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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

An overview of the risk of developing cancer related to oral contraceptive (o.c.) use is presented. A committee of experts affiliated with WHO studied the problem of developing cancer related to o.c. use. O.c. use for more than 2 years prevents the formation of benign breast tumors, even after discontinuing o.c. use. The effect is due to the progestin component. There is no clear indication that o.c. use increases the risk of breast cancer. A higher risk of endometrial cancer is associated with sequential preparation use, but not with the use of combination preparations. Cervical neoplasms and pituitary adenoma may be more frequent among predisposed women who use o.c.s. Studies show a reduced risk of ovarian cancer with o.c. use, but more studies are necessary. There is a marked increase in the relative risk of developing hepatocellular adenoma among women who use o.c.s for longer than 3 years. The risk increases with the hormone dosage, the duration of treatment, and the age of the patient. There is no reliable data to indicate that the risk of malignant melanoma increases with o.c. use. More study is needed to determine the possible cancer risks of injection preparations. Combination preparations can cause an increased risk of vaginal epithelial metaplasia. Diethylstilbestrol taken during early pregnancy can cause vaginal neoplasms in the offspring. More epidemiological studies and clinical and laboratory studies on the carcinogenic effects of o.c.s and the endocrinological effects of o.c.s on younger women should be undertaken. It is recommended that o.c.s with the lowest possible hormone dosages be used. O.c.s should not be prescribed to women with vaginal adenosis.
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PMID:[Oral contraceptives and the risk of neoplasms]. 44 57

Estrogen and/or progestin administration to postmenopausal women with primary hyperparathyroidism lowers serum calcium. We measured cytosolic estrogen receptors (ER) and progesterone receptors (PR) by classical hormone-receptor binding techniques in parathyroid tissue removed from 10 men and 20 women, and ER by immunocytochemistry in tissue from an additional one man and seven women in order to ascertain whether these agents might exert a direct effect upon tissue responsible for hyperparathyroidism. ER were negative (< 3.1 fmol bound estradiol/10 mg tissue) in all 8 adenomas and 4 of 5 secondary hyperplasias removed from men, and from women in 19 of 22 adenomas, 2 of 3 secondary hyperplasias, and 3 of 4 primary hyperplasias. PR were negative (< 10.1 fmol bound progesterone/10 mg tissue) in 7 of 8 adenomas and all 5 secondary hyperplasias removed from men, and from women in 20 of 22 adenomas, all 3 secondary hyperplasias, and all 4 primary hyperplasias. For immunocytochemical studies, quick-frozen specimens were analyzed with a monoclonal antibody (Abbott Laboratory) directed at nuclear ER. All eight samples--five adenoma and three primary hyperplasia--were negative. We conclude that abnormal human parathyroid tissues have nondetectable levels of ER and PR. It is unlikely that estrogen and progesterone exert a direct, ER, or PR-mediated effect upon parathyroid tissue.
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PMID:Measurement of estrogen and progesterone receptors in abnormal human parathyroid tissue. 145 37

Transforming growth factor-alpha (TGF alpha) has been localized to the anterior pituitary, specifically to the lactotroph and somatotroph cell populations, by our previous studies. Since pituitary lactotrophs are known to undergo growth in response to estrogens, we have used an estradiol-induced pituitary hyperplasia/adenoma model. Estradiol treatment resulted in induction of TGF alpha mRNA in anterior pituitary, evident by 48 h, preceding actual macroscopic growth, which attained a maximum greater than 500% by 12 weeks. This rapid effect of estradiol also enhanced PRL mRNA, but did not affect other species of mRNA encoding for proenkephalin, D2 receptor mRNA, or hexosaminidase-A. TGF alpha mRNA remained elevated for the duration of rapid pituitary growth. D2 receptor activation by its agonist bromocriptine resulted in marked attenuation of TGF alpha mRNA preceding regression of growth. Coadministration of bromocriptine with estradiol resulted in an involution of pituitary size, indicating the overriding influence of dopamine in spite of a continued estrogenic stimulus. Epidermal growth factor receptor mRNA was not affected by any of these manipulations, suggesting that the receptor was not coregulated in this tissue similarly to TGF alpha. Estradiol also induced uterine TGF alpha mRNA and marked growth of the organ, but TGF alpha in this location was not regulated by dopamine. These results indicate that TGF alpha in the anterior pituitary is rapidly induced by estrogen in a time course preceding the growth of the gland. Estrogen-induced TGF alpha is rapidly attenuated by D2 dopamine receptor activation and is accompanied by a regression of pituitary growth. Interaction between these opposing hormonal/transmitter responses will determine the growth potential of the anterior pituitary.
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PMID:Dopamine receptor activation inhibits estrogen-stimulated transforming growth factor-alpha gene expression and growth in anterior pituitary, but not in uterus. 153 40

Estrogen receptors (ER) in human gallbladders were examined immunohistochemically using a specific monoclonal antibody against human ER. ER immunoreactivity was positive in 6 (19.4%) of 31 cases of cholelithiasis, 6 (33.3%) of 18 cases of epithelial polyp, 14 (53.8%) of 26 cases of adenoma, and 26 (22.8%) of 114 cases of adenocarcinoma. ER immunoreactivity was located at the nucleus of the epithelium of both non-neoplastic and neoplastic tissues, although the number of ER-immunoreactive cells was small. There was no sex difference in the incidence of ER immunoreactivity. No significant difference in survival rates could be demonstrated between ER-positive and ER-negative carcinomas. Epithelial polyps, adenomas and carcinomas were divided into metaplastic type and non-metaplastic type based on the presence or absence of metaplastic changes for comparison of the incidence of ER immunoreactivity. The incidence of ER immunoreactivity in the metaplastic type was significantly higher than that in the non-metaplastic type. We conclude that ER are present in the gallbladder mucosa in various disease states and suggest that the presence of ER is related to metaplasia of the gallbladder mucosa.
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PMID:Immunohistochemical analysis of estrogen receptors in human gallbladder. 231 69

Clinical and laboratory evidence of an association of oral contraceptive (OC) use with the subsequent development of benign and malignant hepatobiliary neoplasia is growing. The authors present a case in which an adenoma within a large, multicentric anaplastic spindle cell carcinoma occurred in a woman with a long history of OC use. The patient, a 38-year-old gravida 2, para 2, was diagnosed following low-grade fevers and right upper quadrant pain. A partial hepatectomy was performed with no complications; however, a follow-up examination 2 months later revealed widespread intra-abdominal tumor recurrence histologically identical to the original tumor. Immunostaining for alpha 1 antitrypsin and keratin was strongly positive in tumor cells, indicating a biliary derivation. Electron microscopy indicated an epithelial derivation as well, including the presence of intracellular lumens, intermediary filaments, and numerous intercellular junctions. Estrogen and progesterone receptors were negative in the tumor. The tritiated thymidine labeling index was 5.05%, with an estimated potential doubling time of 11 days. This woman had no history of hepatitis, no family or personal history of neoplasms, and no known hepatotoxin exposure. The only medication used by the patient was Norlestrin, an OC containing 1 mg norethindrone and 50 mcg ethinyl estradiol that she had taken continuously for the past 8 years.
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PMID:Hepatic adenoma within a spindle cell carcinoma in a woman with a long history of oral contraceptives. 243 48

Mechanism of action, indications, side effects and contraindications of oral contraceptive agents (OCA) are reviewed. OCA can be divided into two groups: consecutive and combined agents. Combined OCA contain both estrogens and gestagens and are taken for 3 weeks, while consecutive OCA contain only estrogens and are taken for 2 weeks followed by 1 week of combined OCA until the onset of menstruation. Biological activity of synthetic gestagens is estimated by a dosage which results in a delay of menstruation by 2 weeks. Gestagens norethindrone and norethynodrel were shown to be equally effective, while ethinodiol diacetate and norgestrel were 15-30 times more effective. Estrogen component of OCA is represented by ethinyl estradiol or mestranol. Combined OCA are more effective than consecutive OCA; probability of undesirable pregnancy during administration of combined OCA does not exceed 0.2%. The most frequent side-effects of OCA include nausea, headache, uterine hemorrhage, and changes in libido. OCA can affect the endocrine and reproductive systems. Major endocrine effects of OCA include changes in the cortisol metabolism in the adrenal glands, increase in the level of thyroid-binding globulin in the thyroid gland, changes in the glucose metabolism in the pancreas, inhibition of the luteinizing hormone releasing hormone in the hypothalamus with simultaneous decrease in the production of pituitary gonadotropins and inhibition of the ovulation. The most serious side-effects of OCA include cholelithiasis, thrombophlebitis, thromboembolism, liver adenoma, and myocardial infarction. Absolute contraindications to the use of OCA include hypertension, hyperlipidemia, breast or endometrial cancer, pregnancy, cardio-vascular diseases, liver diseases, and kidney insufficiency.
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PMID:[Principles of the use of oral contraceptive preparations]. 307 80

In this preliminary study, we have determined the receptors in normal human prostatic tissue or from patients with benign prostatic hypertrophy and patients with prostatic cancer. A single point assay using a dextran-coated-charcoal treatment of cytosol is utilized. This method permits the elimination of endogenous steroids and is also useful when specimens are too small to provide the larger number of aliquots necessary for multiple steroid receptor analyses. The results are discussed in the light of several problems inherent to this assay. We conclude that adenoma-tissue contains more receptors than neoplasic tissues for the progesterones receptors but that there is no significant difference for the estrogen-receptor and the androgen-receptors. For all the adenoma tissues and some neoplasic tissues the level of the estrogen-receptors is always lower than the one for androgen-receptor which itself is lower than the one for progesterone-receptors. We think that the expression of the results as a ratio of two levels of steroid-receptors gives a better evaluation of the receptors. The ratios Progesterone-receptor Estrogen-receptor and Androgen-receptor/Estrogen-receptor are always greater than 1.5, except for some neoplasic tissues and we think that, as in breast tumors, there are perhaps two kinds of neoplastic tissues, one hormone-dependent, the other not.
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PMID:[Comparative study on the concentrations of steroid receptors in adenomatous and cancerous prostatic tissue]. 618 95

Aspects of the development, morphology, and estrogen binding capacity of mammary tumors in rats exposed prenatally to the synthetic estrogen, diethylstilbestrol (DES), and treated postnatally with 7,12-dimethylbenz(a)anthracene (DMBA) were analyzed as part of a project aimed at understanding the effects of transplacental exposure to DES on estrogen-sensitive tissues. Pregnant Sprague-Dawley rats were given injections of DES (total dose, 1.2 micrograms) or vehicle alone on Days 15 and 18 of gestation. All female offspring were given gastric intubations of DMBA, either a single 10-mg dose on Day 50 or two doses (10 mg each) on Days 50 and 57. Among rats treated postnatally with 10 mg of DMBA, the DES-exposed group had a significantly greater incidence of palpable mammary tumors than did the vehicle-exposed controls. In addition, there was an earlier time of appearance of palpable tumors in the DES-exposed group. When the data from rats treated postnatally with two 10-mg doses of DMBA were analyzed, there were no significant differences in palpable mammary tumor incidence or tumor latency between the DES-exposed and vehicle-exposed groups. When the pathology of the mammary tumors produced in rats treated with 10 mg of DMBA was analyzed, the DES-exposed group had a significantly higher proportion of benign tumors (fibroadenoma, adenoma, lobular hyperplasia) than adenocarcinomata compared to vehicle-exposed controls. Both exposure groups had similar numbers of nonpalpable mammary lesions discovered at necropsy. Estrogen binding capacities of representative adenocarcinomata did not differ significantly between the two prenatal exposure groups treated postnatally with 10 mg of DMBA. These results demonstrate the importance of the dose of the challenge carcinogen in revealing the effects of transplacental drug exposure and may have special significance for women who were exposed to DES in utero.
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PMID:Transplacental action of diethylstilbestrol on mammary carcinogenesis in female rats given one or two doses of 7,12-dimethylbenz(a)anthracene. 641 35

Estrogen affects the synthesis and release of several pituitary hormones. The estrogen receptor (ER), a member of the steroid hormone receptor family, is thought to mediate transcriptional effects in a cell-specific fashion. We investigated whether ER is expressed in specific hormone-producing cell types in the human pituitary and its adenomas. Pituitary adenomas (n = 34) were collected at the time of surgery, and normal glands were obtained from autopsy. Expression of ER messenger ribonucleic acid (mRNA) was determined by reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. ER was also localized with immunohistochemistry and protein extraction. By RT-PCR, ER mRNA was found in the nontumorous pituitary and in pituitary adenomas expressing only PRL, in those producing GH and PRL, and in adenomas expressing the gonadotropic hormones. No ER mRNA was detected in adenomas expressing only GH without PRL or gonadotropins, nor in tumors producing ACTH without PRL or gonadotropins. In situ hybridization was not as sensitive or specific as RT-PCR. Biochemical analysis performed on seven tumors that were positive for ER mRNA by RT-PCR detected ER protein in only one PRL adenoma and one oncocytoma and yielded negative or equivocal results in one PRL adenoma, three GH-PRL adenomas, and one null cell adenoma. ER protein was localized by immunohistochemistry in scattered cells of the nontumorous adenohypophysis and in a few PRL and gonadotroph adenomas. We conclude that ER expression, as determined by RT-PCR, correlates with the expression of PRL or gonadotropins; in contrast, ER mRNA was not detected in adenomas that express only GH or ACTH. These findings implicate ER as a cell-specific transcription factor that may regulate cytodifferentiation in the pituitary.
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PMID:Cell-specific expression of estrogen receptor in the human pituitary and its adenomas. 853 Jun 10


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