Breast Cancer Sequencing Project
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR015688.fastq.gz | Fastqsanger.gz | |||
| ERR015689.fastq.gz | Fastqsanger.gz | |||
| ERR015690.fastq.gz | Fastqsanger.gz | |||
| ERR015691.fastq.gz | Fastqsanger.gz | |||
| ERR015692.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 106 |
Similar Datasets
Project description:Gene expression profiles between normal and breast tumor genomes
| PRJEB2345 | ENA
Project description:The Pan-Cancer Analysis of Whole Genomes (PCAWG) study is an international collaboration to identify common patterns of mutation in more than 2,800 cancer whole genomes from the International Cancer Genome Consortium. Building upon previous work which examined cancer coding regions, this project is exploring the nature and consequences of somatic and germline variations in both coding and non-coding regions, with specific emphasis on cis-regulatory sites, non-coding RNAs, and large-scale structural alterations. Read more on the <a href=\"https://dcc.icgc.org/pcawg\" target=\"_blank\">project website</a>.<br>This is a subset featuring RNA-seq transcription profiling data of 27 cancer subtypes in 19 tissues. Some donors have matched normal tissue. As general reference, a subset of normal tissue samples from the GTEx project were included in this experiment.
2020-02-05 | E-MTAB-5200 | biostudies-arrayexpress
Project description:The Pan-Cancer Analysis of Whole Genomes (PCAWG) study is an international collaboration to identify common patterns of mutation in more than 2,800 cancer whole genomes from the International Cancer Genome Consortium. Building upon previous work which examined cancer coding regions, this project is exploring the nature and consequences of somatic and germline variations in both coding and non-coding regions, with specific emphasis on cis-regulatory sites, non-coding RNAs, and large-scale structural alterations. Read more on the <a href=\"https://dcc.icgc.org/pcawg\" target=\"_blank\">project website</a>.<br>This is a subset featuring RNA-seq transcription profiling data of 27 cancer subtypes in 19 tissues. Some donors have matched normal tissue.<br>This is the alternative view of the experiment for Expression Atlas to show gene expression per donor.
2020-02-05 | E-MTAB-5423 | biostudies-arrayexpress
Project description:The impact of different carcinogenic exposures on the specific patterns of somatic mutations in human tumors remains unclear. To clarify this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by liver fluke Opisthorchis viverrini (OV)-infection and 101 cases due to non-OV etiologies. Whole-exome (N = 15) and prevalence screening (N = 194) revealed recurrent somatic mutations in BAP1 and ARID1A, neither of which has been previously reported to be mutated in CCA. Comparisons between intrahepatic OV and non-OV CCAs demonstrated statistically significant different mutation patterns: BAP1 and IDH1/2 were more frequently mutated in non-OV CCAs, while TP53 displayed the reciprocal pattern. Functional studies demonstrated tumor suppressive roles of BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations even within the same tumor type. Illumina 450k methylation array profiling performed on wild-type (n=23) and mutant (n=9) CCA (cholangiocarcinoma) samples, with adjacent normal tissue (n=4)
2013-10-20 | E-GEOD-49656 | biostudies-arrayexpress
Project description:The impact of different carcinogenic exposures on the specific patterns of somatic mutations in human tumors remains unclear. To clarify this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by liver fluke Opisthorchis viverrini (OV)-infection and 101 cases due to non-OV etiologies. Whole-exome (N = 15) and prevalence screening (N = 194) revealed recurrent somatic mutations in BAP1 and ARID1A, neither of which has been previously reported to be mutated in CCA. Comparisons between intrahepatic OV and non-OV CCAs demonstrated statistically significant different mutation patterns: BAP1 and IDH1/2 were more frequently mutated in non-OV CCAs, while TP53 displayed the reciprocal pattern. Functional studies demonstrated tumor suppressive roles of BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations even within the same tumor type. Affymetrix SNP6 arrays were performed according to the manufacturer's directions on DNA extracted from the 15 tumors and the 15 matched normal discovery samples.
2013-11-03 | E-GEOD-49666 | biostudies-arrayexpress
Project description:This is a continuation of the Chordoma Sequencing Project. All cancers arise due to somatically acquired abnormalities in DNA sequence. Systematic sequencing of cancer genomes allows acquisition of complete catalogues of all classes of somatic mutation present in cancer. These mutation catalogues will allow identification of the somatically mutated cancer genes that are operative and characterise patterns of somatic mutation that may reflect previous exogenous and endogenous mutagenic exposures. In this application, we aim to perform whole genome sequencing on 10 chordoma matched genome pairs. RNA Sequencing/Methylation and SNP6 and an additional sequencing of three cancer cell lines will be added to this work.
2014-06-25 | E-ERAD-128 | biostudies-arrayexpress
Project description:Repetitive sequences are hotspots of evolution at multiple levels. However, due to technical difficulties involved in their assembly and analysis, the role of repeats in tumor evolution is poorly understood. We developed a rigorous motif-based methodology to quantify variations in the repeat content of proteomes and genomes, directly from proteomic and genomic raw sequence data, and applied it to analyze a wide range of tumors and normal tissues. We identify high similarity between the repeat-instability in tumors and their patient-matched normal tissues, but also tumor-specific signatures, both in protein expression and in the genome, that strongly correlate with cancer progression and robustly predict the tumorigenic state. In a patient, the hierarchy of genomic repeat instability signatures accurately reconstructs tumor evolution, with primary tumors differentiated from metastases. We find an inverse relationship between repeat-instability and point mutation load, within and across patients, and independently of other somatic aberrations. Thus, repeat-instability is a distinct, transient and compensatory adaptive mechanism in tumor evolution.
2020-06-02 | PXD012574 | Pride
Project description:Single nucleotide polymorphism (SNP) microarrays are commonly applied to tumors to identify genomic regions with copy number alterations (CNA) or loss of heterozygosity (LOH). However, in typical tumor specimens collected in clinical studies, up to 60% of the DNA derives from stromal cells with a normal genome, resulting in attenuated sensitivity to true somatic aberrations in the tumor. Here we describe SNPfilter, a model-based method to decompose SNP array data from heterogeneous tumor specimens into their corresponding normal and tumor profiles. Unlike existing methods, SNPfilter does not require paired normal control data. We assessed the performance of this method using SNP array data representing cancer cell lines with aberrant genomes, B-cell lymphoblastoid cell lines with normal genomes, and defined mixtures of the two. In the pure tumor samples, SNPfilter identified CNA and LOH regions with accuracy similar to existing methods. In the mixture samples containing 40–80% tumor genomic DNA, SNPfilter yielded prediction sensitivity superior to existing methods. Thus, SNPfilter provides a powerful tool for discovery of clinically relevant somatic aberrations in tumor genomes.
2011-12-30 | GSE34754 | GEO
Project description:The impact of different carcinogenic exposures on the specific patterns of somatic mutations in human tumors remains unclear. To clarify this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by liver fluke Opisthorchis viverrini (OV)-infection and 101 cases due to non-OV etiologies. Whole-exome (N = 15) and prevalence screening (N = 194) revealed recurrent somatic mutations in BAP1 and ARID1A, neither of which has been previously reported to be mutated in CCA. Comparisons between intrahepatic OV and non-OV CCAs demonstrated statistically significant different mutation patterns: BAP1 and IDH1/2 were more frequently mutated in non-OV CCAs, while TP53 displayed the reciprocal pattern. Functional studies demonstrated tumor suppressive roles of BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations even within the same tumor type.
2013-11-03 | GSE49666 | GEO
Project description:The impact of different carcinogenic exposures on the specific patterns of somatic mutations in human tumors remains unclear. To clarify this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by liver fluke Opisthorchis viverrini (OV)-infection and 101 cases due to non-OV etiologies. Whole-exome (N = 15) and prevalence screening (N = 194) revealed recurrent somatic mutations in BAP1 and ARID1A, neither of which has been previously reported to be mutated in CCA. Comparisons between intrahepatic OV and non-OV CCAs demonstrated statistically significant different mutation patterns: BAP1 and IDH1/2 were more frequently mutated in non-OV CCAs, while TP53 displayed the reciprocal pattern. Functional studies demonstrated tumor suppressive roles of BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations even within the same tumor type.
2013-10-20 | GSE49656 | GEO