Navegando por Palavras-chave "endometrial cancer"

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    Association of angiotensin-converting enzyme I gene I/D polymorphism with endometrial but not with ovarian cancer
    (Informa Healthcare, 2012-11-01) Corrêa, Silvana Aparecida Alves [UNIFESP]; Ribeiro de Noronha, Samuel Marcos [UNIFESP]; Alecrim, Cheryl [UNIFESP]; Mesquita, Adriana de Carvalho [UNIFESP]; Silva Brito, Gabriela Soares da [UNIFESP]; Junqueira, Michele Gilvana [UNIFESP]; Leite, Daniela Batista [UNIFESP]; Carvalho, Cristina Valletta de [UNIFESP]; Cotrim Guerreiro da Silva, Ismael Dale [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Associations have been found between the angiotensin-converting enzyme insertion deletion (I/D) polymorphism (ACE I/D) and endometrial and epithelial ovarian cancer (EC and EOC, respectively). in this study, the following frequencies for each of three ACE polymorphisms, DD, ID, and II, respectively, were observed: in the EC group, 55, 24, and 21% versus the control group 39, 40, and 21% (p = 0.033*); in the EOC group 49, 36, and 15% versus the control group 49, 33, and 18% (p = 0.82). According to these allelic distributions, DD carriers are 2.0 times more likely than individuals carrying the ID or II genotypes to develop EC; therefore, the DD genotype seems to be protective against EC. in contrast, no association was observed between ACE (I/D) polymorphism with EOC. the ACE (I/D) polymorphism might play a role in the pathogenesis of EC and it should be considered when identifying genetic markers for EC.
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    Regulation of estrogen target genes and growth by selective estrogen-receptor modulators in endometrial cancer cells
    (Elsevier B.V., 2002-06-01) Dardes, Rita de Cássia de Maio [UNIFESP]; Schafer, J. M.; Pearce, S. T.; Osipo, C.; Chen, B.; Jordan, V. C.; Universidade Federal de São Paulo (UNIFESP); Northwestern Univ
    Objective. Tamoxifen has mixed agonist/antagonist activities, leading to tissue-specific estrogen-like actions and endometrial cancer. the purpose of this study was to evaluate the effects of antiestrogens on the growth of estrogen receptor (ER)-positive ECC-1 endometrial cancer cells in vitro and in vivo.Methods. We performed growth studies and luciferase assays using ERE-tK and AP-1 reporters. ERalpha protein expression was measured by Western blot after antiestrogen treatments. We investigated the actions of antiestrogens on the transcription of the pS2 gene in situ measured by Northern blot and the actions of antiestrogens on the VEGF protein secreted by ELISA. ERa, ERbeta, EGFR, and HER2/neu mRNAs were determined by RTPCR. Last, ECC-1 tumors were developed by inoculation of cells into ovariectomized athymic mice and treated with estradiol (EA tamoxifen, raloxifene, and a combination.Results. E-2 induced cell proliferation while antiestrogens did not. E2 and raloxifene down regulated ERa protein; in contrast, 4OHT did not. IC1182,780 completely degraded the receptor. ECC-1 cells express ER,6 at insignificant levels. Luciferase assays did not show any induction in ERE- nor AP-1-mediated transcription by antiestrogens. E2 caused a concentration-dependent increase in pS2 mRNA but antiestrogens did not. E, increased VEGF expression in a dose-dependent manner and antiestrogens blocked E2 action. E. down regulated HER2/neu while 40HT and raloxifene did not change HER2/neu levels compared to control. in addition, EGFR mRNA was down regulated by E, but raloxifene did not change it. Tamoxifen and raloxifene did not promote tumor growth in vivo. However, raloxifene (1.5 mg daily) only partially blocked E-stimulated growth.Conclusions. Tamoxifen and raloxifene are anti proliferative agents and antiestrogens in ECC-1 endometrial cells in vitro and in vivo. the observation that selective estrogen-receptor modulators do not down regulate EGFR and HER2/neu mRNA may provide a potential role for these oncogenes in the development of raloxifene- or tamoxifen-stimulated endometrial cancer. the ECC-1 cell line could provide important new clues about the evolution of drug resistance to tamoxifen and raloxifene. (C) 2002 Elsevier Science (USA).