{"status":"OK","data":{"id":55608,"identifier":"DVN/DHHH0Y","persistentUrl":"https://doi.org/10.7910/DVN/DHHH0Y","protocol":"doi","authority":"10.7910","separator":"/","publisher":"Harvard Dataverse","publicationDate":"2010-10-19","storageIdentifier":"s3://1902.1/15200","effectiveDatasetFileCountLimit":1000,"datasetFileUploadsAvailable":999,"datasetType":"dataset","locks":[],"latestVersion":{"id":54353,"datasetId":55608,"datasetPersistentId":"doi:10.7910/DVN/DHHH0Y","datasetType":"dataset","storageIdentifier":"s3://1902.1/15200","versionNumber":1,"internalVersionNumber":1,"versionMinorNumber":0,"versionState":"RELEASED","latestVersionPublishingState":"RELEASED","deaccessionNote":"","deaccessionLink":"","lastUpdateTime":"2010-10-18T15:02:19Z","releaseTime":"2010-10-19T00:00:00Z","createTime":"2010-10-18T14:56:10Z","alternativePersistentId":"hdl:1902.1/15200","publicationDate":"2010-10-19","citationDate":"2010-10-19","effectiveDatasetFileCountLimit":1000,"datasetFileUploadsAvailable":999,"license":{"name":"CC0 1.0","uri":"http://creativecommons.org/publicdomain/zero/1.0","iconUri":"https://licensebuttons.net/p/zero/1.0/88x31.png","rightsIdentifier":"CC0-1.0","rightsIdentifierScheme":"SPDX","schemeUri":"https://spdx.org/licenses/","languageCode":"en"},"fileAccessRequest":false,"metadataBlocks":{"citation":{"displayName":"Citation Metadata","name":"citation","fields":[{"typeName":"title","multiple":false,"typeClass":"primitive","value":"Growth Factor Stimulation Induces a Distinct ERalpha Cistrome Underlying Breast Cancer Endocrine Resistance"},{"typeName":"author","multiple":true,"typeClass":"compound","value":[{"authorName":{"typeName":"authorName","multiple":false,"typeClass":"primitive","value":"Mathieu Lupien"},"authorAffiliation":{"typeName":"authorAffiliation","multiple":false,"typeClass":"primitive","value":"Harvard Medical School/Brigham & Women's Hospital"}},{"authorName":{"typeName":"authorName","multiple":false,"typeClass":"primitive","value":"Clifford Meyer"},"authorAffiliation":{"typeName":"authorAffiliation","multiple":false,"typeClass":"primitive","value":"Harvard School of Public Health/Dana-Farber Cancer Institut"}},{"authorName":{"typeName":"authorName","multiple":false,"typeClass":"primitive","value":"et al."}}]},{"typeName":"datasetContact","multiple":true,"typeClass":"compound","value":[{"datasetContactEmail":{"typeName":"datasetContactEmail","multiple":false,"typeClass":"primitive","value":"N/A"}}]},{"typeName":"dsDescription","multiple":true,"typeClass":"compound","value":[{"dsDescriptionValue":{"typeName":"dsDescriptionValue","multiple":false,"typeClass":"primitive","value":"INSTRUCTIONS: Please enter one of the following Topic Classifications in the section below:  Bioinformatics\n& Computational Biology Genes & Environment Genetic & Molecular Epidemiology Medical Genomics Molecular Genetics Proteomics Statistical Genetics, Genomics, and Omics"}},{"dsDescriptionValue":{"typeName":"dsDescriptionValue","multiple":false,"typeClass":"primitive","value":"Estrogen receptor a (ERa) expression in breast cancer is predictive of response to endocrine therapy; however,resistance is common in ERa-positive tumors that overexpress the growth factor receptor ERBB2. Even in the absence of estrogen, ERa can be activated by growth factors, including the epidermal growth factor (EGF). EGF induces a transcriptional program distinct from estrogen; however, the mechanism of the stimulus-specific response is unknown. Here we show that the EGF-induced ERa genomic targets, its cistromes, are distinct from those induced by estrogen in a process dependent on the transcription factor AP-1. The EGF-induced ERa cistrome specifically regulates genes found overexpressed in ERBB2-positive human breast cancers. This providesa potential molecular explanation for the endocrine therapy resistance seen in ERa-positive breast cancers that overexpress ERBB2. These results suggest a central role for ERa in hormone-refractory breast tumors dependent on growth factor pathway activation and favors the development of therapeutic strategies completely antagonizing ERa, as opposed to blocking its estrogen responsiveness alone. [Keywords: ERBB2; breast cancer; cistrome; estrogen receptor; growth factors; transcription]"}}]},{"typeName":"dateOfDeposit","multiple":false,"typeClass":"primitive","value":"2010-10-18"}]}},"files":[{"description":"","label":"Genes Dev.-2010-Lupien-2219-27.pdf","restricted":false,"version":1,"datasetVersionId":54353,"dataFile":{"id":1581692,"persistentId":"doi:10.7910/DVN/DHHH0Y/8DBN5I","pidURL":"https://doi.org/10.7910/DVN/DHHH0Y/8DBN5I","filename":"Genes Dev.-2010-Lupien-2219-27.pdf","contentType":"application/pdf","friendlyType":"Adobe PDF","filesize":1015063,"description":"","storageIdentifier":"s3://dvn-cloud:61866","rootDataFileId":-1,"md5":"32b811a56eb380cb4564a14fa4b472f1","checksum":{"type":"MD5","value":"32b811a56eb380cb4564a14fa4b472f1"},"tabularData":false,"creationDate":"2010-10-18","publicationDate":"2010-10-18","lastUpdateTime":"2010-10-18T15:02:19Z","fileAccessRequest":false}}]}}}