Gene expression profile of breast cancer cells depleted for BRCA1 pseudogene (BRCA1P1)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA448265 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profile of MDA-MB-231 breast cancer cells with BRCA1 pseudogene (BRCA1P1) knockout (KO)
| PRJNA448266 | ENA
Project description:Gene expression profile of breast cancer cells transfected with antisense oligonucleotides (ASO) against BRCA1 pseudogene (BRCA1P1)
| PRJNA448264 | ENA
Project description:Purpose: As estrogen receptor (ER)-positive breast cancer in BRCA1 mutation carriers arises at an older age with less aggressive tumor characteristics than ER negative BRCA1 mutated breast cancer, it has been suggested that these tumors are ?sporadic? and not BRCA1-driven. With the introduction of targeted treatments specific for tumors with a non-functioning BRCA1 or BRCA2 gene, the question whether the BRCA genes are impaired in the tumor, is highly relevant. Therefore, we performed genomic profiling of BRCA1-mutated ER+ tumors. Experimental design: Genomic profiling, BRCA1 promoter methylation assessment, and loss of heterozygosity analysis were done on 16 BRCA1-mutated ER+ tumors. Results were compared with 57 BRCA1-mutated ER- tumors, 36 BRCA2-mutated ER+ associated tumors, and 182 sporadic ER+ tumors [GSE9021, GSE9114, GSE16511, GSE50407] Results: The genomic profile of BRCA1-mutated ER+ tumors was different from BRCA1-mutated ER- breast tumors, but highly similar to BRCA2-mutated ER+ tumors. In 83% of the BRCA1-mutated ER+ tumors, loss of the wildtype BRCA1 allele was observed. In addition, clinico-pathological variables in BRCA1-mutated ER+ cancer were also more similar to BRCA2-mutated ER+ and sporadic ER+ breast cancer than to BRCA1 mutated ER- cancers. Conclusions: As BRCA1-mutated ER+ tumors show a BRCAness copy number profile and LOH, it is likely that the loss of a functional BRCA1 protein plays a role in tumorigenesis in BRCA1-mutated ER+ tumors. Therefore, we hypothesize that these tumors are sensitive to drugs targeting the BRCA1 gene defect, providing new targeted treatment modalities for advanced BRCA-deficient, ER-positive breast cancer.
2016-10-01 | GSE77603 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-03-24 | GSE112574 | GEO
Project description:Analysis of miRNA expression in grade 3 luminal, sporadic and BRCA1 associated basal-like breast cancers 44 primary grade III breast cancer (11 BRCA1 basal, 16 sporadic basal, 17 luminal) and 13 normal breast FFPE (formalin fixed, paraffin embedded) specimens, plus 7 controls and 5 cell lines were analysed. The aim of the study was to derive grade-specific miRNA signatures for sporadic and BRCA1 basal-like breast cancers, and to ascertain an immunohistochemical profile regulated by BRCA1 specific miRNAs for potential diagnostic uses.
2014-09-16 | E-GEOD-61438 | biostudies-arrayexpress
Project description:Purpose: As estrogen receptor (ER)-positive breast cancer in BRCA1 mutation carriers arises at an older age with less aggressive tumor characteristics than ER negative BRCA1 mutated breast cancer, it has been suggested that these tumors are ?sporadic? and not BRCA1-driven. With the introduction of targeted treatments specific for tumors with a non-functioning BRCA1 or BRCA2 gene, the question whether the BRCA genes are impaired in the tumor, is highly relevant. Therefore, we performed genomic profiling of BRCA1-mutated ER+ tumors. Experimental design: Genomic profiling, BRCA1 promoter methylation assessment, and loss of heterozygosity analysis were done on 16 BRCA1-mutated ER+ tumors. Results were compared with 57 BRCA1-mutated ER- tumors, 36 BRCA2-mutated ER+ associated tumors, and 182 sporadic ER+ tumors [GSE9021, GSE9114, GSE16511, GSE50407]. Results: The genomic profile of BRCA1-mutated ER+ tumors was different from BRCA1-mutated ER- breast tumors, but highly similar to BRCA2-mutated ER+ tumors. In 83% of the BRCA1-mutated ER+ tumors, loss of the wildtype BRCA1 allele was observed. In addition, clinico-pathological variables in BRCA1-mutated ER+ cancer were also more similar to BRCA2-mutated ER+ and sporadic ER+ breast cancer than to BRCA1 mutated ER- cancers. Conclusions: As BRCA1-mutated ER+ tumors show a BRCAness copy number profile and LOH, it is likely that the loss of a functional BRCA1 protein plays a role in tumorigenesis in BRCA1-mutated ER+ tumors. Therefore, we hypothesize that these tumors are sensitive to drugs targeting the BRCA1 gene defect, providing new targeted treatment modalities for advanced BRCA-deficient, ER-positive breast cancer.
2016-10-01 | GSE77604 | GEO
Project description:Loss of function of the tumor suppressor BRCA1 (Breast Cancer 1) protein is responsible for numerous familial and sporadic breast cancers. We previously identified PABP1 as a novel BRCA1 partner and showed that BRCA1 modulates translation through its interaction with PABP1. We showed that the global translation was diminished in BRCA1-depleted cells and increased in BRCA1-overexpressing cells. Our findings raised the question whether BRCA1 affects translation of all cytoplasmic cellular mRNAs or whether it specifically targets a subset of mRNAs. In the present study, we investigated which mRNAs are regulated by BRCA1 using a microarray analysis of polysome-associated RNAs from BRCA1-depleted MCF7 cells, a human breast cancer cell line.
2013-12-31 | GSE40730 | GEO
Project description:BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1).
2014-04-25 | GSE47016 | GEO
Project description:BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1). Chromatin Immunoprecipitaitons were performed in triplicate with BCLAF1 antibodies in control 293T cells transfected with siGFP siRNAs and BRCA1 siRNAs (siBRCA1 to deplete BRCA1). Immunoprecipitated genomic DNA was labelled with Cy3 and Input genomic DNA was labelled with Cy5 and hybridized to NimbleGen human 3x720k RefSeq promoter arrays to identify BCLAF1 boundgenomic DNA regions.
2014-04-25 | E-GEOD-47016 | biostudies-arrayexpress
Project description:We have analyzed, using DNA microarrays, putative differences in gene-expression level between hereditary BRCA1 mutation-linked and sporadic breast cancer. Our results show that a previously reported marked difference between BRCA1-mutation linked and sporadic breast cancer was probably due to uneven stratification of samples with different ER status and basal-like versus luminal-like subtype. We observed that apparent difference between BRCA1-linked and other types of breast cancer found in univariate analysis was diminished when data were corrected for ER status and molecular subtype in multivariate analyses. In fact, the difference in gene expression pattern of BRCA1-mutated and sporadic cancer is very discrete. These conclusions were supported by the results of Q-PCR validation. We also found that BRCA1 gene inactivation due to promoter hypermethylation had similar effect on general gene expression profile as mutation-induced protein truncation. This suggests that in the molecular studies of hereditary breast cancer, BRCA1 gene methylation should be recognized and considered together with gene mutation.
2013-09-05 | GSE50567 | GEO