15128 results for "cancer studies using rna-seq"

in 28.31 milliseconds.

• Custom long non-coding RNA capture DAC

  Dac EGAC00001002198

• GLASS-NL RNA-sequencing Study

  Study EGAS00001007551

• We evaluate the PGD/PGS including 129 couples with NGS test and 266 couples with SNP-array test for the detection of embryonic chromosomal abnormalities.

  A total of 395 couples were subjected to IVF-PGD treatment, including 129 couples with NGS test and 266 couples with SNP-array test for the detection of embryonic chromosomal abnormalities. The NGS test was performed using low coverage whole genome sequencing with HiSeq 2000 platform. And the SNP array test was using Affymetrix Gene Chip Mapping Nsp I 262K.

  Study EGAS00001000981

• Gut metagenome/FINRISK 2002 (Salosensaari et al. Nature Comms 2021)

  The main goal of the project is the study the associations between the gut metagenome and human health. The dataset contains data for n=7211 FINRISK 2002 participants who underwent fecal sampling. Demultiplexed shallow shotgun metagenomic sequences were quality filtered and adapter trimmed using Atropos (Didion et al., 2017), and human filtered using Bowtie2 (Langmead and Salzberg, 2012).

  Study EGAS00001005020

• Whole exome sequencing and RNA sequencing of lineage-switched acute myeloid leukemia with KMT2A-AFF1 rearrangement

  We performed whole exome sequencing and RNA sequencing of lineage-switched acute myeloid leukemia (LS AML) with KMT2A-AFF1 rearrangement to elucidate the feature and potential treatment targets. Notably, LS AML possessed gene expression signatures of monocytic myeloid derived suppressor cells (M-MDSCs). Several known genes related to MDSCs were highly expressed in LS AML, which could be novel treatment targets.

  Study JGAS000631

• Identification of Long Non-coding RNA Biomarker of Human Lupus Nephritis Disease Activity

  Total RNA sequencing was performed on whole blood samples from 74 Lupus nephritis (LN) patients and 20 healthy controls. Differential expression analysis and weighted gene co-expression network analysis were performed to characterise expression changes of long non-coding RNAs (lncRNAs) in LN and identify lncRNAs with a key role in disease activity that could be used as potential blood-based biomarkers.

  Study EGAS00001007117

• Single-cell RNA sequencing on single CD45+ immune cells isolated from peripheral blood, lymphnode, ascites, tumour and adjacent normal tissues from six hepatocellular carcinoma patients.

  Single-cell RNA sequencing on single CD45+ immune cells isolated from peripheral blood, lymphnode, ascites, tumour and adjacent normal tissues from six hepatocellular carcinoma patients. The transcriptional properties of these individual cells, were used to delineate the molecular subtypes, lineage, and functional properties of each cell group

  Study EGAS00001003449

• Genotypic data of the individuals in HPP project

  Dataset contains imputed SNP genetics data for human phenotype project https://humanphenotypeproject.org/. The samples are genotypes of 8958 individuals that underwent genetic sequencing based on buccal swab.Sequencing is performed at Neogen GeneSeek Laboratories using Illumina Novaseq at low-pass, targeting coverage levels of 0.5× and 1×. Imputation was done using loimpute-v0.1.0 over the aligned reads. Imputation is done for the autosomal chromosomes (1-22) using The 1000 Genomes phase 3 haplotypes (1KGP3) as a reference panel. The samples are provided in merged PLINK 1 binaries (.bed/.bim/.fam)

  Dataset EGAD00010002714

• stem cell-derived beta cells from cell lines RC9 and HUES8

  stem cell-derived beta cells differentiated using two different cell lines: HUES8 (non-clinical grade) and RC9 (clinical grade). iPSC stem cell lines were differentiated to pancreatic islets using differentiation protocol as detailed by Rajaei et al. (2025, Science Translational Medicine, accepted for publication). scRNAseq was done at stage 7 of differentiation (day 30) using 10X genomics 3' sequencing. Cells were annotated then subsetted for beta cells for downstream analysis

  Dataset EGAD50000001322

• RRBS of 25 pleural mesothelioma samples (Single-end)

  The dataset contains RRBS data (bam files) for 25 pleural mesothelioma samples.The samples were sequenced on NovaSeq6000 (Illumina, San Diego, CA) in single-end 150bp mode. RRBS raw reads were trimmed for adaptor sequences using trim galore (v. 0.6.5) (http://www.bioinformatics.babraham.ac.uk/projects/trim_galore/) and filtered for low-quality sequences using fastQC (v. 0.11.8) (https://www.bioinformatics.babraham.ac.uk/projects/fastqc/). High quality trimmed reads were mapped to the Human reference genome (UCSC genome assembly GRCh38/hg38) using Bismark (v. 0.22.3) with default parameters.

  Dataset EGAD50000002130

• WGS data of paediatric ETV6::RUNX1 B cell acute lymphoblastic leukemia (set1)

  The dataset includes FASTQ and BAM/CRAM files from diagnostic and matched remission (control) samples of five ETV6::RUNX1 ALL patients (ALLT-380, ALLK-114, ALLT-388, ALLT-392, ALLT-394). Sequencing libraries were made using PCR free-based WGS library preparation (PCR-), using NEBNext® Ultra™ II DNA Library Prep Kit (Cat No. E7645). Both diagnostic (90x) and remission (30x) samples were sequenced using Illumina NovaSeq 6000.

  Dataset EGAD50000002285

• Hyperhaploid multiple myeloma

  DNA was obtained from either CD138+ cells from the bone marrow of multiple myeloma patients (tumor) or from stem cell harvests from the same patient (control). 100 ng of DNA was fragmented, end-repaired, and adapters ligated using the HyperPlus kit (KAPA Biosystems). After PCR amplification the libraries were hybridized with probes against either the entire exome (MedExome, Nimblegen) or a targeted panel of 140 genes using SeqCap reagents (Nimblegen). Hybridized libraries underwent further amplification before being sequenced on a NextSeq500 (Illumina) using 75 bp paired end reads.

  Dataset EGAD00001004328

• Carboxylesterase 1 mediates a distinctive metabolic profile of dendritic cells to attain an inflammatory phenotype

  The metabolic profile of dendritic cells (DCs) shapes their phenotype and functions. Carboxylestrase 1 (CES1) enzyme is highly expressed in mononuclear myeloid cells however its exact role in DCs is elusive. We used a CES1 inhibitor (WWL113) and genetic overexpression to explore the role of CES1 in DCs differentiation in inflammatory models. CES1 expression was analyzed during CD14+ monocytes differentiation to DCs (MoDCs) using quantitative PCR. CES1 Inhibitor (WWL113) was applied during MoDCs differentiation. Surface markers, secreted cytokines, lactic acid production, phagocytic and T cell polarization capacity were analyzed. Transcriptomic and metabolic profile were assessed with RNA-sequencing and mass spectrometry. Cellular respiration was assessed with seahorse respirometry. Transgenic mice were used to assess CES1 overexpression in DCs in inflammatory models. CES1 expression peaks early during MoDCs differentiation. Pharmacological inhibition of CES1 led to higher expression of CD209, CD86 and MHCII. WWL113 treated MoDCs secreted higher quantities of IL6, IL8, TNF and IL10 and demonstrated stronger phagocytic ability and higher capacity to polarize Th17 differentiation in autologous DCs-T cells co-culture model. Transcriptomic profiling revealed enrichment of multiple inflammatory and metabolic pathways. Functional metabolic analysis shows impaired maximal mitochondrial respiration capacity, increased lactate production and decreased intracellular amino acids and TCA intermediates. Transgenic human CES1 overexpression in murine DCs generated less inflammatory phenotype and increased resistance to T cell mediated colitis. In conclusion, CES1 inhibition directs DCs differentiation towards more inflammatory phenotype, that shows stronger phagocytic capacity and supports Th17 skewing. This is associated with disrupted mitochondrial respiration and amino acids depletion.

  Study EGAS50000000230

• Transposable Elements in FTLD-TDP and ALS-TDP

  Amyotrophic Lateral Sclerosis (ALS) is a devastating neurodegenerative disease involving the rapid and progressive loss of motor neurons. While a number of inherited mutations have been identified as causing ALS, the vast majority of cases are sporadic with no family history of disease. This has led to the model that ALS may be a complex syndrome with an unknown number of causal molecular pathways. However, nearly all ALS patient tissues display aggregates of the RNA binding protein TDP-43 (TARDBP/TAR DNA-binding protein), and mutations in the gene encoding this protein are known to cause ALS. We show that one of the normal functions of TDP-43 is to bind and regulate retrotransposons, repetitive sequences in the genome that are normally silent, due in part to the function of TDP-43. Furthermore, we demonstrate that many ALS patients with TDP-43 pathology also display de-silencing of retrotransposon RNAs, consistent with a loss of normal TDP-43 function. Those ALS patients that exhibit high levels of retrotransposon expression form a distinct subset of ALS subjects that also show other correlated alterations to the transcriptome. Using unsupervised machine learning algorithms, we identified three distinct molecular subtypes from the whole genomes and transcriptomes of a large cohort of 148 ALS patient samples. The retrotransposon re-activated subset formed 20% of ALS samples; two additional groups displayed signatures of oxidative stress (61%), and glial dysfunction (19%), respectively. Together these results demonstrate that retrotransposon re-activation is common in a subset of ALS patients with TDP-43 pathology.

  Study phs001889

• Non-Coding Autoimmune Risk Variant Defines Role for ICOS in T Peripheral Helper Cell Development

  Our fine-mapping of 76 non-MHC loci associated with risk for rheumatoid arthritis (RA, 11,475 cases, 15,870 controls) has recently identified rs117701653, a non-coding single nucleotide polymorphism (SNP) in the CTLA4/CD28/ICOS locus, as the variant most likely to modulate RA risk within this region, with the minor allele C showing disease protection compared to the major allele A. We found that this SNP exhibits allele-specific protein binding and transcriptional modulation, further supporting its regulatory nature. Here, we aimed to determine whether the functional non-coding variant rs117701653 modulates the expression of genes within the CD28/CTLA4/ICOS locus. To address this question, we employed low-input RNA sequencing using the Illumina SmartSeq2 platform on resting total CD4+ T cells from the blood of 24 healthy subjects (8 AA, 8 AC, 8 CC) recruited based on genotype from the Mass General Brigham biobank. We performed a targeted cis-eQTL mapping analysis for protein coding genes with transcription start sites (TSS) within a 1MB window of SNP rs117701653. These genes included WDR12, NBEAL1, CYP20A1, ABI2, RAPH1, CD28, CTLA4, ICOS, and PARD3B. Surprisingly, allelic variation at rs117701653 correlated strongly with expression of ICOS. This suggests that individuals carrying the protective allele C at rs117701653 express lower levels of ICOS, implicating ICOS as a plausible target gene influenced by this protective allele. The raw sequence data from the 24 healthy individuals are available through dbGAP. Gene expression matrices have been deposited to GEO accession GSE235868.

  Study phs003448

• Structure and evolution of double minutes in diagnosis and relapse brain tumors

  Double minute chromosomes are extrachromosomal circular DNA fragments frequently found in brain tumors. To understand their evolution, we characterized the double minutes in paired diagnosis and relapse tumors from a pediatric high-grade glioma and four adult glioblastoma patients. We determined the full structures of the major double minutes using a novel approach combining multiple types of supporting genomic evidence. Among the double minutes identified in the pediatric tumor, only one carrying EGFR was maintained at high abundance in both samples, whereas two others were resent in only trace amounts at diagnosis but abundant at relapse, and the rest were found either in the relapse sample only or in the diagnosis sample only. For the EGFR-carrying double minutes, we found a secondary somatic deletion in all copies at relapse, after erlotinib treatment, but this was rare at diagnosis, suggesting potential resistance to the EGFR inhibitor. This mutation caused an in-frame RNA transcript to skip exon 16, a novel transcript absent in EST database and in about 700 brain tumors that we reviewed. We observed similar patterns involving longitudinal copy number shift of double minutes in another four pairs (diagnosis / relapse) of adult glioblastoma. Overall, in three of five paired tumor samples, we found that although the same oncogenes were amplified at diagnosis and relapse, they were amplified on different double minutes. Our results suggest that double minutes readily evolve, increasing tumor heterogeneity rapidly. Understanding patterns of double minute evolution can shed light on future therapeutic solutions to brain tumors carrying such variants.

  Study EGAS00001003212

• Beyond BRCA deficiency: Clinical and molecular predictors of survival in patients with BRCA-deficient tubo-ovarian high-grade serous carcinoma

  Homologous recombination DNA repair deficient (HRD) tumors account for about 50% of tubo-ovarian high-grade serous carcinomas (HGSC) and are associated with a high response to platinum-based chemotherapy. However, a subset of patients with HRD tumors have unexpected resistance to chemotherapy and experience short survival. Our study compared BRCA-deficient and proficient HGSC among patients with short (<3 years, the lowest quartile of overall survival (OS)) versus longer-term (>3 year OS) to identify prognostic markers and potential therapeutic opportunities. Primary tumors from a cohort of patients with advanced-stage HGSC (n=154) enriched for those with HRD tumors and short survival (n=42) were analyzed using whole-genome sequencing, bulk RNA-sequencing, and DNA methylation profiling. A subset of HRD tumors (n=143) were characterized for immune cell densities by multiplex immunofluorescence. Clinicopathological features were assessed in 1,389 patients with HGSC, including 282 with pathogenic germline BRCA variants (gBRCApv). Findings were validated in two international HGSC cohorts: the Ovarian Tumor Tissue Analysis consortium (n=5,875) and Multisciplinary Ovarian Cancer Outcome Group (n=895). In gBRCApv-carriers, residual disease following surgical cytoreduction was not associated with shorter OS unlike in non-carriers where it was strongly associated. While most patients with gBRCApv had a more favorable OS compared to non-carriers, a survival advantage was not apparent in those with variants located outside of BRCA1 exon 10/23 and BRCA2 exon 11/27. Patient survival correlated with HRD score, such that those with a score ≥63 had significantly longer OS compared to those with HRD scores of 42-63 and <42. While higher HRD scores were associated with better survival outcomes, most gBRCApv carriers with a short survival had tumor HRD scores that exceeded the threshold typically considered predictive of a good response to carboplatin or PARP inhibitors. BRCA2-deficient HGSC with loss of the tumor suppressor NF1 was associated with exceptionally favorable outcome (median OS 17 years), whereas amplification of both PIK3CA and RAD21, was associated with poor outcome in BRCA2-deficient HGSC (median OS 2.9 years). The density of tumor-infiltrating CD8+ PD-1+ T cells was prognostic for OS in gBRCApv-carriers. In summary, rather than simply the presence or absence of a germline BRCA pathological variant influencing patient survival, the co-occurrence of specific somatic gene alterations, the extent of immune cell infiltration, the level of homologous recombination deficiency, and BRCA-variant location may modify clinical outcomes in patients with BRCA-deficient HGSC. Analysis of exceptional outcome patients, in this case gBRCApv-carriers with an atypically short survival, may identify determinants of outcome applicable to the wider HGSC patient population.

  Study EGAS00001008059

• Detection of MEIS2 inversion using ONT adaptive sequencing

  DNA was extracted from whole blood, and sequenced on a Promethion flow cell. The target region covered chr15:22874354-55370932 (Grch38). The resulting data was aligned to Grch38 using minimap2.

  Dataset EGAD50000000893

• ESGI___Whole_Genome_Sequencing_of_samples_from_the_Cilentogen_isolates

  Deep whole genome sequencing of sampels from the Cilento isolates. The samples are sequenced using the Illumina HiSeq X Ten system.

  Study EGAS00001001116

• Validation of a genome-wide polygenic score for body mass index in South Asians

  Genotyping data of BMI model markers generated using Global Screening Array (Illumina Inc.)

  Study EGAS00001008309

• ESGI___Whole_Genome_Sequencing_of_samples_from_the_Croatian_isolated_populations_

  Whole genome sequencing of sampels from isolated populations from Croatia. The samples are sequenced using the Illumina HiSeq X Ten system.

  Study EGAS00001001119

• Detection of human brain cancers using genomic and immune cell characterization of cerebrospinal fluid through CSF-BAM

  Detection of human brain cancers using genomic and immune cell characterization of cerebrospinal fluid through CSF-BAM

  Dataset EGAD00001015645

• Subtyping Sub-Saharan Esophageal Squamous Cell Carcinoma by Comprehensive Molecular Analysis

  Esophageal squamous cell carcinoma (ESCC) occurs as much as 20x more frequently in sub-Saharan Africa than Western countries. Through the UNC-Malawi project collaboration we obtained whole-exome matched tumor/normal and RNA sequencing of 59 ESCC from Malawi between 2011-2012. DNA analysis revealed similar mutations as other cohorts, while RNA analysis revealed three distinct subtypes. Mutational signature analysis revealed a pattern of mutation not previously reported in other cohorts or more broadly. Taken together this suggests the high prevalence of ESCC in the region is secondary to an as yet identified mutagen.

  Study phs001448

• The Genetic and Transcriptomic Evolution of Melanoma

  The overarching goal of the study was to better understand the evolution of melanoma. To do this, we collected archival tissue of melanomas adjacent to their intact, remnant precursor lesions. We also collected archival tissue of primary melanomas and their matching metastases. From the formalin-fixed paraffin-embedded (FFPE) blocks, we microdissected non-neoplastic (normal), precursor, and descendent portions of tissue. Both RNA and DNA were extracted from the microdissected tissues and subjected to next generation sequencing. In summary, we performed matched DNA/RNA sequencing of melanoma/precursor/normal trios, allowing us to trace the genetic and transcriptomic evolution of melanoma.

  Study phs001550

• Whole Exome Sequencing of Uveal Melanoma

  Uveal melanoma is a rare form of melanoma that occurs in the eye and has no effective treatment once metastatic. To further characterize the genomic events driving uveal melanoma, whole exome sequencing was performed on 61 primary tumors derived from enucleations, 3 liver metasases, and paired normal DNA. Recurrent somatic genetic alterations including point mutations, small insertions and deletions, as well as copy number variations were identified. In addition, RNA sequencing of uveal melanoma cell lines expressing shRNAs was performed from total RNA as well as polysome-associated mRNA in order to identify transcripts regulated by EIF1AX at the level of translation.

  Study phs001370

• Wnt Activity Reveals Context-Dependent Genetic Effects on Gene Regulation in Neural Progenitors

  In this study we aimed to identify context-dependent regulatory functions of common genetic variation after stimulation of the canonical Wnt pathway. Fetal cortical tissue between 14 and 21 gestation weeks was subjected to RNA-Sequencing (242 samples) and ATAC-Sequencing (222 samples) to profile expression and chromatin accessibility, respectively. Considering donor genotypes, we were able to identify eQTLs, caQTLs, as well as response QTLs of both categories. The dataset provided here includes 242 RNA-sequencing files in bam format and 222 ATAC-sequencing files in bam format. We also provide 83 donor genotypes in VCF format (hg38).

  Study phs003642

• Inherited chromosomally-integrated human herpesvirus 6A/B (HHV-6A/B) genome sequences in the Japanese population

  The deposited sequences represent inherited chromosomally-integrated human herpesvirus 6 (iciHHV-6) genomes identified from 10 BioBank Japan (BBJ) subjects based on the analysis of the whole-genome sequencing (WGS) data. In brief, we re-aligned unmapped reads from the WGS to HHV-6A genome (Genbank accession number: KJ123690.1) using BWA-MEM algorithm. Ten out of 3,256 subjects were identified with high depth of coverage of HHV-6. We further distinguished subjects with integrated HHV-6A subtypes from those with integrated HHV-6B based on phylogenetic analysis of concatenated sequences of three viral genes (U27/U43/U83, which show high divergence between viral species). We reconstructed the HHV-6 viral genome of 10 subjects. First, reads that mapped to a reference HHV-6A genome (KJ123690.1) were further aligned against the integrated HHV-6A genome derived from a Japanese individual NA18999 (GenBank Accession number: KY316047.1) using BWA-MEM. Based on the alignment, variant calling was performed using freebayes (version: v1.2.0-2-g29c4002) with parameters ploidy = 1 and min-alternate-fraction = 0.8 {Garrison, 2012}. We generated subject-specific iciHHV-6 viral sequences by applying the resulting variants to the KY316047.1 reference genome using the FastaAlternateReferenceMaker function in the Genome Analysis Toolkit (GATK) v3.7. Please note that HHV-6B-specific variants are unlikely to be sensitively reconstructed using this method.

  Study JGAS000240

• Parallel Genomic Alterations of Antigen and Payload Targets Mediate Polyclonal Acquired Clinical Resistance to the Antibody Drug Conjugate Sacituzumab Govitecan

  Sacituzumab Govitecan (SG), a novel antibody drug conjugate (ADC) incorporating the anti-TROP2 antibody hRS7 conjugated to a topoisomerase-1 inhibitor (SN-38) payload, is the first ADC to be approved for advanced triple negative breast cancer (TNBC). However, mechanisms governing therapeutic resistance to SG are not known. We sought to identify mechanisms of de novo and acquired resistance to SG through unbiased whole-exome sequencing (WES) and RNA sequencing analysis of pre-treatment and multi-site post-progression (autopsy) tumor specimens. We examined three metastatic TNBC cases exhibiting (1) de novo progression, (2) stable disease, and (3) a deep response followed by progression, then mapped the temporal and spatial genomic evolution of acquired resistance in the responding patient. We then conducted additional pre-clinical experiments to validate the observed resistance mechanisms. TROP2 RNA and gene copy number were associated with de novo resistance, as case (1) was found to have absent TROP2 expression in all specimens, case (2) expressed TROP2, while case (3) exhibited both expression and focal genomic amplification of the TACSTD2/TROP2 locus. The genomic phylogeny tree inferred from case (3) post-progression specimens revealed one branch harboring an acquired canonical E418K resistance mutation in TOP1 (encoding topoisomerase 1) and a subsequent sub-clonal TOP1 inactivating frameshift mutation, while a distinct branch exhibited acquisition of a novel T256R missense mutation in TACSTD2 (encoding TROP2). Both the TOP1- and TACSTD2-mutant clones seeded multiple distinct metastatic sites. Through reconstitution experiments in TROP2 negative cells we found that TROP2 T256R is a stable protein with defective cell membrane localization and reduced cell surface binding by RS7 compared to wild-type TROP2. Collectively, these findings underscore TROP2 as a determinant of initial response to SG, and they reveal parallel and mutually exclusive polyclonal molecular mechanisms of acquired resistance involving the direct antibody target and drug payload target in distinct metastatic subclones of a single patient. While further research is needed to extend these novel findings, this study highlights the specificity of SG and illustrates how identifying such mechanisms will inform rational therapeutic strategies to overcome ADC resistance.  

  Study phs002555

• H3K4me3, IgG, and Input ChIP-seq in overexpression of pLV Control, CS-FL and CS-ΔEx4 in SW1116 cells.

  none

  Study EGAS00001008121

• Chromatin accessibility analysis of epidermal keratinocytes from psoriatic, clinically healed, and healthy control skin

  This study uses ATAC-seq to analyze epidermal keratinocytes from psoriatic lesions, clinically healed skin of the same patients, and healthy control skin. The aim is to elucidate chromatin accessibility changes associated with psoriasis pathogenesis and remission from 6 lesional, 6 healed, and 5 control samples.

  Study JGAS000844

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - T=0days, on genome GRCh38

  ChIP-Seq data for 2 monocyte - T=0days sample(s). 7 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002491

• BLUEPRINT release August 2016, ChIP-Seq for inflammatory macrophage, on genome GRCh38

  ChIP-Seq data for 9 inflammatory macrophage sample(s). 58 run(s), 58 experiment(s), 58 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002515

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_BG_T=24hrs_RPMI_T=5days, on genome GRCh38

  ChIP-Seq data for 3 monocyte - RPMI_BG_T=24hrs_RPMI_T=5days sample(s). 7 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002517

• BLUEPRINT release August 2016, ChIP-Seq for Acute Promyelocytic Leukemia - MS-275 (20h), on genome GRCh38

  ChIP-Seq data for 1 Acute Promyelocytic Leukemia - MS-275 (20h) sample(s). 5 run(s), 5 experiment(s), 5 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002493

• BLUEPRINT release August 2016, ChIP-Seq for CD8-positive, alpha-beta thymocyte, on genome GRCh38

  ChIP-Seq data for 1 CD8-positive, alpha-beta thymocyte sample(s). 2 run(s), 2 experiment(s), 2 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002494

• BLUEPRINT release August 2016, ChIP-Seq for memory B cell, on genome GRCh38

  ChIP-Seq data for 1 memory B cell sample(s). 1 run(s), 1 experiment(s), 1 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002510

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_BG_T=24hrs_RPMI_T=5days_LPS_T=4hrs, on genome GRCh38

  ChIP-Seq data for 3 monocyte - RPMI_BG_T=24hrs_RPMI_T=5days_LPS_T=4hrs sample(s). 7 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002512

• BLUEPRINT release August 2016, ChIP-Seq for CD38-negative naive B cell, on genome GRCh38

  ChIP-Seq data for 9 CD38-negative naive B cell sample(s). 48 run(s), 44 experiment(s), 44 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002524

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_T=6days_LPS_T=4hrs, on genome GRCh38

  ChIP-Seq data for 3 monocyte - RPMI_T=6days_LPS_T=4hrs sample(s). 8 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002495

• Tapestri snDNA-seq data along with matched bulk data for validation

  Files from Tapestri snDNA-seq of archival tissue samples from 16 pancreatic ductal adenocarcinoma (PDAC) patients. Matched bulk sequencing (whole-exome, whole-genome, MSK-IMPACT) data are attached for a subset of the patients.

  Dataset EGAD00001009735

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_T=24hrs, on genome GRCh38

  ChIP-Seq data for 3 monocyte - RPMI_T=24hrs sample(s). 7 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002474

• BLUEPRINT release August 2016, ChIP-Seq for conventional dendritic cell, on genome GRCh38

  ChIP-Seq data for 1 conventional dendritic cell sample(s). 4 run(s), 4 experiment(s), 4 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002310

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_LPS_T=24hrs, on genome GRCh38

  ChIP-Seq data for 3 monocyte - RPMI_LPS_T=24hrs sample(s). 8 run(s), 8 experiment(s), 8 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002388

• BLUEPRINT release August 2016, ChIP-Seq for unswitched memory B cell, on genome GRCh38

  ChIP-Seq data for 1 unswitched memory B cell sample(s). 7 run(s), 7 experiment(s), 7 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002282

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_BG_T=1hr, on genome GRCh38

  ChIP-Seq data for 2 monocyte - RPMI_BG_T=1hr sample(s). 6 run(s), 6 experiment(s), 6 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002297

• BLUEPRINT release August 2016, ChIP-Seq for germinal center B cell, on genome GRCh38

  ChIP-Seq data for 4 germinal center B cell sample(s). 24 run(s), 22 experiment(s), 22 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002442

• BLUEPRINT release August 2016, ChIP-Seq for monocyte - RPMI_T=1hr, on genome GRCh38

  ChIP-Seq data for 2 monocyte - RPMI_T=1hr sample(s). 4 run(s), 4 experiment(s), 4 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002453

• BLUEPRINT release August 2016, ChIP-Seq for band form neutrophil, on genome GRCh38

  ChIP-Seq data for 4 band form neutrophil sample(s). 26 run(s), 23 experiment(s), 23 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002454

• BLUEPRINT release August 2016, Bisulfite-Seq for CD3-positive, CD4-positive, CD8-positive, double positive thymocyte, on genome GRCh38

  Bisulfite-Seq data for 2 CD3-positive, CD4-positive, CD8-positive, double positive thymocyte sample(s). 29 run(s), 2 experiment(s), 4 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_bisulphite_analysis_CNAG_20160816

  Dataset EGAD00001002325

• BLUEPRINT release August 2016, ChIP-Seq for segmented neutrophil of bone marrow, on genome GRCh38

  ChIP-Seq data for 4 segmented neutrophil of bone marrow sample(s). 24 run(s), 23 experiment(s), 23 analysis(s) on human genome GRCh38. Part of BLUEPRINT release August 2016. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20160816/homo_sapiens/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002390