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Statements

Subject Item
n2:RIV%2F00064173%3A_____%2F12%3A00003851%21RIV13-MZ0-00064173
rdf:type
n11:Vysledek skos:Concept
dcterms:description
Oestrogen receptor-α (ER) is the defining and driving transcription factor in the majority of breast cancers and its target genes dictate cell growth and endocrine response, yet genomic understanding of ER function has been restricted to model systems1, 2, 3. Here we map genome-wide ER-binding events, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), in primary breast cancers from patients with different clinical outcomes and in distant ER-positive metastases. We find that drug-resistant cancers still recruit ER to the chromatin, but that ER binding is a dynamic process, with the acquisition of unique ER-binding regions in tumours from patients that are likely to relapse. The acquired ER regulatory regions associated with poor clinical outcome observed in primary tumours reveal gene signatures that predict clinical outcome in ER-positive disease exclusively. We find that the differential ER-binding programme observed in tumours from patients with poor outcome is not due to the selection of a rare subpopulation of cells, but is due to the FOXA1-mediated reprogramming of ER binding on a rapid timescale. The parallel redistribution of ER and FOXA1 binding events in drug-resistant cellular contexts is supported by histological co-expression of ER and FOXA1 in metastatic samples. By establishing transcription-factor mapping in primary tumour material, we show that there is plasticity in ER-binding capacity, with distinct combinations of cis-regulatory elements linked with the different clinical outcomes Oestrogen receptor-α (ER) is the defining and driving transcription factor in the majority of breast cancers and its target genes dictate cell growth and endocrine response, yet genomic understanding of ER function has been restricted to model systems1, 2, 3. Here we map genome-wide ER-binding events, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), in primary breast cancers from patients with different clinical outcomes and in distant ER-positive metastases. We find that drug-resistant cancers still recruit ER to the chromatin, but that ER binding is a dynamic process, with the acquisition of unique ER-binding regions in tumours from patients that are likely to relapse. The acquired ER regulatory regions associated with poor clinical outcome observed in primary tumours reveal gene signatures that predict clinical outcome in ER-positive disease exclusively. We find that the differential ER-binding programme observed in tumours from patients with poor outcome is not due to the selection of a rare subpopulation of cells, but is due to the FOXA1-mediated reprogramming of ER binding on a rapid timescale. The parallel redistribution of ER and FOXA1 binding events in drug-resistant cellular contexts is supported by histological co-expression of ER and FOXA1 in metastatic samples. By establishing transcription-factor mapping in primary tumour material, we show that there is plasticity in ER-binding capacity, with distinct combinations of cis-regulatory elements linked with the different clinical outcomes
dcterms:title
Differential oestrogen receptor binding is associated with clinical outcome in breast cancer Differential oestrogen receptor binding is associated with clinical outcome in breast cancer
skos:prefLabel
Differential oestrogen receptor binding is associated with clinical outcome in breast cancer Differential oestrogen receptor binding is associated with clinical outcome in breast cancer
skos:notation
RIV/00064173:_____/12:00003851!RIV13-MZ0-00064173
n11:predkladatel
n12:ico%3A00064173
n3:aktivita
n4:I n4:S
n3:aktivity
I, S
n3:cisloPeriodika
7381
n3:dodaniDat
n18:2013
n3:domaciTvurceVysledku
n17:1293354
n3:druhVysledku
n8:J
n3:duvernostUdaju
n16:S
n3:entitaPredkladatele
n9:predkladatel
n3:idSjednocenehoVysledku
131265
n3:idVysledku
RIV/00064173:_____/12:00003851
n3:jazykVysledku
n7:eng
n3:klicovaSlova
grade; sites; reveals; prognosis; resistance; FOXA1; survival; Chip-seq; ER-alpha; gene-expression signature
n3:klicoveSlovo
n5:FOXA1 n5:survival n5:ER-alpha n5:sites n5:resistance n5:grade n5:gene-expression%20signature n5:reveals n5:prognosis n5:Chip-seq
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[41A69808CF2E]
n3:nazevZdroje
Nature
n3:obor
n10:FD
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
15
n3:rokUplatneniVysledku
n18:2012
n3:svazekPeriodika
481
n3:tvurceVysledku
Gojiš, Ondřej
n3:wos
000299210600048
s:issn
0028-0836
s:numberOfPages
6
n15:doi
10.1038/nature10730