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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen replacement therapy is effective for the prevention and treatment of postmenopausal osteoporosis and should be offered to all women at high risk for osteoporosis. Such therapy is particularly beneficial for prevention of spinal compression fractures; in addition, it alleviates menopausal symptoms (hot flushes, genitourinary symptoms, and changes in mood). In each patient, these benefits must be weighted against the potential risks of endometrial hyperplasia and carcinoma, breast tenderness, hypertension, vascular headaches, and the inconvenience of menstrual bleeding if the uterus is intact. The risk of endometrial cancer associated with estrogen replacement therapy can be considerably reduced by the addition of a progestin, and other side effects can be diminished or eliminated by use of the new transdermal estrogen preparations. Thus, estrogen replacement therapy should be considered in all women who have experienced natural or surgically induced menopause, and it is advisable in women who have osteoporosis or an increased risk for this disorder and no contra-indications to its use. Estrogen replacement therapy should be instituted as soon after menopause as possible and seems to be well tolerated until at least 75 years of age.
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PMID:Estrogen replacement therapy: current recommendations. 328 71

The joint effect of risk factors on endometrial cancer was examined by applying general statistical models to the data of a hospital-based case-control study conducted in Copenhagen, Denmark. The analysis included 149 cases of histologically confirmed adenocarcinoma of the endometrium and 154 age-matched controls with cervical cancer. Information on risk factors derived from the medical records. Estrogen use and body mass were found to be the main predictors of endometrial cancer risk. In the model proposed, women who ever used non-contraceptive estrogens had a 10-fold increased risk irrespective of their weight and height. Among non-users of estrogen, the risk of endometrial cancer rose with increasing body mass, the largest showing a five-fold increased risk. These data provide further evidence of the significant role that excess estrogens play, whether exogenous from replacement therapy or endogenous from enhanced androgen conversion, in the etiology of endometrial cancer.
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PMID:The joint effect of risk factors on endometrial cancer. 335 5

Symptoms due to estrogen deficiency begin in the perimenopausal years and progress as serum levels of this hormone decrease Vasomotor instability, manifested by hot flushes or night sweats, may persist for several months to a few years. Psychologic symptoms include anxiety, tension, depression, insomnia, palpitations, and headaches. Atrophy of the genital epithelium may result in senile vaginitis with symptoms of irritation, burning, pruritus, dyspareunia, and even vaginal bleeding. Even the lower urinary tract mucosa is dependent upon estrogen. Postmenopausal osteoporosis affects 25 to 50% of older women and increases the risk for vertebral, hip, and other fractures. Estrogen therapy for menopausal complaints has received adverse publicity because several reports have indicated that unopposed estrogens increase the risk of endometrial cancer. Added progestogen not only negates this risk but reduces the incidence of endometrial adenocarcinoma in estrogen-progestogen users to less than that observed in untreated women. Estrogen replacement therapy does not increase the risk of breast cancer; the incidence of this malignancy, however, was also less in the estrogen-progestogen users when compared with either the untreated women or from that expected from the national cancer surveys. In evaluating postmenopausal women for hormone replacement, the benefits of estrogen-progestogen therapy must be weighed against possible risks.
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PMID:The menopause. 351 23

Unopposed estrogen replacement is known to cause endometrial carcinoma in a small percentage of postmenopausal women, but the effects on ovarian and breast tissue remain uncertain. The increased risk of endometrial carcinoma seems to be related to both the dosage and duration of unopposed estrogen treatment. Until very recently, the morbidity and costs that result from the need for endometrial biopsy because of abnormal bleeding and from the need for hysterectomy due to hyperplasia have been ignored, but recent data suggest that they are likely to be considerable. Progestogens are known to protect against endometrial hyperstimulation, but the optimal duration of therapy each month and the maximally protective agent and dose remain to be determined. Estrogen replacement therapy may reduce the risk of arterial disease; however, the comparative effects of the various preparations, as well as their respective mechanisms of action, must be subjected to further study.
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PMID:Controversies concerning the safety of estrogen replacement therapy. 355 93

Estrogen therapy for postmenopausal women has received adverse publicity since the mid-1970s because several reports implicated estrogens with an increased risk of endometrial cancer. Other studies indicated that the risk of endometrial malignancy is reduced when a progestogen is added to the estrogen. Not all postmenopausal women need estrogen replacement, since many are symptom free because they continue to produce endogenous estrogens. Within this group may be the women at greatest risk for adenocarcinoma of the endometrium. The progestogen challenge test was devised to identify women at greatest risk for endometrial cancer. The number of endometrial malignancies declined at Wilford Hall U.S. Air Force Medical Center with increasing use of this test from 1975 through 1983. The lowest incidence of endometrial cancer was observed in the estrogen-progestogen users (49.0 per 100,000) and was significantly lower than that found in either the unopposed estrogen users (390.6 per 100,000; p less than or equal to 0.0001) or in the untreated women (245.5 per 100,000; p less than or equal to 0.005). The incidence of breast cancer was also significantly lower in the estrogen-progestogen users (66.8 per 100,000) than in the untreated group (343.5 per 100,000) and lower than that expected from two national cancer surveys (188.3 and 229.2 per 100,000; p less than or equal to 0.01). Progestogens should be added to estrogen replacement therapy in women who have undergone a hysterectomy, as well as in those with an intact uterus.
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PMID:Use of progestogen therapy. 357 52

The analysis of compliance with hormonal replacement therapy in postmenopausal women must take into account the physician's knowledge of and willingness to prescribe such treatment and the patient's acceptance of the risks and benefits. Studies have shown that most women receiving oral therapy take their medication only sporadically, and those who discontinue treatment usually do so because of the fear of endometrial cancer. Both physicians and patients should be made aware that the addition of progestogen can greatly lessen this risk. Estrogen therapy has been shown to offer significant benefits, notably a reduction in the incidence of osteoporosis-related fractures. Epidemiologic models can be useful in showing both physicians and patients that hormonal treatment is safe and effective. Noncompliance, stemming from side effects or the problem of forgetting to take medications, can be improved through the use of the transdermal estrogen formulation. This product has been associated with excellent tolerability; local and systemic adverse reactions have been minimal, and any problems with unscheduled bleeding or hyperplasia can be circumvented through the addition of progestogens.
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PMID:Compliance with hormone therapy. 357 53

Estrogen replacement therapy (ERT) prevents fractures and relieves vasomotor symptoms, but it increases the risk of endometrial cancer. Previous studies and national prescribing patterns show that physicians are conservative in their approach to this therapy. The authors interviewed physicians and perimenopausal women to assess their utilities for the various health outcomes of estrogen replacement therapy. On all outcomes, physicians rated illness episodes followed by recovery as being closer to perfect health than did perimenopausal women. Physicians, in judging which outcomes were most important to women, estimated relief of symptoms above fracture prevention, whereas women rated fracture prevention above symptom relief. These results emphasize the need to assess patients' utilities directly, particularly when utilities for the outcome of a particular therapy may influence the choice of a therapeutic regimen.
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PMID:Women's and physicians' utilities for health outcomes in estrogen replacement therapy. 358 72

Estrogen-noncompatible antiestrogen binding sites (AEBS) as well as estrogen receptors (ER), and the growth-inhibitory effect of tamoxifen were investigated in two human endometrial cancer cell lines, IK-90 and HEC-IA cells. IK-90 cells contained specific AEBS, but no ER was found in these cells. Scatchard plot analysis of AEBS in 12,000 g supernatant from IK-90 cells showed a high affinity binding site for tamoxifen (Kd:5.6 +/- 1.0 nM) with the maximum binding site of 457 +/- 47 fmol/mg protein. However, no measurable ER or AEBS was found in HEC-IA cells. The effect of tamoxifen on the growth of cells was found to be identical in both cell lines; the addition of 10 microM tamoxifen to culture medium was cytocidal whereas tamoxifen at lower concentrations (1 nM-1 microM) did not significantly affect the growth of both IK-90 and HEC-IA cells. These results demonstrate for the first time the presence of AEBS in human endometrial cancer cells. The present results also suggest that AEBS does not play a fundamental role in mediating the growth-inhibitory effect of tamoxifen in endometrial cancer cells.
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PMID:Roles of antiestrogen binding sites in human endometrial cancer cells. 361 70

For examination of the effect of prior exogenous estrogen use on survival after diagnosis of endometrial cancer, 244 endometrial cancer cases newly diagnosed at North Carolina Memorial Hospital, Chapel Hill, North Carolina, between 1970 and 1976 were followed until 1982. Estrogen users (n = 46) were younger, had less advanced disease, and were more likely to be nonobese and white than were nonusers (n = 198). The estimated probability of surviving (Kaplan-Meier) five years after diagnosis was 0.89 for users and 0.53 for nonusers. When adjusted for age, grade, stage, obesity, race, and treatment (using the Cox proportional hazards regression model), the survival probabilities throughout the period of observation for estrogen users continued to be higher. The adjusted hazard rate for a nonuser was 2.05 (95% confidence interval (Cl) 0.96-4.39) times that for an estrogen user. The adjusted hazard rate from endometrial cancer only was 4.01 (95% Cl 1.22-13.21) times greater among estrogen nonusers. The more frequent occurrence of endometrial cancer in an earlier stage and grade among estrogen users may not be the sole cause of their lower hazard rate from this disease.
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PMID:The influence of exogenous estrogen use on survival after diagnosis of endometrial cancer. 366 33

Previously we demonstrated the polymorphism of estrogen receptors (ER) in cytosol of various tissues based upon properties of size, shape and surface charge. This study describes the application of a multidimensional approach utilizing HPLC for characterization of ER. Cytosols from human uterus and endometrial carcinomas were characterized sequentially by high performance size exclusion chromatography (HPSEC) on Spherogel TSK-3000 SW, and high performance ion-exchange chromatography (HPIEC) using SynChropak AX-1000 anion exchange columns. Using HPSEC, specific estrogen binding was exhibited by a 30 A isoform and by one appearing after the V0 (approximately 60 A) in human uterus. However, in endometrial carcinoma other smaller binding components with Stoke's radii of less than 20 A were observed also. In buffers containing 400 mM KCl, predominantly a 28-30 A species was observed by HPSEC. Further characterization of the 28-30 A isoform from low and high salt elution from HPSEC was accomplished with an AX-1000 column. With either condition, 2 forms were eluted on HPIEC, 1 in the column wash (retention time 8-9 min), and the other at 50-70 mM phosphate. The elution profile of the larger species (approximately 60 A by HPSEC) on the ion-exchange column was time dependent. Immediate analysis (within 15 min) showed a profile similar to that of the original cytosol which contained minor components eluting in wash buffer and at 50-70 mM phosphate and a major isoform at 180 mM phosphate. However delayed analysis (after 2 h) of the 60 A isoform showed a similar profile (components in buffer wash and at 50-70 mM phosphate) obtained with the 30 A species. This time dependent change was not observed for the 30 A species or for the original cytosol. Estrogen receptors in cytosol sedimented at 10S and 4S in low ionic strength gradients and at 4S in sucrose gradients containing 400 mM KCl. The 28-30 A and 60 A species recovered from HPSEC sedimented at 3.5S. This multidimensional approach indicates that native estrogen receptors dissociated into a number of smaller molecular isoforms, which were distinguishable by different surface charge properties.
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PMID:HPLC analysis of estrogen receptor by a multidimensional approach. 373 41


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