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Results for “Estrogens--indications”

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At least 19 recordsLinked to original sources

Increased peptidylarginine deiminase expression during induction of prolactin biosynthesis in a growth-hormone-producing rat pituitary cell line, MtT/S.

Insulin and type I insulin-like growth factor (IGF-I) suppressed growth hormone (GH) expression followed by the induction of prolactin (PRL) biosynthesis in MtT/S cells cultured with normal sera. Insulin also increased the peptidylarginine deiminase activity in a dose-dependent manner. The increase was detectable at 1 ng/ml and reached a maximum (about 16-fold higher than the control) at 1 micrograms/ml. IGF-I showed similar but less prominent effects. The enzyme activity started to increase by 15 hr after the addition of insulin (500 ng/ml), and reached a plateau level at 48 hr. There were concurrent increases in the enzyme mRNA level, enzyme biosynthesis, and enzyme protein contents detected by Northern blot hybridization, [35S]-amino-acid incorporation, and Western immunoblot analysis, respectively. Two-color immunofluorescence staining at 1 day after the insulin addition detected a small number of peptidylarginine-deiminase-positive cells (about 1% of the total cells) which were also GH-positive. The enzyme-positive cells increased to 12% on day 2 and to 24-26% on days 4-6. PRL-positive cells first appeared in the enzyme-positive cell population on day 2, and PRL-positive, enzyme-negative cells appeared later. These results suggest that peptidylarginine deiminase expression increases in association with the hormone switching in MtT/S cells. When the cells were cultured in a steroid-depleted medium, insulin failed to increase the enzyme activity. The insulin action could be specifically restored by estrogen, indicating estrogen-insulin synergism in regulation of the enzyme expression.

Animals↗

A risk-benefit analysis of elective bilateral oophorectomy: effect of changes in compliance with estrogen therapy on outcome.

A bilateral oophorectomy at the time of elective hysterectomy is often performed to prevent ovarian cancer. The assumption that endogenous estrogen can be easily replaced with supplemental medication fosters the decision for routine oophorectomy. Published reports on the use of postmenopausal estrogen indicate that compliance is less than perfect. This fact could affect the overall outcome. Decision analysis techniques with Markov cohort modeling were used to evaluate the policy of elective bilateral oophorectomy. Results from studies judged methodologically sound were combined to determine values representing the influence of estrogen on coronary heart disease, breast cancer, and osteoporotic fracture. The decision tree also explicitly incorporated patient compliance. When compliance with estrogen therapy is assumed to be perfect, oophorectomy yields longer life expectancy than retaining the ovaries. When actual drug-taking behavior is considered, retaining the ovaries results in longer survival. This analysis highlights the importance of including the effects of patient compliance with treatment recommendations when the impact of a health policy decision such as prophylactic surgery is assessed.

Adult↗

Management of cavernous hemangioma of the liver.

Cavernous hemangioma of the liver was diagnosed in 12 of 60 patients (20 percent) evaluated for surgery of neoplastic liver disease. All were female, from 29 to 77 years old. Six patients presented with abdominal pain and seven had taken estrogens. Indications for surgery included uncertain diagnosis, symptoms, large lesion greater than or equal to 6 cm, and hypoproliferative anemia. Three right lobectomies, one left lateral segmentectomy, one open biopsy, and one right trisegmentectomy were performed. There were no deaths, one subphrenic abscess, and one bile leak. The remaining seven patients were observed and at 2 to 6 years post operatively had followed a benign course. Resectional therapy may be considered for superficial large or symptomatic lesions in the appropriate patient, but most hepatic hemangiomas follow a benign course.

Adult↗

Overexpression and hormonal regulation of pro-cathepsin D in mammary and endometrial cancer.

Pro-cathepsin D is overexpressed in breast cancer cells compared to normal mammary epithelial cells. Moreover, its processing and maturation are altered resulting in increased secretion. In estrogen-responsive breast cancer cell lines such as MCF7 cells and ZR75-1 cells, the 2.2-kb cathepsin D mRNA is accumulated specifically by estrogens and growth factors. Estrogen regulation is mostly transcriptional, while growth factors stabilize the mRNA and act indirectly. In estrogen-receptor-negative cell lines, there is a constitutive high production of cathepsin D mRNA. Moreover in uterine cells, progesterone is the inducer rather than estrogen, indicating the complexity of regulation by steroids, depending on the tissue. The increased production of cathepsin D appears to be correlated with the aggressiveness of the tumour, as shown by retrospective clinical studies, suggesting a role in mammary carcinogenesis.

Breast↗

Estrogen regulation of Xenopus laevis gamma-fibrinogen gene expression.

Albumin gene expression in Xenopus is regulated by estrogen through changes in the stability of its mRNA. The goal of the present study was to determine whether a similar pathway regulates gamma-fibrinogen. Degenerate oligonucleotides directed to conserved regions of the carboxyl-terminal half (domain D) of human and lamprey gamma-fibrinogen were used to isolate a full-length cDNA clone for Xenopus gamma-fibrinogen. Analysis of codon utilization from the DNA sequence of this clone revealed that Xenopus gamma-fibrinogen mRNA shows the same bias against CG dinucleotides as present in human, but not lamprey, fibrinogen mRNA. Features of the protein shared with the human homologue include all of the cysteine residues, an N-linked glycosylation site at amino acid 50, and 75% sequence identity in domain D. Much of the same region is conserved in lamprey gamma-fibrinogen. There is only a single size mRNA encoding gamma-fibrinogen in Xenopus, unlike rats where two mRNAs of different length are generated by alternate splicing. Administration of estrogen to male Xenopus results in the disappearance of gamma-fibrinogen mRNA from the cytoplasm, with no effect on steady-state levels in the nucleus. This process can be blocked by prior treatment with anti-estrogen, indicating that, like the regulation of serum albumin mRNA, gamma-fibrinogen is regulated posttranscriptionally through an estrogen receptor dependent mechanism. It is postulated that a consensus sequence flanking the AAUAAA polyadenylation signal in gamma-fibrinogen and the 68- and 74-kDa albumin mRNAs, but not vitellogenin or beta-globin mRNA, may play a role in the hormonal regulation of mRNA stability.

Amino Acid Sequence↗

Activation of estrogen receptor transfected into a receptor-negative breast cancer cell line decreases the metastatic and invasive potential of the cells.

Breast cancers containing estrogen receptors are responsive to antiestrogen treatment and have a better prognosis than estrogen receptor-negative tumors. The loss of estrogen and progesterone receptors appears to be associated with a progression to less-differentiated tumors. We transfected the human estrogen receptor into the estrogen receptor-negative metastatic breast cancer cell line MDA-MB-231 in an attempt to restore their sensitivity to antiestrogens. Two stable sublines of MDA-MB-231 cells (HC1 and HE5) expressing functional estrogen receptors were studied for their ability to grow and invade in vitro and to metastasize in athymic nude mice. The number and size of lung metastases developed by these two sublines in ovariectomized nude mice was not markedly altered by tamoxifen but was inhibited 3-fold by estradiol. Estradiol also significantly inhibited in vitro cell proliferation of these sublines and their invasiveness in Matrigel, a reconstituted basement membrane, whereas the antiestrogens 4-hydroxytamoxifen and ICI 164,384 reversed these effects. These results show that estradiol inhibits the metastatic ability of estrogen receptor-negative breast cancer cells following transfection with the estrogen receptor, whereas estrogen receptor-positive breast cancers are stimulated by estrogen, indicating that factors other than the estrogen receptor are involved in progression toward hormone independence. Reactivation or transfer of the estrogen receptor gene can therefore be considered as therapeutic approaches to hormone-independent cancers.

Animals↗

Study on reproductive endocrinology of human placenta (II)--Hormone secreting activity of cytotrophoblast cells.

The capability of cytotrophoblast cells to produce hCG, progesterone, estrogen, cGnRH and beta-endorphin in vitro has been demonstrated in serum-free culture medium. Before experiment, a 24-h preculture was carried out in order to remove the endogenous hormones of the tissue. During a period of 8 days' culture, the cytotrophoblast cells could constantly produce a small amount of hCG. The production of progesterone rose rapidly and became doubled within six days. The estrogen secretion showed a similar pattern in the presence of androstenedione, a precursor of estrogen, indicating the elevation of aromatase activity in the cells. The elevation of the enzyme activity has been further demonstrated not to be induced by androstenedione. In both cytotrophoblast and syncytiotrophoblast cell cultures, cGnRH was only detected in the culture of cytotrophoblast cells, with a value up to 4 pg/10(5) cells/24 h. However, beta-endorphin was identified both in cytotrophoblast and syncytiotrophoblast cells. Its content increased significantly in the medium of cytotrophoblast cell culture from the 4th to 6th days, but declined in the medium of syncytiotrophoblast cell culture. The results demonstrate clearly that the cytotrophoblast cells are the sole origin of GnRH in human placenta and are also able to synthesize beta-endorphin and steroid hormones. The findings indicate that there is no such a sharp functional demarcation existing between these two kinds of trophoblast cells as suggested before. The data are of significance for a better understanding of the mechanism of hormonal regulation in placenta.

Chorionic Gonadotropin↗

Estrogen therapy for severe persistent depressions in women.

Positive results are reported from a double-blind study of estrogen therapy administered to severely depressed, inpatient women who had failed to respond to various conventional treatments of depression. Large doses of oral conjugated estrogen were administered for a three-month period to 23 premenopausal and postmenopausal inpatient women. Placebos were administered for a comparable period to 17 similar patients. The posttreatment Hamilton ratings of depression were significantly reduced in the estrogen-treated group, but not in the placebo group. Possible physiological mechanisms are discussed. The risk-benefit ratio for estrogen therapy of depression in these patients was judged to be favorable. However, periodic endometrial biopsies are required to monitor the endometrial response of women receiving high doses of estrogens.

Adult↗

Effects of long-term estrogen replacement therapy. I. Metabolic effects.

Two groups of hypoestrogenic women are analyzed by retrospective comparisons. Patients were observed by a single group of physicians for at least five years; 301 patients were treated with replacement estrogen and 309 patients were untreated. Incidence figures for various metabolic diseases present at entry and both during and after estrogen therapy were compared by the usual statistical analysis and by statistical adjustments for certain group differences (Mantel-Haenszel statistic). The long-term administration of estrogen to these relatively young women with hypoestrogenism was associated with significantly lower rates of development of cardiovascular disease, hypertension, osteoporosis, and fractures. Detrimental effects were a higher rate of abnormal uterine bleeding and an increase in the likelihood of developing adenocarcinoma of the endometrium. Effects of estrogen preparation, dosage, method of therapy, duration of therapy, and the addition of synthetic progestins are presented.

Adenocarcinoma↗

Effects of long-term estrogen replacement therapy. II. Neoplasia.

Two groups of hypoestrogenic women are analyzed by retrospective comparison. Patients were observed by a single group of physicians for at least five years -- 301 patients treated with replacement estrogen and 309 untreated patients. Of each group, 207 women had uteri in situ. Incidence figures for neoplasia (gynecologic, breast, and all sites) were compared between the two groups and with the Third National Cancer Survey, yielding a risk ratio for the development of adenocarcinoma of the endometrium among estrogen-treated women of 3.8 and 9.3, respectively. There was no increase among any other malignancies. The addition of synthetic progestin to estrogen therapy provided significant protection against the likelihood of developing endometrial cancer and did not reduce previously reported metabolic benefits of estrogen treatment. Data pertaining to estrogen use and details of the patients with endometrial carcinoma are presented.

Adenocarcinoma↗

Mestranol.

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Animals↗

Estrogen therapy.

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Adolescent↗