{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["109(10)"],"submitter":["Giessrigl B"],"pubmed_abstract":["<h4>Background</h4>Breast cancer is the leading cause of cancer death in women living in the western hemisphere. Despite major advances in first-line endocrine therapy of advanced oestrogen receptor (ER)-positive breast cancer, the frequent recurrence of resistant cancer cells represents a serious obstacle to successful treatment. Understanding the mechanisms leading to acquired resistance, therefore, could pave the way to the development of second-line therapeutics. To this end, we generated an ER-positive breast cancer cell line (MCF-7) with resistance to the therapeutic anti-oestrogen fulvestrant (FUL) and studied the molecular changes involved in resistance.<h4>Methods</h4>Naive MCF-7 cells were treated with increasing FUL concentrations and the gene expression profile of the resulting"],"journal":["British journal of cancer"],"pagination":["2751-62"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3833203"],"repository":["biostudies-literature"],"pubmed_title":["Fulvestrant induces resistance by modulating GPER and CDK6 expression: implication of methyltransferases, deacetylases and the hSWI/SNF chromatin remodelling complex."],"pmcid":["PMC3833203"],"pubmed_authors":["Giessrigl B","Kalipciyan M","Jeitler M","Krieger S","Mader RM","Krupitza G","Gollinger M","Schmidt WM","Jager W","Bilban M"],"additional_accession":[]},"is_claimable":false,"name":"Fulvestrant induces resistance by modulating GPER and CDK6 expression: implication of methyltransferases, deacetylases and the hSWI/SNF chromatin remodelling complex.","description":"<h4>Background</h4>Breast cancer is the leading cause of cancer death in women living in the western hemisphere. Despite major advances in first-line endocrine therapy of advanced oestrogen receptor (ER)-positive breast cancer, the frequent recurrence of resistant cancer cells represents a serious obstacle to successful treatment. Understanding the mechanisms leading to acquired resistance, therefore, could pave the way to the development of second-line therapeutics. To this end, we generated an ER-positive breast cancer cell line (MCF-7) with resistance to the therapeutic anti-oestrogen fulvestrant (FUL) and studied the molecular changes involved in resistance.<h4>Methods</h4>Naive MCF-7 cells were treated with increasing FUL concentrations and the gene expression profile of the resulting","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Nov","modification":"2025-04-26T17:40:15.319Z","creation":"2019-03-27T03:08:51Z"},"accession":"S-EPMC3833203","cross_references":{"pubmed":["24169358"],"doi":["10.1038/bjc.2013.583"]}}