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dc.contributor.authorTorres-Arzayus, Maria I.
dc.contributor.authorFont de Mora, Jaime
dc.contributor.authorYuan, Jing
dc.contributor.authorVazquez, Francisca
dc.contributor.authorBronson, Roderick
dc.contributor.authorRué i Monné, Montserrat
dc.contributor.authorSellers, William R.
dc.contributor.authorBrown, Myles
dc.date.accessioned2016-05-19T08:53:52Z
dc.date.issued2004
dc.identifier.issn1535-6108
dc.identifier.urihttp://hdl.handle.net/10459.1/57053
dc.description.abstractThe gene encoding AIB1, an estrogen receptor coactivator, is amplified in a subset of human breast cancers. Here we show that overexpression of AIB1 in transgenic mice (AIB1-tg) leads to mammary hypertrophy, hyperplasia, abnormal postweaning involution, and the development of malignant mammary tumors. Tumors are also increased in other organs, including the pituitary and uterus. AIB1 overexpression increases mammary IGF-I mRNA and serum IGF-I protein levels. In addition, IGF-I receptor and downstream signaling molecules are activated in primary mammary epithelial cells and mammary tumor cells derived from AIB1-tg mice. Knockdown of AIB1 expression in cultured AIB1-tg mammary tumor cells leads to reduced IGF-I mRNA levels and increased apoptosis, suggesting that an autocrine IGF-I loop underlies the mechanism of AIB1-induced oncogenesis.ca_ES
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.ccr.2004.06.027ca_ES
dc.relation.ispartofCancer Cell, 2004, vol. 6, núm. 3, p. 263-274ca_ES
dc.rights(c) Cell Press, 2004ca_ES
dc.titleHigh tumor incidence and activation of the PI3K/AKT pathway in transgenic mice define AIB1 as an oncogeneca_ES
dc.typearticleca_ES
dc.identifier.idgrec009164
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1016/j.ccr.2004.06.027
dc.date.embargoEndDate2025-01-01


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