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

Approximately 20,000 women are diagnosed with ovarian cancer in the United States each year, and some 12,000 women die because of it. Epithelial ovarian cancer, the most common histopathologic type, is uncommon before age 40 years, after which incidence rates increase steeply until age 70-79 years and then decrease somewhat. In the United States, the lifetime risk from birth to age 85 years is about 1.5%. There is general agreement that residence in North America or northern Europe, nulliparity, and having a mother or sister with ovarian cancer are associated with an elevated risk, and that increasing number of pregnancies (whether or not full term), increasing length of oral contraceptive use, and increasing duration of lactation are protective. A history of breast or endometrial cancer appears to be associated with a slight elevation in risk. Apart from oral contraceptive use, none of these characteristics can be modified easily to reduce ovarian cancer risk. However, long-term oral contraceptive use before the menopause could prevent as much as half of all ovarian cancer. At present, the subgroup of the population at highest risk consists of women with a mother or sister with the disease; the lifetime ovarian cancer risk in these women is about 9%. A small fraction of them have families with multiple cases of ovarian cancer and early-onset breast cancer, due largely or entirely to mutated alleles of the gene BRCA1. These women, who have a lifetime risk of breast or ovarian cancer of 85-100%, need aggressive screening and possibly prophylactic surgery.
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PMID:Characteristics relating to ovarian cancer risk: implications for prevention and detection. 863 61

The use of agonistic analogues of luteinizing hormone releasing hormone (LHRH) is an established therapy for hormone-dependent metastatic pre-menopausal breast cancer. Their mechanism of action in this disease is the suppression of ovarian oestrogen production (medical castration). In the treatment of post-menopausal metastatic breast cancer, LHRH agonists also have some effect, although minor, probably through a suppression of ovarian androgen production. Convincing evidence has been accumulated that LHRH analogues can directly inhibit the proliferation of breast cancer cells in vitro. The clinical impact of these findings, however, is still controversial. Experimental data and several pilot clinical trials suggest that in epithelial ovarian cancer and sex-cord-stromal tumours of the ovary, LHRH agonists might have antitumour activity through the suppression of gonadotrophin secretion (selective medical hypophysectomy). Phase III clinical trials, evaluating this hypothesis, are in progress. Direct antiproliferative effects of LHRH analogues on epithelial ovarian cancer cells have been demonstrated in vitro. In endometrial cancer, experimental and early clinical results support the concept of a direct antiproliferative activity of LHRH analogues. Recently, potent antagonistic analogues of LHRH, devoid of relevant side-effects have become available for clinical testing. These new antagonists might be superior to agonistic LHRH analogues with respect to the rapidity and efficacy of selective medical hypophysectomy and medical castration. Modern LHRH antagonists might also permit a better exploitation of direct antitumour effects. A further therapeutic improvement in gynaecological oncology might result from a combination of LHRH agonists or antagonists with other peptide hormone analogues such as agonists of somatostatin or antagonists of bombesin/gastrin releasing peptide which have antitumour activity. Since 50% of breast cancers and 80% of epithelial ovarian cancers and endometrial cancers have high affinity binding sites for LHRH, cytotoxic LHRH analogues might provide a targeted chemotherapy, which would be more efficacious and less toxic than conventional regimens.
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PMID:The use of luteinizing hormone releasing hormone agonists and antagonists in gynaecological cancers. 1096 15

Specimens from 344 cases of endometrial carcinoma, 289 cases of ovarian carcinoma, 177 cases of cervical carcinoma, 10 vulva and 4 fallopian tube carcinoma were assayed for cytosol estrogen and progesterone receptor (ER, PR) contents with dextran-coated charcoal (DCC) method. Positive rates of ER and PR in these malignant tumors in relation to menstrual cycle, histological differentiation, clinical stage and prognosis of disease were studied. The results suggested that the contents of ER and PR may play a role in building endocrine therapy and prognosis in the postoperative period. Further study on vulvar and fallopian tube carcinomas should be undertaken.
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PMID:[Cytosol estrogen and progesterone receptors in female genital system malignant tumors]. 803 16

Autologous blood transfusion, as an alternative to homologous blood, must be considered for those patients who require blood. Transfusion in gynecologic oncology surgery is often required and autologous blood transfusion has been utilized. Between January 1988 and December 1992 a total of 162 surgical procedures for gynecologic cancers were performed in the same number of patients. Of these only 102 were eligible for autologous blood transfusion as predonation. The mean age of patients was 57.8 years (range 35-81). Forty-three patients were affected with endometrial carcinoma, 31 with carcinoma of the cervix, 21 with ovarian carcinoma and 7 with vulvar cancer. Collected autologous blood units were 138 (mean 1.35 every patient). Indications for predeposited blood transfusion was given by a hemorrhage greater than 100 cc intraoperatively or hemoglobin level less than 10 g/dl until 1988 or less than 8 g/dl since 1989. Forty-eight (34.8%) of the collected units were transfused to 39 autologous donors (mean 1.2 units every patient). There was a significant difference in transfusion rate in patients: endometrium 25.8%, ovary 28%, cervix 45%, vulva 72.7%. Unused autologous blood units were discarded at the expiration date: they were 90, 65% of collected ones. In 6 patients homologous blood was necessary other than autotransfusions. Our experience demonstrates that the transfusion requirement in gynecologic cancer surgery depends on pattern of neoplasm and consequently of surgical procedure. Patients with carcinoma of the cervix and vulva are at risk for transfusion and have appropriate indications for autologous donation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autologous blood collection in gynecologic oncologic surgery]. 806 87

Steroid sulfatase (STS) desulfates a number of 3 beta-hydroxysteroid sulfates, converting inactive steroid hormone to the active form. We have established an enzyme-linked immunosorbent assay (ELISA) of STS by using polyclonal antibody against STS purified from human placenta to measure the amount of the enzyme protein in sera. ELISA was performed by a 'Sandwich' method using a peroxidase conjugated anti-STS IgG Fab' fragment. A range of STS of 10-1,500 ng/ml in serum was assayed by this method. When the serum STS from the patients with gynecologic carcinomas was assayed by the ELISA, the level was significantly elevated in endometrial carcinoma (P < 0.05) and ovarian carcinoma (P < 0.01), respectively, as compared with that of normal healthy women.
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PMID:Serum levels of steroid sulfatase protein in gynecologic carcinomas. 807 Jan 31

The inactivation of the tumor suppressor gene p53 has been demonstrated in a variety of human tumors. Herein, we performed a p53 gene analysis of human gynecologic tumor cell lines and tumor tissues. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of p53 gene. Transcripts were not detectable by either Northern or PCR analysis. Sequencing analysis of the entire coding region revealed mutations changing the p53 amino acid composition in all six endometrial carcinoma cell lines tested (Ishikawa, Hec1-A, Hec1-B, KLE, RL95-2, and AN-3), and four cell lines in ovarian carcinoma cell lines (Caov-3, -4, OVCAR-3, and Kuramochi). Of the seven cervical carcinoma cell lines, two (HT-3 and C-33A) contained p53 codon changes. We were unable to detect the human papilloma virus (HPV) in these two cell lines. By contrast, five HPV-positive cervical carcinoma cell lines (HeLa S-3, Caski, SiHa, C-41, and ME-180) contained wild-type p53 gene sequences. Examination of loss of heterozygosity (LOH) by PCR revealed that about 30% of the human ovarian carcinoma tissues has LOH at the locus of p53 gene. We suggest that, in the HPV-positive cervical tumors, p53 inactivation occurred via the known mechanism of viral E6/cellular p53 protein association, whereas in all other tumors (ovarian carcinoma, endometrial carcinoma, HPV-negative cervical carcinoma) p53 function was compromised by changes in the amino acid sequence.
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PMID:[Analysis of p53 gene in gynecologic tumors]. 815 58

This review addresses possible associations between depot-medroxy-progesterone acetate (DMPA) and endometrial and epithelial ovarian cancers. Two unexpected endometrial carcinomas were observed at autopsy of rhesus monkeys treated for 10 years with 50 times the human doses of DMPA. A record linkage in the USA did not suggest any association between DMPA and endometrial cancer. A multicentre case-control study in Thailand showed a strong protective effect of DMPA for endometrial cancer. Studies from the USA, Mexico and Thailand did not observe any association between use of DMPA and epithelial ovarian cancer. The available information, therefore, indicates that use of DMPA protects against endometrial cancer and is not associated with epithelial ovarian cancer.
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PMID:Depot-medroxyprogesterone acetate (DMPA) and cancer of the endometrium and ovary. 820 Feb 14

Less than 100 cases have been reported involving coexistent pregnancy and endometrial cancer of epithelial ovarian cancer. Only one case, histologically an endometrioid adenocarcinoma, demonstrated simultaneous involvement of endometrium and ovary. We report an additional case involving both uterus and ovary coexisting with pregnancy but of a serous papillary histology. A viable preterm infant was delivered. The mother is currently without evidence of disease on cisplatin-based chemotherapy.
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PMID:Pregnancy coexisting with serous papillary adenocarcinoma involving both uterus and ovary. 820 13

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.
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PMID:[Do sex steroids cause breast and genital cancers? Epidemiologic data--the current status (July 1993)]. 827 Jan 46

We have previously documented the responsiveness of a cell line of human ovarian epithelial carcinoma (Bowman Gray 1) heterotransplanted in nude mice to treatment with the GnRH agonist Lupron-SR. In this study we used another human ovarian epithelial carcinoma cell line, OVCAR-3, and the human endometrial carcinoma cell line HEC-1A. After a latent period, OVCAR-3 tumors showed significant inhibition of growth on Days 17, 21, and 24 (P < 0.03) compared to controls. The effect was transient and did not persist beyond Day 24. HEC-1A tumors showed no inhibition of growth. Radioreceptor assay studies utilizing native radiolabeled GnRH and [D-Lys6]-GnRH revealed no specific GnRH receptors in any of the tumor samples (BG-1, OVCAR-3, HEC-1A, University of Nebraska cell line, and two fresh human ovarian epithelial tumor samples) compared to male rat anterior pituitary cells. Binding studies and the latency and transience of effect would suggest that the mechanism of action in this animal model may be indirect. This activity may be via altered circulating steroids, gonadotropins, cell-cycle regulatory events, or some other as-yet-undefined action related to GnRH agonist administration or indirectly via effects of the metabolic products of degraded GnRH agonist such as D-amino acids, which are incorporated into the cells by constitutive or adsorptive pinocytosis. This study confirms latency and transience of effect of GnRH agonist therapy on an in vivo model of ovarian cancer.
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PMID:GnRH agonist therapy in human ovarian epithelial carcinoma (OVCAR-3) heterotransplanted in the nude mouse is characterized by latency and transience. 830 97


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