11936 results for "cancer rna-seq"

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• Reference epigenome Islet-derived_MSC06 h3k27ac ChIP-Seq data generated from KEP study

  Islet-derived_MSC06 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007895

• Reference epigenome Islet-derived_iPSC04 h3k27me3 ChIP-Seq data generated from KEP study

  Islet-derived_iPSC04 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007889

• Reference epigenome Islet-derived_MSC06 h3k9me3 ChIP-Seq data generated from KEP study

  Islet-derived_MSC06 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007900

• Reference epigenome Islet-derived_MSC06 input ChIP-Seq data generated from KEP study

  Islet-derived_MSC06 input ChIP-Seq paired end data

  Dataset EGAD00001007901

• Reference epigenome Islet-derived_iPSC04 input ChIP-Seq data generated from KEP study

  Islet-derived_iPSC04 input ChIP-Seq paired end data

  Dataset EGAD00001007894

• Reference epigenome Islet-derived_MSC06 h3k4me3 ChIP-Seq data generated from KEP study

  Islet-derived_MSC06 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007899

• Reference epigenome Islet-derived_MSC08 h3k27ac ChIP-Seq data generated from KEP study

  Islet-derived_MSC08 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007902

• Reference epigenome Islet-derived_iPSC04 h3k27ac ChIP-Seq data generated from KEP study

  Islet-derived_iPSC04 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007888

• Reference epigenome Islet-derived_MSC08 h3k36me3 ChIP-Seq data generated from KEP study

  Islet-derived_MSC08 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007904

• STAG1 and STAG2-ChIP-seq in RAD21-mutant adult acute myeloid leukemia

  STAG1 and STAG2-ChIP-seq in RAD21-mutant adult acute myeloid leukemia

  Dataset EGAD00001015361

• RNA sequencing of lung fibroblasts

  RNA sequencing of lung fibroblasts

  Study EGAS00001007857

• RNA Splicing Dysregulation in the Pathogenesis of Chronic Lymphocytic Leukemia

  RNA splicing dysregulation is a hallmark of cancers, promoting the onset and progression of disease. In chronic lymphocytic leukemia (CLL), spliceosome mutations leading to aberrant splicing occurs in approximately 20% of patients. However, the underlying mechanism for splicing defects in spliceosome unmutated CLL cases remains elusive. To discover posttranscriptional regulation of RNA splicing, we performed RNA sequencing using RNA derived from B cells from 6 healthy donors and 36 CLL patients, along with MAZTER sequencing from 9 CLL patients (8 matched with RNA sequencing cohort) and B cells from 5 healthy donors. We found that CLL cells have dysregulated m6A modification sites on transcripts from splicing factors, suggesting a critical role of m6A modification in RNA splicing dysregulation.

  Study phs003191

• mFAST-SeqS

  Recent progress in the analysis of cell-free DNA fragments (cell-free circulating tumor DNA, ctDNA) now allows monitoring of tumor genomes by non-invasive means. However, previous studies with plasma DNA from patients with cancer demonstrated highly variable allele frequencies of ctDNA. The comprehensive analysis of tumor genomes is greatly facilitated when plasma DNA has increased amounts of ctDNA. Therefore, a fast and cost-effective pre-screening method to identify such plasma samples without previous knowledge about alterations in the respective tumor genome could assist in the selection of samples suitable for further extensive qualitative analysis. To address this, we adapted the recently described FAST-SeqS method, which was originally established as a simple and effective, non-invasive screening method for fetal aneuploidy from maternal blood. We show that our modified FAST-SeqS method (mFAST-SeqS) can be used as a pre-screening tool for an estimation of the ctDNA percentage. Using a combined evaluation of genome-wide and chromosome-arm specific z-scores from dilution series with cell line DNA and by comparisons of plasma-Seq profiles with data from mFAST-SeqS, we established a detection limit of 10% or more of mutant alleles. Plasma samples with an mFAST-SeqS z-score above 5 showed highly concordant results compared to copy number profiles obtained from our previously described plasma-Seq approach.

  Study EGAS00001001133

• BLUEPRINT EpiVar ChIP-seq for naive CD4+ T-cells

  BLUEPRINT EpiVar ChIP-seq for naive CD4+ T-cells

  Study EGAS00001000753

• Genomic Analysis of Prostate Tumor Heterogeneity in Metastasis

  To investigate the molecular changes, mutations, and signaling pathways that characterize the initial steps of prostate cancer metastasis to the lymph nodes, we analyzed 19 discrete lymph node (LN) metastases, 97 primary tumor foci, 39 benign lymph nodes, and 10 normal adjacent prostate tissue samples from 43 patients enrolled in a clinical trial (NCT01808222) of extended lymphadenectomy and metastasis excision guided by [18F]-fluciclovine PET imaging for high risk, newly diagnosed prostate cancer conducted at Emory University. These patients fell within high or very high-risk groups (T3a, Gleason score 8-10, or PSA greater than 20 ng/ml). Of these patients, 16 had LN metastases at least 4 mm in diameter, and 20 patients had no metastases. For metastatic patients, we performed RNA and Whole Exome Sequencing (WES) on three primary tumor foci, one benign LN, and all LN metastases greater than 4mm in diameter. For non-metastatic patients, we sequenced two primary tumor foci and one benign LN. In total, RNAseq was performed on 165 tissue samples from 43 patients, and WES was performed on 137 samples from 35 patients.

  Study phs003404