment decreased, whereas OH-TAM increased, epidermal growth factor receptors in Ishikawa cells. Both estradiol and the antiestrogens decreased TGF-beta 1 mRNA abundance when cells were grown in media containing 1% ctFBS. In summary, the response of human endometrial adenocarcinoma cells to estrogen and antiestrogens varied between cell lines and was dependent upon the culture conditions used. In addition, OH-TAM, unlike the other two antiestrogens tested, had growth-stimulating effects on Ishikawa cells.
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PMID:Differential effects of estrogen and antiestrogen on transforming growth factor gene expression in endometrial adenocarcinoma cells. 155 Nov

To prevent hyperplasia and carcinoma of the endometrium during Estrogen Replacement Therapy (ERT), addition of progestogens once a month is considered mandatory. There is, however, no good scientific basis for this assumption. Since the addition of progestogens has several disadvantages, it is important to minimise the frequency of progestogen addition. Vaginosonography is a rather new technique, which has not yet been used for monitoring ERT. This study uses the growth of the endometrium, as it was measured by vaginosonography, as a parameter for stimulation of the endometrium by estrogens. ERT with Estraderm 50 twice a week was started in postmenopausal women. The endometrial thickness at the beginning was less than 3 millimeters. During estrogen treatment the endometrial thickness was determined every 6 to 10 weeks. As long as there was little or no increase during the estrogen treatment, no progestogen was added. Where there was a considerable growth, progestogen was added. With the use of vaginosonography, it is possible, to distinguish "fast growers" (women whose endometrium responded fast) from "slow growers".
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PMID:[Endometrial growth in continuous, estrogen substitution monotherapy with Estraderm TTS (0.05 mg/die) in 31 postmenopausal females]. 163 98

In a study carried out in Germany between 1985-89 unintended pregnancy was found in 7.9% of girls aged 15-21 in 1985 and in 5.2% in 1989. A study of 2905 young people aged 14-18 in Austria indicated that 75% of girls and 55% of boys had sexual intercourse by age 18 making contraception vital for adolescents. Among oral contraceptives (OCs) micropills with 20 mcg ethinyl estradiol barely affect the follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels, but the gestagen component can induce bleeding, spotting, and breast symptoms. Discontinuation quickly restores the normal connection of the hypophysis and ovary without affecting later pregnancy. 5.1 years after the end of high-dose combination OC use for 9-46 months only 3 out of 13 women did not become pregnant. OCs reduce bleeding disorders, anemia, and dysmenorrhea, ovarian cancer, and endometrial cancer. Their effect on breast cancer is not clear. Phenobarbital and rifampicin accelerate OC metabolism, and OCs reduce the effect of anticonvulsives and tolbutamide (for hypoglycemia). Neogynon and Stediril D are postcoital pills used within 48 hours of intercourse. IUDs are not recommended, as adnexal infection is 1.5-2 times higher in girls 14018 using IUDs. The effectiveness of the diaphragm and condom depend on motivation; creams and vaginal sponges are useful but they may cause irritation. The Billings method produced only a 2.9 Pearl-index reliability in 7000 cycles, thus natural methods often fail. Before age 14 girls must have parental consent for prescription of OCs, after 14 the physician is not liable for OC prescription, but induced abortion still requires parental consent until age 18.
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PMID:[Contraception in adolescents]. 174 70

Estrone sulfate (E1-S) in the serum and tissues of patients with breast cancer or endometrial cancer was measured by a direct radioimmunoassay without hydrolysis. The concentration of E1-S in breast cancer tissue was 1.64 +/- 0.28 ng/g wet wt (+/- SE), lower than in surrounding normal breast tissue (4.46 +/- 1.23). Estradiol-17 beta(E2)/E1-S was higher in endometrial cancer tissue than normal endometrial tissue. Estrone sulfatase activity in breast cancer tissue was 0.81 +/- 0.23 nmol/h/mg protein, higher than in surrounding normal breast tissue (0.35 +/- 0.11). These results suggest that E1-S, which is abundant in the peripheral circulation, is hydrolyzed by sulfatase in breast cancer tissue or endometrial cancer tissue and liberates free estrogens, which may stimulate the growth of these malignant tumors.
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PMID:Estrone sulfate and sulfatase activity in human breast cancer and endometrial cancer. 255 48

Estradiol receptors of plasma membranes (PM), PM lipids, the activity of membrane-bound enzymes and plasma levels of hormones have been tested in patients of postmenopausal ages with various endometrial diseases (glandular fibrous and glandular cystic polyps, highly, moderately and poorly differentiated adenocarcinomas). Test findings were similar in patients with the glandular cystic polyps and poorly and moderately differentiated adenocarcinomas. Therefore, the patients with the glandular cystic endometrial polyps are at high risk of endometrial cancer. Since the risk increases with higher estrogen plasma levels, the patients with proliferative endometrial conditions may benefit from intake of antiestrogens.
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PMID:[The estrogen receptors of the endometrial plasma membranes in proliferative processes in the postmenopause]. 262 27

Studies of hormonal growth regulation in cultured human endometrial cancer cells are limited by the requirement of exogenous growth factors, usually supplied by addition of serum. The present report provides evidence that estradiol can stimulate proliferation of endometrial cancer cells of the Ishikawa line in the absence of serum or added growth factors. Mitogenic effects of estrogen were demonstrated in two different experimental systems, in cells attached to the substratum of mammalian tissue culture dishes, and in cells forming colonies in soft agar under anchorage-independent conditions. Addition of estradiol to a mixture of serum-free, phenol red-free Dulbecco's minimal essential medium and Ham's F-12 medium, supplemented with L-glutamine and 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid [basal medium: (BM)] significantly increased the proliferation of cells attached to culture dishes. Dose-response experiments revealed maximal estradiol stimulation at 10 nM; significant responses were also observed at 1 nM and at 100 nM concentrations. The mitogenic effect of 10 nM estradiol was comparable to that of 1% charcoal-treated fetal bovine serum and the two effects were additive. The presence of estradiol in serum-free BM resulted in a shortening of the doubling time of exponentially proliferating cells from 38 to 29 h. From the labeling index, measured after exposure to a pulse of [3H]thymidine, and from the mitotic index, both determined in exponentially proliferating cells, the lengths of the S and M phases were calculated to be 11 and 1 h, respectively. From these data it was estimated that estradiol shortened the G1 phase by approximately 40%, from 22 to 13 h. Estradiol doubled the colony formation efficiency of cells plated in BM containing 0.3% agar in the absence of serum as well as in the presence of 1% charcoal-treated fetal bovine serum. The stimulation of colony formation by estradiol was influenced by medium components, since no effects were observed in minimal essential medium. The colony formation efficiency was positively related to the serum concentrations and remained significantly lower in minimal essential medium than in BM at comparable serum levels. The observed positive relationship between colony formation efficiency and cell densities at plating suggests a cooperative mitogenic effect, likely due to autocrine and paracrine action of secreted growth factors. These results define a model to evaluate hormonal growth regulation mediated by autocrine mitogens in human endometrial cancer cells in the absence of interfering exogenous growth factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Proliferation and responsiveness to estrogen of human endometrial cancer cells under serum-free culture conditions. 272 Jun 84

The Authors studied the concentration of cytosolic and nuclear receptor for Estradiol and Progesterone in endometrial hyperplasia and carcinoma, compared with a control group. Comparative study of hormone receptor concentrations in different populations shows: 1) A significant increase in Estradiol receptors in endometrial hyperplasia (p less than 0.01); 2) A decreasing concentration of estradiol receptors with the decreasing of cellular differentiation in endometrial carcinoma (p less than 0.01); 3) A similar tendency and significance for Progesterone receptors; 4) For both receptors the tendency in the nuclear compartment is similar to that in cytosol but the significance is smaller (p less than 0.05).
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PMID:Hormonal receptors in endometrial neoplasias. 297 93


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