Locally, E2 can be formed either via the so-called aromatase pathway from androstenedione (A-dione), which originates from dehydroepiandrosterone-sulfate (DHEA-S) and DHEA, or from testosterone (T), by the actions of aromatase and the reductive 17β-hydroxysteroid dehydrogenases (enzymes 17β-HSD, HSD17B Figure ). Local estrogen formation has an important role in the development of EC and increased estradiol (E2) concentrations have been detected in cancerous, as compared to normal endometrium (). Although, type II EC was considered to be estrogen independent ( ), experimental data suggest involvement of estrogens ( ). Prank Programs Blogspot Comics more.ĮC can be classified into estrogen-dependent type I, which comprises 80% of all cases, and the poorly differentiated, more aggressive, type II. Introduction Endometrial cancer (EC) is the fifth-most-common cancer in women in Western Europe and the USA, with the majority of cases arising after menopause ( ). Our data demonstrate that in cancerous endometrium, E2 is formed from E1-S via the sulfatase pathway, and not from A-dione via the aromatase pathway. At the protein level, there were no differences in the levels of STS and HSD17B2 between cancerous and adjacent control tissue by Western blotting, and immunohistochemistry revealed intense staining for STS and HSD17B2, and weak staining for SULT1E1 and HSD17B1 in cancerous tissue. The mRNA levels of CYP19A1 and HSD17B1 were low, and HSD17B14, which promotes inactivation of E2, was significantly down-regulated in cancerous endometrium, especially in patients with lymphovascular invasion.
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There was no significant difference in expression of the key genes of the aromatase ( CYP19A1) and the sulfatase ( STS, HSD17B1, HSD17B2) pathways in cancerous endometrium compared to adjacent control tissue. In cancerous endometrium, A-dione was metabolized to testosterone, and no E2 was formed.īoth, E1-S and E1 were metabolized to E2, with increased levels of E2 seen in cancerous tissue. Furthermore, we studied expression of the key genes for estradiol formation via the aromatase and sulfatase pathways.Ī-dione and E2 were detected in cancerous and adjacent control endometrium.
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To investigate the local formation of estradiol (E2), we first measured the concentrations of the steroid precursor androstenedione (A-dione) and the most potent estrogen, E2, and we evaluated the metabolism of A-dione, estrone-sulfate (E1-S), and estrone (E1) in cancerous and adjacent control endometrium.
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Kanker hati – Sindrom nefrotik – Kanker ovarium, kanker endometrium – Pankreatitis – Kanker pankreas.ġ, 1, Maja Anko 1, Neli Hevir 1, Katja Vouk 1, Aleš Jerin 2, 3 and 1 * Hiperplasia endometrium adalah pertumbuhan yang berlebih dari kelenjar, dan stroma disertai pembentukan vaskularisasi dan infiltrasi limfosit pada endometrium. Hiperplasia Endometrium 2 ~ Dokter's Blog. Kanker ovarium bisa menyebar melalui system getah bening dan melalui sistem pembuluh darah menyebar ke hati dan paru – paru. Kanker ovarium adalah tumor ganas yang tumbuh pada ovarium (indung telur) yang paling sering ditemukan pada wanita berusia 50 – 70 tahun.