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Authordc.contributor.authorPlaza Parrochia, Francisca 
Authordc.contributor.authorRomero Osses, Carmen 
Authordc.contributor.authorValladares Boasi, Luis 
Authordc.contributor.authorVega Blanco, María Margarita 
Admission datedc.date.accessioned2018-06-27T14:23:34Z
Available datedc.date.available2018-06-27T14:23:34Z
Publication datedc.date.issued2017
Cita de ítemdc.identifier.citationSteroids 126 (2017): 85–91es_ES
Identifierdc.identifier.other10.1016/j.steroids.2017.08.007
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/149269
Abstractdc.description.abstractNormal endometrial function requires of cell proliferation and differentiation; therefore, disturbances in these processes could lead to pathological entities such as hyperplasia and endometrial adenocarcinoma, where cell proliferation is increased. The development of these pathologies is highly related to alterations in the levels and/or action of sexual steroids. In the present review, it has been analyzed how steroids, particularly estrogens, androgens and progestagens are involved in the etiopathogenesis of hyperplasia and endometrial endometrioid adenocarcinoma. The emphasis is given on pathological and pharmacological conditions that are presented as risk factors for endometrial pathologies, such as obesity, polycystic ovarian syndrome and hormone replacement postmenopausal women therapy, among others. Steroids alterations may promote changes at molecular level that enhance the development of hyperplasia and endometrioid cancer. In fact, there are solid data that indicate that estrogens stimulate cell -proliferation in this tissue; meanwhile, progestagens are able to stop cell proliferation and to increase differentiation. Nevertheless, the role of androgens is less clear, since there is contradictory information. It is most likely that the major contribution of steroids to the development of cell proliferation pathologies in endometria would be in early stages, where there is a high sensitivity to these molecules. This phenomenon is present even in stages previous to the occurrence of hyperplasia, like in the condition of polycystic ovarian syndrome, where the endometria have a greater sensitivity to steroids and high expression of cell cycle molecules. These abnormalities would contribute to the pathogenesis of hyperplasia and then in the progression to endometrioid adenocarcinoma.es_ES
Patrocinadordc.description.sponsorshipFONDECYT 1100299 1130053 CONICYT 24121153 CONICYT Doctoral National Fellowship 21100275es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherElsevieres_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceSteroidses_ES
Keywordsdc.subjectEndometriaes_ES
Keywordsdc.subjectCanceres_ES
Keywordsdc.subjectSteroidses_ES
Keywordsdc.subjectHyperplasiaes_ES
Keywordsdc.subjectAdenocarcinomaes_ES
Títulodc.titleEndometrium and steroids, a pathologic overviewes_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadortjnes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile