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

To study the role of prostacyclin (PGI2) and thromboxane A2 (TxA2) in uterine tumors, pieces of endometrial cancer (n = 12) and leiomyomas (n = 12) were incubated in vitro, and the productions of 6-keto-prostaglandin F1a (6-keto-PGF1a, a hydration product of PGI2) and thromboxane B2 (TxB2, a hydration product of TxA2), measured by radioimmunoassay, were compared to those of corresponding healthy tissues. The production of 6-keto-PGF1a by endometrial cancer (20.8; 15.1-85.0 ng/mg protein/min, median and interquartile range), by healthy endometrium (25.5; 10.0-55.0), by healthy myometrium (34.9; 25.0-59.9) and by leiomyoma (20.3; 10.2-45.1) was similar. The production of TxB2 was increased by endometrial cancer (55.5; 10.5-155.2, p less than 0.02) in comparison with endometrium (9.8; 4.3-35.1), myometrium (3.8; 2.1-8.0) and leiomyoma (1.9; 1.0-3.8). The 6-keto-PGF1a/TxB2 ratio in endometrial cancer (0.9; 0.3-1.5) was smaller (p less than 0.02) than that in healthy endometrium (3.3; 1.9-4.8). Thus, TxA2 may be a factor in endometrial cancer.
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PMID:Prostacyclin and thromboxane synthesis by endometrial cancer and leiomyomas. 211 Oct 34

The risks and benefits of specific types of postmenopausal estrogens and progestogens are explored: those affecting serum lipids, clotting elements, hepatic proteins synthesis, blood pressure, glucose tolerance, endometrial, breast and cervical cancer. Ethinyl estradiol taken orally is the only estrogen likely to cause gall bladder disease. It also induces liver protein synthesis when taken orally or vaginally. Natural estrogens do not heighten coagulation factors, and may shift towards fibrinolysis. Both ethinyl estradiol and equine estrogens may increase blood pressure, while natural estrogens may decrease it. Similarly natural estrogens induce prostacyclin synthesis, while ethinyl estradiol activates both prostacyclin and thromboxanes. Progestagens, especially so the norprogestins, disturb carbohydrate metabolism and tend to reverse the beneficial effects of estrogens on serum lipids, a 40-70% reduction in risk of mortality from coronary heart disease. A meta- analysis of 23 studies concluded that menopausal estrogens do not increase the risk of breast cancer by a measurable degree, except in high doses and in those predisposed by family history. There is an increased risk of endometrial carcinoma for those taking unopposed estrogens for more than 3-6 years. This can be attenuated by taking combined estrogen-progestins, which will eventually result in absence of bleeding, or a 12-day progestogen course every 4-6 cycles. Oral micronized progesterone decreases blood pressure. The relative androgenic effects of progestins other than the norprogesterone derivatives are less significant. As an alternative to taking a progestogen, a woman could have regular endometrial sampling or abdominal or vaginal sonograms to detect endometrial cancer.
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PMID:Risks of estrogens and progestogens. 217 Aug 23

The production of the antiaggregatory and vasodilatory prostacyclin (PGI2) in patients with gynaecological tumours was studied by assaying urinary 6-keto-prostaglandin F1a (= 6-keto-PGF1a), a hydration product of PGI2), by radioimmunoassay following high performance liquid chromatography (HPLC) in 59 patients with gynaecological tumours and 12 non-tumourous control women. Urinary 6-keto-PGF1a excretion in patients with cervical cancer (28.3 +/- 3.6 pmol/mmol creatinine, mean +/- S.E., n = 12), endometrial cancer (22.8 +/- 3.7 pmol/mmol creatinine, n = 12, uterine fibroids (26.0 +/- 3.5 pmol/mmol creatinine, n = 12) benign ovarian cysts (22.4 +/- 1.8 pmol/mmol creatinine, n = 12) did not differ from that in the control women (29.9 +/- 3.6 pmol/mmol creatinine, n = 12). However, patients with ovarian cancer excreted increased amounts of 6-keto-PGF1a (55.4 +/- 10.4 pmol/mmol creatinine, n = 11, P less than 0.05), although this bore no relation to tumour histology, clinical stage or the outcome of the patients. Thus, ovarian cancer is accompanied by increased PGI2 production, perhaps in the kidneys and/or in the cancer tissue.
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PMID:Urinary 6-keto-prostaglandin F1a in patients with gynaecological tumours. 354 43

Several lines of evidence suggest that estrogen is an important determinant of cardiovascular risk in women. Epidemiologic data document low rates of coronary heart disease (CHD) in premenopausal women, a narrowing of the gender gap in CHD mortality after menopause, and elevated risk of CHD among young women with bilateral oophorectomy not treated with estrogen. Nearly all of the more than 30 observational studies of exogenous estrogen replacement therapy have indicated a reduced risk of CHD among women receiving estrogen therapy. In a meta-analysis comparing estrogen users and nonusers, the estimated reduction of CHD among users was 44%. In angiographic studies, women taking estrogen were less likely to have coronary artery stenosis. Estrogen is known to affect a wide range of physiologic processes that may have an impact on CHD risk. Use of oral estrogen has favorable effects on serum lipid profiles; it increases high-density lipoprotein cholesterol levels by 10% to 15% and decreases low-density lipoprotein cholesterol levels by a similar magnitude. Other proposed mechanisms include inhibition of endothelial hyperplasia, reduced arterial impedance, enhanced production of prostacyclin, increased insulin sensitivity, and inhibition of oxidation of low-density lipoprotein. Nevertheless, the role of hormone replacement therapy in preventing clinical atherosclerotic events in women remains inconclusive because of the absence of randomized trial data. The benefit-to-risk ratio must be reliably assessed, because estrogen has complex actions, including postulated benefits (CHD, osteoporosis, and menopausal symptoms) and postulated risks (endometrial cancer, breast cancer, and gallstones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postmenopausal hormone therapy and atherosclerotic disease. 797 16

Prostanoids are bioactive lipids that interact with 7-membrane-spanning G-protein-coupled receptors on target cells to impart their biologic effects. They include prostaglandins, prostacyclin, and thromboxane. Prostanoids are widely distributed; mediate several diverse biologic effects like platelet aggregation and smooth-muscle contraction; and are known to be involved in allergies, acquired immunity, and cancer metastasis. Prostanoids have also been associated with breast and endometrial cancer promotion, and with the inhibition of melanoma. The role of prostanoids in the development of lung disease has been poorly understood. In particular, prostacyclin possesses significant anti-inflammatory and antimetastatic properties and is the main product of cyclooxygenase-2 activity in the lung. In fact, the balance of the various members of the prostanoids family, specifically the prostaglandins PGE(2) and prostacyclin (PGI(2)), seems to play an increasingly important role in the development of lung cancer. Gaining a better understanding of prostanoids and their associated pathways is critical to the future development of molecular-based and pharmaceutical treatments of lung disease.
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PMID:The role of prostacyclin in lung cancer. 2012 85