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

Proliferating tumor cells obtained from ovarian, mammary, and endometrial tumors in tissue culture were tested for the influence of proteohormones and steroid hormones on cellular DNA synthesis and cell growth. The gonadotropic hormones stimulated DNA synthesis of ovarian tumor cells by single administration, or in combination with cortisol, up to the 11-fold of the comparable controls. The hormone sensitivity of the cell lines was variable, resulting in individual reaction patterns. There was no correlation to the histological diagnosis of the primary tumors with respect to the grade of differentiation. The results suggest that ovarian tumor cells in tissue culture can maintain sensitivity to organotropic hormones. Compared to the ovarian carcinoma lines, mammary or endometrial tumor cells did not respond to a similar extent. Progesterone decreased DNA synthesis of endometrial carcinoma cells.
J Cancer Res Clin Oncol 1979 Jul 27
PMID:Hormone sensitivity of gynecological tumor cells in tissue culture. 47 69

A case-control study was undertaken of use of permanent and semipermanent hair dyes by women with cancers of several sites, including breast and endometrium. In London, Ontario, 50 cases of of breast cancer and in Toronto 35 cases of breast cancer and 36 cases of endometrial cancer were identified in cancer treatment centers. In London, controls were selected from hospitalized women with diseases other than cancer; in Toronto, controls were selected from women living in the same neighborhood as the patients with cancer. The results did not suggest an increased risk of either breast or endometrial cancer in users of permanent or permanent and semipermanent dyes combined. Although the numbers of cases and controls were small, the consistency of the results for both sites, in both study centers, and the absence of any clear positive relationship between various measures of intensity of use and risk of cancer provided evidence that a large increase in risk was not missed.
J Natl Cancer Inst 1979 Oct
PMID:Case-control study of hair dye use by patients with breast cancer and endometrial cancer. 48 Mar 86

The author reviews the literature on the possible association of breast cancer and endometrial cancer, and on the hormonal environment of patients affected with one or both. Knowledge of this supposed association is minimal early diagnosis and correction of hormonal disorders are extremely important. Demographic and endocrine characteristics, and also sterility, make some women more susceptible than others to breast and endometrial cancer. Some estrogens, such as estrone and estriol, are reputed by some authors to be responsible for these types of cancer.
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PMID:[Hormonal correlations between cancer of the breast and atypical hyperplasia of the endometrium in premenopausal women]. 48 15

Controversy over the relationship between the use of exogenous estrogens and endometrial cancer persists and will be dissipated only by well designed prospective studies. Most epidemiological investigations, both descriptive and etiological, have reported a relationship between estrogen use and endometrial cancer, but the association may have been artifically inflated by a number of factors. The evidence for an association between less invasive forms of endometrial cancer and estrogen use is more convincing. Descriptive studies have reported an increase in the incidence of endometrial cancer in a number of regions in the U.S. from 1960 to the mid-1970s, and this observed increase has been attributed to the corresponding increase in estrogen usage during the same period. The high endometrial cancer rates may have been inflated by the inclusion of nonmalignant hyperplasia cases stemming from the recent adoption of more sensitive diagnostic criteria. The association between endometrial cancer and estrogen use revealed in a number of case control studies may have been exaggerated because: 1) cancer is more likely to be detected among women taking estrogens since they are under closer medical scrutiny; 2) women with a typical hyperplasia may have been assigned disease status; and 3) retrospectively ascertained medication records on women with cancer may be more complete than those obtained for controls. Prospective studies are needed to clarify the degree of association despite the high cost involved in this type of undertaking. In the meantime, it is suggested that clinicians in treating menopausal women 1) refrain from estrogen therapy if pretreatment endometrial biopsy findings indicate the presence of hyperplasia; 2) use low estrogen doses; 3) consider the addition of progesterone in the treatment regimen; and 4) perform yearly biopsies on women receiving treatment. Line graphs depict 1) duration of estrogen use by risk ratio of endometrial cancer and 2) comparison of cumulative risk of endometrial cancer by years of follow-up for a hypothetical 50 year old patient treated with estrogens and one not treated.
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PMID:Review of epidemiologic studies of endometrial cancer and exogenous estrogen. 49 41

Horwitz and Feinstein (1) conclude from their epidemiologic study of endometrial cancer that "no association exists between the use of oral contraceptive pills and the subsequent development of endometrial cancer." They correctly point out that a limitation of their data is that only a small number of patients and control subjects had previously used contraceptive pills. Their data may also be limited by the relatively short time from the introduction of contraceptive pills to the present. A typical latent period from exposure to known chemical carcinogens until detection of cancer is 20 to 40 years (2-4). Oral contraceptive pills were introduced in the early 1960s (higher estrogen pills in 1960 and "average" estrogen pills after 1963) (5). Thus, an excess of cancers resulting from oral contraceptive use might not yet be detectable. Horwitz and Feinstein's hypothesis ought to be considered unproven until one can study a group of women at least 20 years after their initial exposure to oral contraceptives.
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PMID:Oral contraceptive pills and endometrial cancer. 49 28

Estradiol and testosterone levels in the peripheral and ovarian circulation of patients with endometrial cancer and of postmenopausal women were studied. These levels proved to be the same in the two groups. The ovaries of neither group secreted estradiol. The testosterone level in the ovarian circulation of all examined women was four times higher than that in the peripheral circulation, thus indicating the ovarian origin of testosterone.
Cancer 1979 Nov
PMID:Estradiol and testosterone levels in the peripheral and ovarian circulations in patients with endometrial cancer. 49 50

By a high dose gestagen therapy following primary radiation therapy of endometrial carcinoma it was possible to reduce the recurrence-rate 12 months after therapy in comparison with a control-group without gestagen therapy by more than 50%. Therefore this method is recommended not only for treatment of far advanced carcinoma of the endometrium but also as prophylactic therapy in cases of early endometrium cancer.
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PMID:[High dose gestagen therapy following primary radiation therapy of endometrial carcinoma (author's transl)]. 50 94

For many years, a variety of abnormal endometrial lesions have been linked to endometrial cancer but have been designated as hyperplasia and classified by modifying adjectives such as cystic, adenomatous, atypical, moderate, and severe. Though descriptively distinctive, there are enough consistent histologic transitions between them to designate the entire group as belonging to a continuous spectrum from benign to malignant. Furthermore, because these epithelial lesions demonstrate not just hyperplasia but significant disorderly growth patterns, it has been suggested that they be referred to as dysplasias. In order to evaluate the association of these types of dysplasia to cancer, two groups of patients were studied. In one group, the histologic states of the endometrium of patients with endometrial cancer were retrospectively analyzed. In the second group of patients, who were selected for study because the endometria were diagnosed as belonging to the dysplastic groups, the subsequent endometrial histology was prospectively studied. The findings suggest that there is a recognizable group of endometrial lesions with an association to endometrial cancer strong enought to label and treat them as neoplastic.
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PMID:The precursors of endometrial carcinoma. 50 34

Electrophoresis of cytosol prepared from normal and malignant tissue samples of uterine cervix and endometrium revealed interesting differences which may be relevant to the characteristic alterations in glucose metabolism associated with tumour development. Hexokinase II was detected in 30% of the cancer material from both sources, but in none of the samples of normal cervix. A duplet band of 6-phosphogluconate dehydrognease was seen in the majority of the cancer samples but in no sample of normal cervix; it appeared to be partly due to ageing of the sample, and is not phenotypically related to the malignant process. Analysis of genetic variance for phosphoglucomutase at the PGM1 locus revealed a highly significant excess of the PGM1-1 phenotype in patients with cancer of the endometrium, which may reflect susceptibility to endometrial cancer in patients with this phenotype. At the PGM2 locus, samples of malignant cervix were deficient in "Band f" compared with normal cervix samples, all of which showed this band. Conversely, gene products of the PGM3 locus were found in most samples of malignant cervix and a small minority of normal cervix samples. Compared with the isomorphic distribution of lactate dehydrogenase enzymes in normal uterine tissue, cancers showed a shift towards either a more anodal or a more cathodal pattern. The former may be associated with tumours enjoying a good oxygen supply, and the latter with tumours which, because of their depth or poor blood supply have to function under less aerobic conditions.
Br J Cancer 1979 Sep
PMID:Isoenzymes of hexokinase, 6-phosphogluconate dehydrogenase, phosphoglucomutase and lactate dehydrogenase in uterine cancer. 50 67

The effects of 17beta-estradiol and progesterone on the rate of growth and the morphological changes of human endometrial adenocarcinoma cells were studied in in vitro culture. 17beta-Estradiol enhanced their growth and produced no cellular morphological changes at low concentrations of less than 1 microgram/ml, whereas it suppressed their growth and produced such cellular changes as enlargement of nuclei, karyorrhexis, and karyolysis at high concentrations of more than 5 microgram/ml. On the other hand, progesterone did not affect the cells at less than 1 microgram/ml, but it suppressed their growth and induced differentiation at more than 5 microgram/ml. Specific morphological changes produced by progesterone were characterized by multinucleation, multinucleolation, prominent Golgi apparatus, occurrence of vacuoles, and papillary-like arrangement of cells. These features suggested that progesterone acted directly on the endometrial carcinoma cells and induced their histological differentiation. These changes could not be detected by the adminstration of 17beta-estradiol.
Cancer Res 1977 Dec
PMID:Effects of 17beta-estradiol and progesterone on growth and morphology of human endometrial carcinoma cells in vitro. 56 9


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