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Tamoxifen resistance: Emerging molecular targets

dc.creatorRondón Lagos, Milena
dc.creatorVillegas Gálvez, Victoria Eugenia
dc.creatorRangel, Nelson
dc.creatorSanchez-Corredor, Magda-Carolina
dc.creatorZaphiropoulos, Peter G.
dc.creator.googleRondón-Lagos, M.spa
dc.creator.googleVillegas, V.E.spa
dc.creator.googleRangel, N.spa
dc.creator.googleSánchez, Magda Carolinaspa
dc.creator.googleZaphiropoulos, P.G.spa
dc.date.accessioned2020-05-11T22:12:38Z
dc.date.available2020-05-11T22:12:38Z
dc.date.created2016
dc.date.issued2016
dc.description.abstract17β-Estradiol (E2) plays a pivotal role in the development and progression of breast cancer. As a result, blockade of the E2 signal through either tamoxifen (TAM) or aromatase inhibitors is an important therapeutic strategy to treat or prevent estrogen receptor (ER) positive breast cancer. However, resistance to TAM is the major obstacle in endocrine therapy. This resistance occurs either de novo or is acquired after an initial beneficial response. The underlying mechanisms for TAM resistance are probably multifactorial and remain largely unknown. Considering that breast cancer is a very heterogeneous disease and patients respond differently to treatment, the molecular analysis of TAM’s biological activity could provide the necessary framework to understand the complex effects of this drug in target cells. Moreover, this could explain, at least in part, the development of resistance and indicate an optimal therapeutic option. This review highlights the implications of TAM in breast cancer as well as the role of receptors/signal pathways recently suggested to be involved in the development of TAM resistance. G protein—coupled estrogen receptor, Androgen Receptor and Hedgehog signaling pathways are emerging as novel therapeutic targets and prognostic indicators for breast cancer, based on their ability to mediate estrogenic signaling in ERα-positive or -negative breast cancer.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.3390/ijms17081357
dc.identifier.issn1661-6596
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/21958
dc.language.isoengspa
dc.relation.citationTitleInternational Journal of Molecular Sciences
dc.relation.citationVolumeVol. 17
dc.relation.ispartofInternational Journal of Molecular Sciences, ISSN: 1661-6596 Vol. 17, (Agosto 2016); 31 ppspa
dc.relation.urihttps://www.mdpi.com/1422-0067/17/8/1357spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subject.ddcIncidencia & prevención de la enfermedadspa
dc.subject.keywordTamoxifenspa
dc.subject.keywordBreast cancerspa
dc.subject.keywordG protein-coupled estrogen receptor (gper)spa
dc.subject.keywordEstrogen receptors (ers)spa
dc.subject.keywordAndrogen receptor (ar)spa
dc.subject.keywordHedgehog (hh) signaling pathwayspa
dc.subject.keywordEndocrine resistancespa
dc.subject.keywordAntibiotic sensitivityspa
dc.subject.keywordBiological activityspa
dc.subject.keywordNeu differentiation factorspa
dc.titleTamoxifen resistance: Emerging molecular targetsspa
dc.typerevieweng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaRevisiónspa
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