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

The benefits of combined oral contraceptives are put into perspective, considering their effectiveness as a contraceptive, actual risks for breast, ovarian, endometrial and cervical cancer, and effects of reproductive and other body systems. Combined oral contraceptives are the best contraceptives available except for injectable progestogens, therefore they an reduce the risk of maternal mortality by at least 5 in nonsmoking western women, or over 100 in developing countries. No data are available on mortality risk of the presumed safer low-dose pills. Pills reduce ectopic pregnancy to virtually nil. They decrease the risk of endometrial cancer, and of ovarian cancer for up to 15 years after use. Although they protect against benign breast disease, both fibrocystic disease and fibroadenoma, which are risk factors for breast cancer, it is unsettled whether pills affect breast cancer incidence. Cervical cancer risk may be slightly higher. Functional ovarian cysts requiring surgery are cut about 10-fold; corpus luteum and follicular cysts are also reduced. Fibroids are decreased in proportion to duration of use. Pelvic inflammatory disease rates fall 50% during use. Chlamydial infections have not fallen in pill users, but it is not known whether sexual activity is a factor. Combined pills cut abnormal uterine bleeding by about half, reduce the incidence of iron deficiency anemia and of premenstrual tension. Seizures related to menses also are controlled. Some studies find a reduction in rheumatoid arthritis. Most of the cardiovascular complications of pills are thought to be dose related. Since today's pills contain approximately the same dose as a whole cycle of the original pills, it is expected that these risks will be greatly reduced, especially with better screening of candidates that is now the rule.
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PMID:The benefits of combined oral contraceptives. 269 95

Central nervous system (CNS) involvement by endometrial carcinoma is uncommon. Among 1069 patients registered for endometrial carcinoma at our institution between 1982 and 1994, 10 (0,9%) developed brain metastases. Median age at the time of CNS metastasis diagnosis was 59 years. Median interval between diagnosis of endometrial cancer and documentation of brain involvement was 26 months. Clinical manifestation of brain metastasis included headache (80%), motor weakness (50%), seizures (20%), confusion (10%), balance (10%), and visual disturbances (10%). All lesions (4 multiple, 6 single) were contrast enhancing on computed tomography (CT) scans, and were located in the cerebrum in seven cases, in the cerebellum in one case, and in both in two cases. The CNS was the only site of detectable disease in six patients with recurrent disease. Nine patients died and one is alive with disease 3 months after surgical resection of a single cerebral deposit. Median survival from diagnosis of brain metastases for the entire series was 1 month (range 1-83). Six patients receiving only steroids died within 1 month from the diagnosis. One patient received radiotherapy (survival, 3 months) and two underwent surgical resection of solitary metastasis followed by radiotherapy (survival = 28 and 83 months). Prognosis of patients with CNS metastases from endometrial carcinoma appears poor; however, in a selected group of patients early diagnosis followed by multimodal treatment may result in a palliation of the disease.
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PMID:Brain metastases from endometrial carcinoma. 862 15

Angiogenesis plays an important role in neovascularization in tumors. Glycodelin, a hormone-responsive protein, has been detected in tumors of reproductive organs and is found in high levels in the plasma of subjects with gynecological malignancies. Glycodelin is also found in the endothelial cells of the umbilical cord and in the blood vessels of tumors. In this study, we tested whether glycodelin-rich amniotic fluid and a synthetic peptide derived from the sequence of glycodelin peptide (Gp) might promote angiogenic response by examining the migration and tube formation in human umbilical cord vein endothelial cells (HUVECs). Increased migration and tube formation of HUVECs were found in the presence of amniotic fluid and Gp, and this increase was blocked by antibody to Gp and by an anti-vascular endothelial growth factor (VEGF) antibody, suggesting that the angiogenic effects of glycodelin might be mediated by VEGF. The results also showed that Gp significantly increased the release of VEGF protein and mRNA expression in HUVECs, RL-95 (human endometrial carcinoma cells), OVCAR-3 (human ovarian adenocarcinoma cells), EM42 (human endometrial epithelial cells), THP-1 (human monocyte), and MCF-7 and MDA-MB-231 (human breast adenocarcinoma cells) cell lines. VEGF receptor Fit-1 mRNA expression in HUVECs was also increased in the presence of Gp. These findings, together with the suggestion from the literature that glycodelin may have immunosuppressive properties, suggest that glycodelin might play an important role in neovascularization during embryogenesis and tumor development.
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PMID:Angiogenic role for glycodelin in tumorigenesis. 1145 32

Somatic inactivation of PTEN occurs in different human tumors including glioblastoma, endometrial carcinoma and prostate carcinoma. Germline mutations in PTEN result in a range of phenotypic abnormalities that occur with variable penetrance, including neurological features such as macrocephaly, seizures, ataxia and Lhermitte-Duclos disease (also described as dysplastic gangliocytoma of the cerebellum). Homozygous deletion of Pten causes embryonic lethality in mice. To investigate function in the brain, we used Cre-loxP technology to selectively inactivate Pten in specific mouse neuronal populations. Loss of Pten resulted in progressive macrocephaly and seizures. Neurons lacking Pten expressed high levels of phosphorylated Akt and showed a progressive increase in soma size without evidence of abnormal proliferation. Cerebellar abnormalities closely resembled the histopathology of human Lhermitte-Duclos disease. These results indicate that Pten regulates neuronal size in vivo in a cell-autonomous manner and provide new insights into the etiology of Lhermitte-Duclos disease.
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PMID:Pten regulates neuronal soma size: a mouse model of Lhermitte-Duclos disease. 1172 27