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

A new human endometrial carcinoma cell line, designated OMC-2, was established from the endometrial adenocarcinoma of a 59-year-old woman. This cell line has grown well for 51 months and has been subcultured more than 50 times. Monolayer cultured cells are polygonal in shape, showing a pavement-like arrangement and a piling up tendency without contact inhibition. The chromosomal number shows aneuploidy and the modal chromosomal number is in the diploid range. The cells were transplanted into the subcutis of nude mice and produced tumors resembling the original tumor. 1 X 10(5) OMC-2 cells produced CA 125 (184-682 U) during 19 days in culture media. CA 125 was demonstrated immunohistochemically in the original tumor, heterotransplanted tumor, and OMC-2 cells. The cells contain no estrogen or progesterone receptors. Twenty-nine other reports of endometrial carcinoma cell lines are reviewed.
Asia Oceania J Obstet Gynaecol 1989 Dec
PMID:Establishment and characterization of CA 125 producing cell line (OMC-2) originating from a human endometrial adenocarcinoma. 262 81

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.
Akush Ginekol (Mosk) 1989 Dec
PMID:[The estrogen receptors of the endometrial plasma membranes in proliferative processes in the postmenopause]. 262 27

Thyroid cancer is well known to be hormone sensitive as well as breast cancer, prostatic cancer, and endometrial cancer of the uterus. Various experimental results suggest that the growth regulation for thyroid cancer, as well as the normal thyroid gland, appears to depend upon the TSH (Thyroid stimulating hormone) receptor on cell membranes. Differentiated thyroid carcinoma cells possess TSH receptor, although anaplastic carcinoma cells do not; therefore suppression therapy of TSH with thyroid hormone is considered to be effective against differentiated thyroid carcinoma. It has been recognized that some recurrent differentiated thyroid cancers cause regression in size in response to treatment with thyroid hormone. But the administration of the thyroid hormone after the operation for the differentiated thyroid carcinoma does not necessarily enhance the survival rate. To analyze the difference in survival rate is very difficult because of the excellent survival rate of thyroid cancer patients after the operation. It is hoped that further clinical study and laboratory investigation about suppression in adjuvant therapy for differentiated thyroid cancer will give us a conclusive answer.
Gan To Kagaku Ryoho 1989 Dec
PMID:[The effect of thyroid hormone on the growth of thyroid cancer]. 268 57

Unopposed estrogen stimulates mitotic activity in endometrial and breast tissue. Numerous case-control studies have evaluated the relationship between estrogen use and the risk of endometrial and breast cancers. In general, exogenous, unopposed estrogen use increases the risk of endometrial cancer by tenfold and of breast cancer by twofold after long-term use of high doses. Estrogen's positive effects on osteoporosis and coronary heart disease must be considered when evaluating the potential risks associated with its use in postmenopausal women.
Am J Obstet Gynecol 1989 Dec
PMID:The cancer question: an overview of recent epidemiologic and retrospective data. 269 Jun 39

The goal of contemporary hormone replacement is to minimize net predictable lifetime risk; success therefore depends upon quantitative assessments of the net quality of life, of net morbidity and of net mortality. Estrogens ameliorate menopausal symptoms, maintain bone integrity, and produce endometrial cancer; these facts and their quantitative aspects can be stimulated. Other links are gradually becoming clear: estrogens increase biliary disease, but prevent heart disease, and, it now seems, stroke. Conventional wisdom to the contrary notwithstanding, a critical review suggests that breast cancer is probably increased in frequency by long-term estrogen use; the increase is modest as a risk factor but because breast cancer is a common disease, it is substantial in absolute terms. The addition of progestin seems attractive as a method of opposing undesirable estrogenic effects on the endometrium. In fact, there is reason for concern about the effect of an added progestin upon the risks from breast cancer, heart disease, and stroke; even the magnitude of the expected reduction in endometrial cancer may not be great when the hormone is administered sequentially. Using a simple deterministic model of post-menopausal life with hormone replacement, we have inserted available estimates of the regimen-specific relative risk for each outcome, and translated each net impact into common denominators of morbidity and mortality. While estrogens probably increase net morbidity, as measured by either the number of hospitalizations to be anticipated or by the more arbitrary measure of expected days of disability, these negative changes are mostly due to gallbladder disease and endometrial cancer, both largely treatable conditions. Largely because of protection against heart disease, estrogen replacement in modest dose is likely to reduce substantially the number of deaths to be expected in women treated through age 75 and even into more advanced age. Hormone replacement which includes systemic progestin supplementation has not been empirically tested; it may be beneficial, but it is at least as likely to be harmful. Either a modest increment in the number of additional breast cancers produced by estrogens, a modest reduction in the number of cardiac events prevented by estrogens, or a simultaneous minor shift in the same direction for each condition, would have the effect of shifting the net reduction in cumulative deaths into an increase in the number of deaths as a result of treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
Schweiz Med Wochenschr 1989 Dec 16
PMID:Risks and benefits of long-term treatment with estrogens. 269 47

Previous studies have suggested that alcoholic beverage consumption may lead to a decrease in a woman's oestrogen levels. It is possible that any such alcohol-associated decrease could lead to a decrease in endometrial cancer risk. To study the association between alcohol consumption and endometrial cancer, we examined data from the Cancer and Steroid Hormone Study, a multi-centre, population based, case-control study. A total of 351 women with primary epithelial endometrial cancer and 2247 women selected from the same geographical areas as the cases were interviewed for the study. As part of the interview, the participants provided information regarding their alcohol consumption during the preceding five years. Analysis of these data revealed that women who were non-drinkers had a risk of endometrial cancer of 1.83 relative to the risk of women who had consumed an average of 150 grams or more of alcohol per week (95% Cl, 1.11, 3.01). Women who drank, but who consumed less than 150 grams of alcohol per week, were at an intermediate risk. The increased risk associated with abstinence from alcohol consumption was particularly great in overweight women and was virtually absent in lean women. These results argue that alcohol ingestion may reduce a woman's risk of endometrial cancer, particularly if she is overweight.
Int J Epidemiol 1989 Dec
PMID:Alcoholic beverage consumption and the risk of endometrial cancer. Cancer and Steroid Hormone Study Group. 269 74

In recent years the incidence in endometrial cancer is rising. The relation of cervical to endometrial cancer has shifted to almost 1:1. The peak of age distribution is between 50 and 60 years of age. Accompanying diseases are obesity, diabetes and hypertension. The endometrial cancer has its precancerous stages. The pertinent estrogenic stimulus is probably significant for the development of precancerous lesions: adenomatous hyperplasia of the endometrium without atypias is known as an optional, that with atypia as an obligatory precancerous lesion. The range of morphologic variation extends from mature endometrial adenocarcinoma with favorable prognosis to immature neoplasias with unfavorable outcome. Besides various other parameters of neoplastic disease the depths of infiltration into the myometrium is known to be significant. The leading sign of endometrial cancer is uterine bleeding. The histological diagnosis is established by the examination of the tissue produced by curettage from the cervical canal and from the uterine cavity. A true early diagnosis--in comparison to the early detection of cervical cancer--does still not exist for endometrial cancer. Exfoliative cytology from the uterine cavity or ultrasonography does still not allow the final and definite diagnosis. Among the therapeutic alternatives abdominal hysterectomy in combination with bilateral adnexectomy plays the most important role. Depending from more specific morphologic criteria of a given case additional pelvic and paraaortic lymphnode-dissection is advised. Surgical therapy in general accounts for a 10 to 20 percent better survival. In patients who cannot surgically be treated because of the local extension of the tumor or due to a general high risk situation the primary therapy is pelvic irradiation both by packing and percutaneously. Disseminated neoplasms, adenocarcinomas in particular, respond well to large dosages of progestins, whereas combinations of cytostatics have failed to show favorable results, perhaps with the exception of those containing adriamycin. All endometrial cancer patients need special posttreatment care, because early recurrences still have a certain chance of survival when recognized and appropriately treated.
Ther Umsch 1989 Dec
PMID:[Precancerous conditions and cancer of the endometrium]. 269 33

In contrast to cancers of non-hormone-dependent sites, cancers of the breast, ovary and endometrium show a slowing down of the rate of increase in incidence at around age 50, as if ceasing menstrual activity reduced risk. Also nulliparous women appear more prone to these three cancers as compared to parous women, thus suggesting that pregnancies also represent a 'protected' time. Epidemiological studies on breast cancer, the only ones sufficiently large to try to disentangle meaningfully the effects of collinear reproductive variables such as parity and ages at first and last birth, show, however, that the effect of pregnancy is not simple and depends on how many births take place and at what age. Larger population-based investigations able to obtain with greater precision information not only on reproductive factors but also on possible confounding variables (e.g. socio-economic status, dietary habits, etc.) are mandatory, particularly as regards ovarian cancer and endometrial cancer. The lesson from the recent studies on pregnancy-related events and breast cancer is, however, that initially a decrease of old certainties must be expected to derive from the accumulation of new, better epidemiological data.
Eur J Cancer Clin Oncol 1989 Dec
PMID:Reproductive factors and cancers of the breast, ovary and endometrium. 269 9

This review focuses on the effects of oral contraceptives (OC) and estrogen replacement therapy (ERT) on the risk of breast, ovarian and endometrial cancer. The relationship between OC and cancer risk is first placed in a historical perspective. Since 1960, when OC were introduced, the hormonal composition of OC as well as the characteristics of the OC user have changed considerably. Studies conducted in the 1970s were generally reassuring, but it was not until the 1980s that studies could evaluate the effect of prolonged OC use after an extended follow-up period. Although the relationship between breast cancer and OC has been investigated in about 40 studies, the issue still remains essentially unresolved. Most studies report no association between ever use of OC and breast cancer risk. Several studies find increased risk for prolonged use and other studies report elevated risks for women who used OC very early in their reproductive years. The inconsistent results of recent studies are attributed to bias or to geographical variation in latency period elapsed, types of OC preparations, or prevalence of other risk factors. In contrast, the use of combined OC has consistently been shown to reduce the risk of ovarian and endometrial cancer. The risk further decreases with increasing duration of use and the protective effect seems to persist in ex-users for at least 5 years. Some evidence indicates that higher parity reduces the protective effect. Though studies relating ERT to breast cancer are far from consistent, overall, there is evidence for a moderately increased risk with high dose and/or long duration. The effect seems to be modified by mode of administration (injections vs. pills) and by type of ERT, but this needs confirmation. The number of adequate studies on the relationship between ERT and ovarian cancer is too small to draw firm conclusions. The positive relationship between ERT and endometrial cancer is now well established. The ERT effect is dose- and duration-dependent and is characterized by a short latency period. The cyclic addition of progesterone (greater than 10 days/cycle) may reduce the risk increase.
Eur J Cancer Clin Oncol 1989 Dec
PMID:The role of exogenous hormones in the epidemiology of breast, ovarian and endometrial cancer. 269 11

Previous epidemiological studies have demonstrated that obesity increases endometrial cancer risk two- to 10-fold. To test the hypothesis that abdominal adiposity further increases this relative risk, we conducted a nested case-control study of endometrial cancer incidence in a cohort of 41,873 women ages 55-69 years. Women were recruited by mail and asked to have a friend measure circumferences of several body parts using a tape measure and written instructions. Two-year follow-up for cancer incidence was conducted using a state-wide cancer registry. Compared to random controls (n = 1,274), cases (n = 63) had higher age-adjusted mean values of waist-to-hip circumference ratio (P = 0.10) and trunk-to-limb circumference ratio (waist plus hip circumferences divided by arm plus calf circumferences, P = 0.008). Other anthropometric variables, including current body mass index and current weight, were also greater (P less than 0.001) in cases than controls. After accounting for the association with body mass index, neither the waist-to-hip ratio nor the trunk-to-limb ratio remained associated with endometrial cancer incidence (P greater than 0.40). A 5 kg/m2 increase in body mass index was associated with an adjusted relative risk of endometrial cancer of 1.80 [95% CI = 1.46, 2.22] when other significant risk factors, namely age, education level, extended use of exogenous estrogens, and age at menopause, were taken into account. We conclude that endometrial cancer risk is increased in relation to the amount but not the distribution of adiposity. This is in contrast with several other diseases in which, in addition to overall body mass, the distribution of adiposity is also important.
Cancer Res 1989 Dec 01
PMID:Association of incident carcinoma of the endometrium with body weight and fat distribution in older women: early findings of the Iowa Women's Health Study. 281 22


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