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

The serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and, prolactin (PRL) were measured before and after gonadotrophin releasing hormone (GnRH) and thyrotrophin releasing hormone (TRH) stimulation in 17 patients with endometrial cancer, in 15 patients with uterine fibroids, in 11 patients with ovarian cystadenomas or cancer and in 14 age-matched controls. The women with fibroids had a low FSH level and a diminished FSH response to GnRH but an excessive PRL response to TRH while the other patient groups did not differ from the controls. The results indicate no relation between pituitary function and endometrial or ovarian tumor.
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PMID:Pituitary gonadotrophins and prolactin in patients with endometrial cancer, fibroids or ovarian tumours. 11 72

Within a period of 1966-1970 in the three republics according to standardized indices for 100.000 females cancer of the female genitalia was found in 42.32 (in Georgia--29.1; in Kazakhstan--43.02; in Latvia--54.85). Dynamically, there was noted a stabilization of indices on cervial cancer and growth in ovarian and, especially, endometrial cancer incidence. In dynamics there is an "ageing" of cancer of the female gentalia.
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PMID:[Comparative study of the female genital cancer morbidity in the Georgian SSR, Latvian SSR and Kazakh SSR]. 12 11

A so-called "endometrial" adenocarcinoma of the prostate has been studied by light and electron microscopy, and by histochemical techniques. The previously proposed utricular origin and estrogen dependence of such tumors is questioned. Strong acid phosphatase staining, and the ultrastructural demonstration of multivacuolated, lipid, and lysosome-containing tumor cells, suggest a prostatic ductal origin for this type of carcinoma despite the histologic similarity to carcinoma of the endometrium.
Cancer 1976 May
PMID:"Endometrial" adenocarcinoma of the prostate: a distinctive tumor of probable prostatic duct origin. 13 Sep 69

The histochemical method was used for determining glycogen, phosphorylase, glycogensynthetase, and glucose-6-phosphatase in order to evaluate the effect of progesterone on different morphological forms of cancer of the endometrium in man. On the basis of histochemical analysis of changes in the carbohydrate metabolism in 29 cases of cancer before and after treatment with progesterone a conclusion is drawn that sensitivity of tumours of the endometrium to hormonotherapy only partially depends upon the degree of their morphological differentiation.
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PMID:[A histochemical study of the effect of progesterone on the carbohydrate metabolism enzymes of different morphologic forms of endometrial cancer]. 17 78

All cases of endometrial cancer occurring among the residents of an affluent retirement community were compared with controls chosen from a roster of all women in the same community. Evidence of estrogen and other drug use and of selected medical conditions was obtained from three sources: medical records of the principal care facility, interviews, and the records of the local pharmacy. The risk ratio for any estrogen use was estimated from all available evidence to be 8.0 (95 per cent confidence interval, 3.5 to 18.1). and the for conjugated estrogen use to be 5.6 (95 per cent confidence interval, 2.8 to 11.1). Increased risk from estrogens was shown for invasive as well as noninvasive cancer, and a dose-response effect was demonstrated. For an estrogen user, the risk from endometrial cancer appeared to exceed by far the base-line risk from any other single cancer.
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PMID:Estrogens and endometrial cancer in a retirement community. 17 70

Sera from cancer patients and healthy individuals, obtained from two independent sources, were examined for their abilities to react with herpes simplex virus-associated tumor antigens, AG-4 and NVA-TAA (nonvirion antigen-tumor-associated antigen). Both antigens were prepared by infection of HEp-2 cells with herpes simplex virus type 2, and all antigen-antibody interactions were measured by the micro-complement fixation test. Of sera from 16 patients with cancer of the uterine cervix, 81% (P less than 0.01) reacted with NVA-TAA, whereas 78% (P less than 0.001) of 18 sera examined reacted with AG-4. These values differed significantly from those for normal sera, of which 14% reacted with NVA-TAA and 13% with AG-4. Of sera for 8 patients with squamous cell carcinoma of head and neck or vulva, 75% (P less than 0.02) reacted with NVA-TAA, whereas 63% (P less than 0.05) reacted with AG-4. As a group, other cancers (including adenocarcinoma of lung, breast, ovary, and cervix; liposarcoma; sarcoma; melanoma; and carcinoma of the endometrium) did not differ significantly from controls in reactive patterns with AG-4 or NVA-TAA. These studies partly supported the reported preferential reactivity of AG-4 and NVA-TAA with sera of patients with squamous cell carcinoma, especially of the uterine cervix.
J Natl Cancer Inst 1976 Sep
PMID:Comparative diagnostic aspects of herpes simplex virus tumor-associated antigens. 18 98

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

205 patients with endometrial carcinoma, excluding carcinoma in situ, were seen in 1 private practice between 1947-1976. A control for each case was chosen from patients who had had a hysterectomy for a benign condition. Average age of patients with cancer was 56.5 years and parity 1.5. The cancer patients weighed significantly more than controls. A history of diabetes was recorded for 8 study patients, and 1 control. Of the 205 cancer patients, 55, and of the control patients, 31, had used some form of estrogen-containing medication. The relative risk (RR) for all users of systemic estrogens was 2.6. Most had used conjugated estrogens giving an RR of 3.1 for this form of the drug. There was no increased risk associated with vaginal estrogenic preparations or oral contraceptives. The RR increased with increasing duration of use, with no appreciable increase in the risk for those using the medication for less than 5 years. Those using these drugs for 5-9 years had a risk 11.5 times that of nonusers. Those using the 1.25 mg tablet had a risk markedly above that for users of the .3 or .625 mg tablets. The study group had more frequent histories of abnormal uterine bleeding than the control group. The lifetime risk of developing endometrial cancer is estimated as 2.2% for whites and 1.1% for blacks. A 70.9% 5-year survival rate and a 55.8% 10-year survival rate have been recorded. With early diagnosis, the cure rate may approach 95%. Many of the symptoms of women in the manopause may be alleviated by estrogenic therapy. Many of these women will have had a hysterectomy and no longer be at risk of endometrial cancer. Therefore, such therapy seems justified.
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PMID:Estrogens and endometrial carcinoma. 19 72

Feminizing ovarian tumors and polycystic ovarian disease may cause endometrial cancer by abnormal, unopposed endogenous estrogenic stimulation. We reviewed the clinical course of 72 endometrial cancer patients with a concomitant feminizing ovarian tumor or polycystic ovarian disease and compared tumor characteristics and treatment results with those exhibited by 523 patients treated for endometrial cancer alone. With functioning ovarian tumor and with polycystic ovaries, the cancer tended to be more often low-grade, low-stage, and superficial than did endometrial cancer alone. The high 5-year and 10-year survival rates observed in our functioning ovarian tumor-polycystic ovary patients support the conclusion that endometrial carcinoma with a coexistent endogenous estrogenic stimulus has a more favorable prognosis (P less than 0.01) than endometrial carcinoma alone.
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PMID:Endometrial cancer associated with feminizing ovarian tumor and polycystic ovarian disease. 19 78

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79


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