title: Disorders in cytokine gene expression in endometrial hyperplasia and effect of hormone therapy.
abstract: We studied local expression of insulin-like growth factor 1, insulin-like growth factor receptor, epithelial growth factor, transforming growth factor beta2, PCNA, TNF-alpha, type I TNF receptor, Fas, FasL, IFN-gamma, IL-1beta, IL-4, IL-6, IL-8, IL-10, and IL-12 genes in intact and hyperplastic endometrium. Endometrial hyperplasia was associated with reduced production of TNF-alpha (p<0.05), PCNA (p<0.05), and epithelial growth factor mRNA and enhanced production of Fas mRNA (p<0.01). The expression of TNF-R1, IL-1beta, and IL-12 genes decreased only in glandular cystic hyperplasia (p<0.05 for all genes), expression of insulin-like growth factor 1 gene decreased only in adenomatous hyperplasia (p<0.05). Dufaston therapy of glandular cystic hyperplasia and zoladex therapy of adenomatous hyperplasia normalized expression of Fas receptor, PCNA, and insulin-like growth factor 1 genes, while the expression of IFN-gamma and IL-6 genes, which was normal in hyperplasia, decreased (p<0.05). Zoladex therapy decreased the production of transforming growth factor beta2 (p<0.05) and IL-1beta (p<0.01) mRNA, dufaston therapy decreased production of TNF-alpha (p<0.05) and IL-4 mRNA (p<0.05). Hence, both apoptosis and proliferative activity were suppressed in endometrial hyperplasia, and hormone therapy created prerequisites for transition of the endometrium into the normal proliferation stage.
authors: Research Center of Obstetrics, Gynecology, and Perinatology, Russian Academy of Medical Sciences, Moscow.
authors: G T
authors: GT
authors: Sukhikh
authors: A V
authors: AV
authors: Zhdanov
authors: M P
authors: MP
authors: Davydova
authors: T V
authors: TV
authors: Slukina
authors: G E
authors: GE
authors: Chernukha
authors: T E
authors: TE
authors: Samoilova
authors: V P
authors: VP
authors: Smetnik
mesh_terms: D017209:Apoptosis; D049109:Cell Proliferation; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004394:Dydrogesterone / Q000627:therapeutic use*; D004714:Endometrial Hyperplasia / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D017273:Goserelin / Q000627:therapeutic use*; D006801:Humans; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D017273:Goserelin; D004394:Dydrogesterone