sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_4 ;
    pav:version "1.4" .
  sub:_3 prov:value "In breast cancers, estrogen receptor (ER) levels are highly correlated with response to endocrine therapies. We sought to define mechanisms of estradiol (E) signaling in a solid breast tumor model using gene expression profiling. ER+ T47D-Y human breast cancer cells were grown as xenografts in ovariectomized nude mice under four conditions: i. E for 8 weeks (E); ii. without E for 8 weeks (controls, C); iii. E for 7 weeks followed by 1 week of E withdrawal (Ewd), or iv. E for 8 weeks with Tamoxifen for the last week (E+Tam). E-regulated genes were defined as those that differed significantly between C and E, and/or between E and Ewd. These protocols generated 188 in vivo E-regulated genes that showed two major patterns of regulation. Approximately 46% returned to basal states after Ewd (Class I genes); 53% did not (Class II genes). In addition, more than 70% of Class II regulated genes also failed to reverse in response to Tamoxifen. These genes may be interesting to study hormone resistance issues. A subset of in vivo E-regulated genes appears on lists of clinical  \\\"ER discriminator \\\" genes. These may be useful therapeutic targets or markers of E activity. Comparison of in vivo E-regulated genes to those regulated in identical cells in vitro after 6 and 24 h of E treatment demonstrate only 11% overlap. This indicates the extent to which gene expression profiles are uniquely dependent on hormone treatment times and the cellular microenvironment." ;
    prov:wasQuotedFrom pubmed:16239301 .
  sub:_4 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:16239301 ;
    prov:wasDerivedFrom beldoc: , sub:_3 .
}