Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although there is a slightly increased risk of endometrial cancer from estrogen therapy for menopausal women, progestogens given along with the estrogen significantly decrease the incidence of this malignancy to a rate lower than that of untreated women. Postmenopausal women predisposed to adenocarcinoma of the endometrium because of increased endogenous estrogens can be identified with the progestogen challenge test and treated with cyclic progestogens for 10 days each month to prevent endometrial cancer. Oral contraceptives containing both estrogens and progestogens in each tablet are protective against developing adenocarcinoma of the endometrium, whereas the sequential birth control pills provided less protection. The incidence of breast cancer is significantly lower in both estrogen and estrogen-progestogen users than in postmenopausal women never using these hormones. In those women found to have breast cancer while using these hormones, the prognosis is better than that found in women never exposed to exogenous estrogens, most likely due to an earlier detection. No clear-cut pattern of either abnormal hormone production or milieu has been found in women with carcinoma of the breast. Oral contraceptives reduce the risk of benign breast disease and afford some protection from the subsequent development of breast cancer. The mortality rate from breast cancer developing in oral contraceptive users is significantly lower than that of the non-users.
 ...
PMID:Role of hormones in the etiology and prevention of endometrial and breast cancer. 704 35

In Canada depot medroxyprogesterone acetate (DMPA) (Depo-Provera, Upjohn Company of Canada) has been cleared for use in the management of endometriosis in the nonpregnant woman and for palliation of advanced endometrial cancer. There remains some question as to whether physicians are authorized to use this drug for other clinical conditions. The health protection branch of the Department of National Health and Welfare, after a review of the world literature and data on the clinical use of this drug for indications other than those mentioned, has concluded that the available clinical experience with DMPA shows a favorable risk/benefit ratio and that the drug does not present an undue health hazard. Since the 1st clinical studies began in the early 1960s experience with DMPA for contraception has totalled more than 10 million women years. It is estimated that over 1.2 million women in various countries are currently using DMPA for contraception and that several thousand women have used it for 10 years or longer. Available data indicate that the risk/benefit ratio for DMPA in a appropriately selected population is as favorable as that for oral contraceptives (OCs) or IUDs. These statements have been supported by many international organizations concerned with family planning. The special advisory committee on reproductive physiology of the health protection branch reviewed the October 1981 publication concerning the use of DMPA in the Ontario government facilities for the mentally retarded. Its authors considered "of borderline significance" the finding of 3 deaths from carcinoma of the breast in 533 women treated with DMPA at some time during their lives. The evidence for a causal relationship was very tenuous. The composition of the study cohort and the control group as well as the incomplete data collection made the statistical evaluation questionable. Also the higher prevalence of carcinoma of the breast in mentally retarded individuals and in patients with epilepsy and the fact that the other medications many of these patients must have taken were not reported or commented upon further confuse the issue and invalidate the inferences. From a review of the world literature it was learned that among 11,500 DMPA users in the US there have been only 4 reported cases of carcinoma of the breast, for a rate that is lower than that expected in a Canadian control population. The committee reaffirms its opinion tha DMPA is safe in the management of specific clinical problems. It is believed that there is no undue health hazard when DMPA is used to produce amenorrhea in physically or mentally handicapped individuals unable to cope satisfactorily with menstrual hygiene.
 ...
PMID:Should depot medroxyprogesterone acetate be considered for additional uses? 713 35

We present 6 cases illustrating some of the gynaecological complications associated with tamoxifen treatment of women with breast cancer. The first 2 represent cases of myometrial hypertrophy secondary to tamoxifen use, a postmenopausal woman and a premenopausal women with recurrent carcinoma of the breast. The third is a case of probable ovulation induction in a perimenopausal women with recurrent breast cancer who was commenced on tamoxifen 20 mg daily. The other 3 cases illustrate some of the endometrial effects associated with tamoxifen therapy in women with a history of breast cancer, namely cystic glandular hyperplasia, endometrial polyps and endometrial cancer.
 ...
PMID:Gynaecological complications of women treated with tamoxifen for breast cancer. 767 89

Present literature on epidemiology shows, that estrogens administered either in the form of contraceptives or as replacement therapy will reduce the relative risk of ovarian carcinoma to less than 0.5. Likewise this result was also seen in all studies without exception. The reduction becomes manifest after four months and is maintained for many years following discontinuation. The same applies to corpus carcinoma, provided estrogens are administered concomitantly with gestagens. Administration of estrogens alone results in enhancing the relative risk up to 3-4. Hyperproliferation can lead to carcinoma of the endometrium. No data are presently available for cervical carcinoma, that would justify the assumption, that the relative risk for squamous cell carcinoma of the cervix is increased. This statement does not apply to the adenocarcinoma of the cervix, since too few cases have been studied. The following statements apply to carcinoma of the breast: OC's (oral contraceptives) taken before the age of 45 do not increase the relative risk. This is also true of females, for whom a risk factor exists, as for example family case history, period of administration, benign diseases of the breast, use of OC's before the first pregnancy, nulliparity, no breast-feeding. Possible, but not proven is a slight increase in relative risk to 1.3 in females, in whom carcinoma of the breast had been diagnosed before the age of 34. If this increase is accepted, one must likewise expect a decrease in relative risk after the age of 45. A hormonal replacement therapy for up to four years will not increase the relative risk. This applies also to replacement therapy with gestagens, even though only few data are available at present. It has been concluded from the results of some studies, that a slight increase in relative risk to 1.3 is possible after long-term therapy (more than 15 years). However, no causal relationship to cancer of the breast has been established. It has not been claimed so far, that estrogens cause cancer of the breast. Should the slight relative risk increase be confirmed, this would mean, that in a small group of very young females, estrogens may promote the growth of an already existing cancer of the breast.
 ...
PMID:[Do sex steroids cause breast and genital cancers? Epidemiologic data--the current status (July 1993)]. 827 Jan 46

Familial ovarian cancer is described as a familial aggregation of ovarian cancer. The disease is heterogeneous, with at least three genotypes prodisposing to distinctive hereditary syndrome, site-specific ovarian cancer, wherein familial cancer risk is restricted to ovarian carcinoma; breast/ovary carcinoma syndrome, that is ovarian carcinoma in association with carcinoma of the breast; and Lynch syndrome II, characterized by hereditary nonpolyposis colorectal cancer with proximal colonic cancer predominance, endometrial carcinoma, and ovarian carcinoma. When a familial aggregation of ovarian cancer is observed, unaffected women in the family should have periodic gynecologic examinations, including cytologic and ultrasonographic, radiologic studies and magnetic resonance imaging, in an effort to detect preinvasive ovarian cancer. Until more reliable diagnostic methods are developed, however, the physician should consider the advisability of prophylactic oophorectomy and oral contraceptives when counseling women who have several close relatives with ovarian cancer.
 ...
PMID:[Familial ovarian cancer, uterine cancer]. 853 42

Deletion of certain chromosomal regions can be demonstrated in malignant cells. Chromosome 16q is one of the regions where allelic loss is frequently detected in carcinoma of the breast and many other tumors, suggesting that gene(s) which retard tumor growth may exist here. To elucidate the clinicopathological significance of chromosome 16q, loss of heterozygosity (LOH) was investigated using microsatellite polymorphism analysis in 58 patients with endometrial lesions (50 with endometrial carcinoma and 8 who had hyperplasia with or without atypia). When 11 regions of chromosome 16q were examined, LOH was found in 20 patients with carcinoma (40%) and none of the patients with hyperplasia. The tumors of 9 of the 20 patients (45%) showed total loss of 16q, while the others (55%) showed partial deletion. Tumors with LOH were histologically less differentiated than those without LOH (P = 0.038, chi2 test). Patients with tumors showing LOH of 16q had a worse prognosis than those without LOH according to Kaplan-Meier survival analysis (P=0.0158, log-rank test). In addition, LOH of 16q showed a significant relationship to prognosis by Cox regression analysis. Deletion mapping of 16q demonstrated that two regions (16q22.1 and 16q22.2-23.1) were frequently involved. Patients with 16q22.1 LOH had a poorer prognosis than those with intact 16q22.1 (P=0.0003, log-rank test). These findings suggest that gene(s) of which defect is possibly related to the aggressiveness of endometrial cancer are localized on a limited region of 16q that includes 16q22.1.
 ...
PMID:Allelic loss of chromosome 16q in endometrial cancer: correlation with poor prognosis of patients and less differentiated histology. 904 49

A key to successful metastasis is the formation of new vasculature, known as angiogenesis. Therefore, it is of great interest to unravel the underlying molecular mechanisms of tumor angiogenesis. Cadherins are a major class of cell surface receptors. The loss of cadherins, especially E-cadherin, is a well-established marker for tumor metastasis. Loss of E-cadherin is also a defining characteristic of several carcinomas, such as lobular carcinoma of the breast, and de-differentiated endometrioid carcinoma of the endometrium and ovary, which are known to be associated with more aggressive tumor behavior. Although E-cadherin is synthesized as a transmembrane molecule, its extracellular domain can be enzymatically cleaved off and released as a soluble E-cadherin (sE-cad), and this accounts for the loss of E-cadherin function or expression that has been implicated in tumor progression and metastasis. Importantly, sE-cad is present at high levels in the serum and malignant ascites of ovarian carcinoma patients. Nevertheless, little is known about how this essential protein dictates metastasis. Hitherto, many studies have given attention only to the dominant negative role of the loss of E-cadherin in weakening cell-cell adhesion, however, it is not known if sE-cad has biological activity in itself. In addition, the release mechanism of sE-cad has remained elusive. Here we show for the first time that sE-cad is a pivotal regulator of angiogenesis. We further show that exosomes are a novel major platform for the cleavage and release of sE-cad in vitro, in vivo and in patients' derived samples (Nat Commun, 9: 2270).
 ...
PMID:New insights into the role of soluble E-cadherin in tumor angiogenesis. 2989 38


<< Previous 1 2