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

The cytologic diagnosis of endometrial cancer using material obtained with the Endocyte endometrial sampler was assessed for 874 patients. The samples obtained were smeared directly on slides for fixation and staining; the smears were more difficult to assess than cervicovaginal smears, however, due to the presence of blood, the small size and density of the cells and the flattened three-dimensional architecture of the tissue fragments obtained. Only 8.2% of the samples were classified as inadequate; repeat sampling in some of those cases produced diagnostic material. All 12 cases of carcinoma (including one case in a woman less than 40 years of age) were diagnosed by cytology as malignant; however, the original cytologic sample in one of those cases was inadequate. For the diagnosis of benign versus malignant, cytology had a sensitivity of 92%, a specificity of 100% and predictive value of 100%. Cytology also diagnosed as suspicious the smears from 5 of 13 cases of endometrial hyperplasia and 2 of the 9 cases of endometrial polyps. The cytologic findings for benign and malignant samples are described and illustrated in detail. Relative to other endometrial sampling devices, the Endocyte is inexpensive and was easily used by the gynecologist and well tolerated by the patients, with no complications and minimal discomfort.
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PMID:Endocyte endometrial smears in the cytodiagnosis of endometrial carcinoma. 234 95

Much evidence has been suggested that cystic, adenomatous, and atypical hyperplasia as well as adenocarcinoma in situ of the endometrium may ultimately progress to invasive cancer. Consequently, these lesions should be considered to be precursors of endometrial cancer. Twelve postmenopausal and three perimenopausal women with vaginal bleeding due to endometrial hyperplasia received 400 mg/d of danazol orally for 3 months. After 15 to 30 days of continuous danazol therapy, the endometrial glands ceased to grow and became smaller and rounder. The lumina of glands were narrow and contained no secretion. The nucleic mitosis of the glands disappeared. All women showed regression of hyperplastic endometrium within 2 to 3 months of initial treatment. In the 15 cases treated, endometrial hyperplasia could be controlled successfully with danazol without further recurrence and/or progression of the disease. In summary, danazol should be an effective and safe alternative therapy to progesterone for the treatment of endometrial hyperplasia.
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PMID:Clinical effects of danazol on endometrial hyperplasia in menopausal and postmenopausal women. 238 26

For patients with previous endometrial cancer, ERT is not the accepted practice in the U.S. The therapeutic dictum that estrogen is contraindicated in patients with previous uterine adenocarcinoma is, however, not substantiated by clinical data. The relation of unopposed estrogen stimulation to endometrial hyperplasia and carcinoma, and the published studies relating ERT to endometrial cancer, have resulted in the clinical perception--and cautionary statements to that effect--that estrogen is contraindicated for patients with a history of endometrial carcinoma. The exact biologic effects of ERT on endometrial adenocarcinoma have not yet been studied adequately, however; the initial clinical data suggest that there is no increase in recurrence or mortality. In the meantime, the clinician is left with contradictory data as a basis for determining the proper management of symptomatic patients. The total impact of estrogen deficiency on the health of women and the ratio of benefits and risks of ERT are yet to be defined completely. The preponderance of evidence suggests that estrogen has a beneficial effect on the major cause of death in women, coronary heart disease, by increasing the high-density lipoprotein (HDL) fraction of cholesterol. It is established that estrogen prevents the demineralization of bone and delays the ravages of osteoporosis. No one has died from vaginal atrophy, bladder dysfunction, or hot flashes; the quality of life and marriage have been improved, however, by relieving these symptomatic conditions with ERT. Several studies have attempted to analyze with various statistical models the ratio of benefits to risks, and the majority of authors have concluded that the beneficial effect on cardiovascular disease alone clearly outweighs any known risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estrogen-replacement therapy in patients with previous endometrial carcinoma. 240 7

As to endometrial cancer and endometrial hyperplasia, this study represents the localizations of the placental proteins and the tumor-associated antigens by both immunohistochemical light microscopy (ILM) and immunoelectron microscopy (IEM). The reagents examined include human placental lactogen (HPL), placental alkaline phosphatase (PAP), pregnancy-associated plasma protein A (PAPP-A), pregnancy-specific beta 1-glycoprotein (SP1), alpha 1-anti-trypsin (alpha-AT), and tissue polypeptide antigen (TPA). The tumor cells stained for HPL are localized and the SP1-positive cancer cells are almost entirely restricted to an infiltrating front. alpha-AT is shown in both tumor cells with marked cellular atypism and ones in deeply infiltrating foci. The immunoreactive frequency for the above six reagents in endometrial cancer is higher than that in endometrial hyperplasia. In endometrial cancer, the high frequency of an immunoreaction is confirmed in TPA (p less than 0.05). The combined stainings, i.e. either for TPA and SP1 or for TPA and PAPP-A, are efficient immunohistochemical screening methods to use in diagnosing endometrial cancer in the biopsied specimens (p less than 0.05).
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PMID:Immunohistochemical localization of placental proteins and tumor-associated antigens in endometrial cancer and endometrial hyperplasia. 244 80

The use of megestrol acetate in treatment of malignancy (endometrial carcinoma, ovarian cancer, prostate cancer, breast cancer, renal cell carcinoma, malignant melanoma), endometrial hyperplasia, benign prostatic hypertrophy, contraception, anorexia, cachexia and weight loss is reviewed, concluding with a toxicity profile. Megestrol acetate was introduced in 1971 for treatment of endometrial carcinoma. Megestrol acetate is probably effective in proportion to the number of cytoplasmic progesterone receptors, but it has not been tested in a Phase III trial. For ovarian cancer it has been reported to be effective in 1 trail at doses of 800 mg/day. Prostate cancer, although difficult to assess, responds to megestrol acetate at doses of 120 mg/day because of its suppression of gonadotropins, its inhibition of 5alpha-reductase and its binding to the dihydrotestosterone receptor. Megestrol acetate permits a lower dose of diethylstilbestrol, and thus lower toxicity. There is apparently a dose-response between megestrol acetate and breast cancer, along with a response dependent on the number and type of estrogen and progestin receptors. Responses are better in postmenopausal women, and additive with other agents such as tamoxifen and mitomycin C. The medium duration of effect is 6-8 months. It has no effect on renal cancer or malignant melanoma. Megestrol acetate can be considered as an effective medical alternative to surgery for endometrial hyperplasia or benign prostatic hypertrophy. As a contraceptive in inhibits sperm transport rather than ovulation, but also causes irregular bleeding. Megestrol acetate has few side effects, and has the advantage of stimulating appetite and weight gain, a benefit in cancer patients.
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PMID:Megestrol acetate: clinical experience. 247 90

In order to achieve the long-term benefits from hormone replacement therapy of a markedly reduced incidence of heart disease and osteoporosis, a high degree of compliance is essential. In an effort to obtain high compliance, it was decided to introduce a cyclic therapy of 6 months duration using conjugated oestrogens supported by a 10-day course of progestogens. A total of 85 patients were treated prospectively. Compliance was assessed by the number of patients continuing treatment, and endometrial response was assessed by office biopsy and cytological or histological examination. Five patients withdrew, giving an overall compliance rate of 94%. Two have subsequently resumed therapy, thus 98% of those enrolled are currently receiving hormone replacement therapy. No cases of endometrial carcinoma were detected during the trial period of 4 years. Two cases of mild atypical endometrial hyperplasia were detected but both were mild and reverted to secretory or inactive endometrium following progestogen therapy. This regimen provides a viable alternative for those women who are troubled by progestogenic side-effects and monthly withdrawal bleeding.
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PMID:An alternative regimen of hormone replacement therapy to improve patient compliance. 256 74

Estrogen therapy for postmenopausal women has received adverse publicity since the mid-1970s because several reports linked 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 replacement. Not all postmenopausal women need estrogen replacement. Because some continue to produce significant amounts of endogenous estrogens, many need progestogen replacement to reduce the risk for endometrial hyperplasia and adenocarcinoma. It has been well demonstrated that estrogen replacement therapy does not increase the risk for breast cancer. However, added progestogen may actually reduce the risk for this malignancy in some women. Where estrogen therapy retards the development of and helps to prevent osteoporosis, added progestogen may restore bone which has been lost by promoting new bone formation. The greatest benefit to accrue to postmenopausal estrogen users is prevention of cardiovascular disease. Concern has been expressed that added progestogen may negate this benefit by adverse effects on lipids. Side effects of added progestogen occur, but these may be managed by changing to another progestogen or adding a mild diuretic.
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PMID:Use of progestogens in postmenopausal women. 257 91

This review of endometrial cancer summarizes the demographic characteristics of patients with the disease, their hormonal risk factors related to endogenous and exogenous estrogens and medical history, and other risk factors. Endometrial cancer increased in incidence in the US in the early 1970s, but then declined again in the last 2 decades. Possible reasons are classification including estrogen- induced hyperplasia, but also increased use of exogenous estrogens primarily in post-menopausal women, who are the predominant victims. Postmenopausal estrogen usage decreased at the same time. The highest incidence occurs in Polynesian women, although US Caucasians have more endometrial cancer then Blacks or European women. Endometrial cancer is common in women with estrogen-secreting ovarian cancer. Women with polycystic ovaries, where the steroid androstenedione is secreted and converted to estrone in peripheral tissues, but progesterone is lacking, are higher risk for endometrial hyperplasia and cancer. Obese women are also at risk (estimated 20-fold), as they have low sex binding globulin and higher estrogen levels. Any exogenous estrogen, by any route, even if stopped for a week per month confers higher risk for endometrial cancer, as shown by virtually all case control studies. Very little data exists on the actual effect of taking progestins with postmenopausal estrogens. These tumors are less invasive, more differentiated, and often detected earlier than non-estrogen dependent endometrial cancers. Other putative risk factors, e.g., diabetes, hypertension, gall bladder disease, radiation exposure, and family history of breast cancer have no solid evidence for association. Smoking, however, is associated with a lower risk of endometrial cancer.
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PMID:Epidemiology of endometrial cancer. 257 97

Strong immunoreactivity with polyclonal S-100 protein antisera and monoclonal S-100 alpha subunit antiserum was found in glandular cells of the decidua basalis and cervical polyps during early pregnancy. Immunoreactive S-100 protein was negative in glandular cells of the endometrium and cervix of nonpregnant women. It was also negative in endometrial hyperplasia and endometrial carcinoma. While the function of S-100 protein is not known, a relationship between humoral factors related to pregnancy and expression of S-100 protein gene is suggested by the results of this study.
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PMID:S-100 protein in glands within decidua and cervical glands during early pregnancy. 259 51

Endometrial carcinoma found in patients younger than 50 years of age were analyzed clinicopathologically in comparison with those of other age groups. The results were 1) Out of 150 patients with endometrial carcinoma, 44 (29.3%) were diagnosed in those younger than 50 years of age and 17(11.3%) were under the age of 40. The average age of endometrial cancer was 53.6 years and that of atypical endometrial hyperplasia was 49.2. 2) The majority of these patients (93.4%) had ever complained of vaginal bleeding, whereas those younger than 40 years of age had in 82.4%. 3) History of irregular menstrual cycle was only observed in 25.6% of the patients with the age 50 or older, whereas it was complained of in 61.5% of those among forties and in 56.3% of those younger than 40. 4) Nulliparity was found in 19.8% among 50 and older, whereas 70.4% and 64.7% were seen respectively in those among forties and younger than 40. 5) Hypertension was found more frequently in older patients, but diabetes mellitus and obesity did not correlate with age. 6) Seventy cases (46.7%) has history of receiving screening for cervical cancer without detecting endometrial cancer. 7) Well differentiated adenocarcinoma (G1) and adenoacanthoma was observed frequently in younger age group. Endometrial hyperplasia was often combined with cancer in young women. Having the data above mentioned, importance of screening for endometrial cancer in younger women is discussed.
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PMID:[Clinicopathological analysis of endometrial carcinoma in young women]. 261 74


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