Comparative oncogenomics
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30443 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3020840.fastq.gz | Fastqsanger.gz | |||
| ERR3020850.fastq.gz | Fastqsanger.gz | |||
| ERR3020860.fastq.gz | Fastqsanger.gz | |||
| ERR3020870.fastq.gz | Fastqsanger.gz | |||
| ERR3020880.fastq.gz | Fastqsanger.gz |
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Project description:In order to identify new targets for basal-like breast cancers, we performed Methyl-Seq of 10 breast cancer cell lines. Basal-like cell lines (MDAMB231, MDAMB436, HCC1937, SUM149, SUM1315 and MCF10A) were compared to luminal cell lines (MCF7 and T47D). Moreover we could also study BRCA1 influence on methylome of basal-like breast cancer. 4 of our cell lines are indeed BRCA1 mutated (MDAMB436, HCC1937, SUM149 and SUM1315) and we also developed 2 cell lines that come from the BRCA1 mutated SUM1315 cell line stably transfected with empty LXSN plasmid (SUM1315-LXSN) or with a BRCA1 coding plasmid (SUM1315-BRCA1).
2017-02-14 | E-MTAB-5468 | biostudies-arrayexpress
Project description:In order to identify new targets for basal-like breast cancers, we performed RNA-Seq of 10 breast cancer cell lines. Basal-like cell lines (MDAMB231, MDAMB436, HCC1937, SUM149, SUM1315 and MCF10A) were compared to luminal cell lines (MCF7 and T47D). Moreover we could also study BRCA1 influence on transcriptome of basal-like breast cancer. 4 of our cell lines are indeed BRCA1 mutated (MDAMB436, HCC1937, SUM149 and SUM1315) and we also developed 2 cell lines that come from the BRCA1 mutated SUM1315 cell line stably transfected with empty LXSN plasmid (SUM1315-LXSN) or with a BRCA1 coding plasmid (SUM1315-BRCA1).
2017-02-14 | E-MTAB-5465 | 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: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.
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Project description:Comparative oncogenomics identifies breast tumors enriched in functional tumor initiating cells
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Project description:The Long-read POG dataset comprises a cohort of 189 patient tumours and 41 matched normal samples sequenced using the Oxford Nanopore Technologies PromethION platform. This dataset from the Personalized Oncogenomics (POG) program and the Marathon of Hope Cancer Centres Network includes accompanying DNA and RNA short-read sequence data, analytics, and clinical information. We show the potential of long-read sequencing for resolving complex cancer-related structural variants, viral integrations, and extrachromosomal circular DNA. Long-range phasing of variants facilitates the discovery of allelically differentially methylated regions (aDMRs) and allele-specific expression, including recurrent aDMRs in the cancer genes RET and CDKN2A. Germline promoter methylation in MLH1 can be directly observed in Lynch syndrome. Promoter methylation in BRCA1 and RAD51C is a likely driver behind patterns of homologous recombination deficiency where no driver mutation was found. This dataset demonstrates applications for long-read sequencing in precision medicine, and is available as a resource for developing analytical approaches using this technology.
2024-10-15 | GSE270257 | GEO
Project description:We hypothesized that the transcriptome of primary cultures of morphologically normal ovarian surface epithelial cells could be altered by the presence of a heterozygous BRCA1 or BRCA2 mutation. We aimed to discover early events associated to ovarian carcinogenesis, which could represent putative targets for preventive strategies of this silent killer tumor. We identified the first molecular signature associated with French Canadian BRCA1 or BRCA2 founder mutations in morphologically normal ovarian epithelial cells. We discovered that wild-type and mutated BRCA2 allelic transcripts were expressed not only in morphologically normal but also in tumor cells from 8765delAG BRCA2 carriers. Further analysis of morphologically normal ovarian and tumor cells from C4446T BRCA1 carriers lead to the same observation. Our data support the idea that one single hit in BRCA1 or BRCA2 is sufficient to alter the transcriptome of phenotypically normal ovarian epithelial cell. The highest level of BRCA2 mutated allele transcript expression was measured in cells originating from the most aggressive ovarian tumor. The penetrance of the mutation and the aggressiveness of the related tumor could depend on a dosage effect of the mutated allele transcript. We studied the molecular profiles associated with 5 a priori classes of samples : 4 non-familial morphologically normal ovarian surface epithelium (NOSEs) : NM class, 2 BRCA1-mutated NOSEs : M1 class, 3 BRCA2-mutated NOSEs : M2 class, 3 BRCA1-mutated ovarian tumor cells (TOVs) : TM1 class and one BRCA2-mutated TOV :TM2 class. No technical replicates were included in this study. The following contrasts were computed : NM vs. M1, NM vs. M2, M1 vs. M2, M1 vs. TM1 and M (M1 union M2) vs. TM (TM1 union TM2).
2012-06-14 | E-GEOD-34928 | biostudies-arrayexpress
Project description:Breast tumors from BRCA1 germ line mutation carriers typically exhibit features of the basal-like molecular subtype. However, the specific genes recurrently mutated as a consequence of BRCA1 dysfunction have not been fully elucidated. In this study, we utilized gene expression profiling to molecularly subtype 577 breast tumors, including 73 breast tumors from BRCA1/2 mutation carriers. Focusing on the RB1 locus, we analyzed 33 BRCA1-mutated, 36 BRCA2-mutated and 48 non-BRCA1/2-mutated breast tumors using a custom-designed high-density oligomicroarray covering the RB1 gene. We found a strong association between the basal-like subtype and BRCA1-mutated breast tumors and the luminal B subtype and BRCA2-mutated breast tumors. RB1 was identified as a major target for genomic disruption in tumors arising in BRCA1 mutation carriers and in sporadic tumors with BRCA1 promoter-methylation, but rarely in other breast cancers. Homozygous deletions, intragenic breaks, or microdeletions were found in 33% of BRCA1-mutant tumors, 36% of BRCA1 promoter-methylated basal-like tumors, 13% of non-BRCA1 deficient basal-like tumors, and 3% of BRCA2-mutated tumors. In addition, RB1 was frequently inactivated by gross gene disruption in BRCA1-related hereditary breast cancer and BRCA1-methylated sporadic basal-like breast cancer, but rarely in BRCA2-hereditary breast cancer and non-BRCA1-deficient sporadic breast cancers. Together, our findings demonstrate the existence of genetic heterogeneity within the basal-like breast cancer subtype that is based upon BRCA1-status. Gene expression profiling of breast tumors. Dual color common reference gene expression study using 55K oligonucleotide microarrays.
2012-06-26 | E-GEOD-25307 | biostudies-arrayexpress
Project description:Purpose: Loss-of-function mutations of the breast cancer type 1 susceptibility protein (BRCA1) are associated with breast (BC) and ovarian cancer (OC). We assessed responses to histone deacetylase inhibitors (HDACi) and performed genome-wide RNA and chromatin immunoprecipitation (ChIP)-sequencing in isogenic OC cells UWB1.289 (carrying a BRCA1 mutation) and UWB1.289 transduced with wild type BRCA1. Experimental Design: Gene expression profiles of cells harboring mutated vs. functional BRCA1 and treated with the HDACi were integrated with chromatin mapping of histone H3 lysine 9 or 27 acetylation (H3K9ac, H3K27ac) at active promoters and enhancers. Key pathways found deregulated in BRCA1 mutated cells were validated. Results: Gene networks activated in BRCA1-mutated vs. BRCA1+ OC cells relate to Cellular Movement, Cellular Development, Cellular Growth and Proliferation and shared upstream regulators included TGFb1, TNF, and IFN-g. The IFN-g pathway was significantly altered in response to HDACi in BRCA1+ vs. BRCA1-mutated cells and in BRCA1-mutated/or low vs. BRCA1-normal ovarian tumors profiled in the TCGA database. Key IFN-γ-induced genes upregulated at baseline in BRCA1-mutated vs. BRCA1+ OC and BC cells included CXCL10, CXCL11, and IFI16. Increased localization of STAT1 to the promoters of these genes was observed in BRCA1-mutated cells, resulting in diminished cellular responses to IFN-γ or to STAT1 knockdown. The IFN-g signature was associated with improved survival among tumors profiled by the TCGA. Conclusions: Transcriptomic changes affecting IFN-γ response are associated with inactivating BRCA1 mutations in OC. These alterations could contribute to diminished anti-tumor immunity in BRCA1 mutated cells or tumors.
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Project description:Purpose: Loss-of-function mutations of the breast cancer type 1 susceptibility protein (BRCA1) are associated with breast (BC) and ovarian cancer (OC). We assessed responses to histone deacetylase inhibitors (HDACi) and performed genome-wide RNA and chromatin immunoprecipitation (ChIP)-sequencing in isogenic OC cells UWB1.289 (carrying a BRCA1 mutation) and UWB1.289 transduced with wild type BRCA1. Experimental Design: Gene expression profiles of cells harboring mutated vs. functional BRCA1 and treated with the HDACi were integrated with chromatin mapping of histone H3 lysine 9 or 27 acetylation (H3K9ac, H3K27ac) at active promoters and enhancers. Key pathways found deregulated in BRCA1 mutated cells were validated. Results: Gene networks activated in BRCA1-mutated vs. BRCA1+ OC cells relate to Cellular Movement, Cellular Development, Cellular Growth and Proliferation and shared upstream regulators included TGFb1, TNF, and IFN-g. The IFN-g pathway was significantly altered in response to HDACi in BRCA1+ vs. BRCA1-mutated cells and in BRCA1-mutated/or low vs. BRCA1-normal ovarian tumors profiled in the TCGA database. Key IFN-γ-induced genes upregulated at baseline in BRCA1-mutated vs. BRCA1+ OC and BC cells included CXCL10, CXCL11, and IFI16. Increased localization of STAT1 to the promoters of these genes was observed in BRCA1-mutated cells, resulting in diminished cellular responses to IFN-γ or to STAT1 knockdown. The IFN-g signature was associated with improved survival among tumors profiled by the TCGA. Conclusions: Transcriptomic changes affecting IFN-γ response are associated with inactivating BRCA1 mutations in OC. These alterations could contribute to diminished anti-tumor immunity in BRCA1 mutated cells or tumors.
2019-12-31 | GSE131085 | GEO