11805 results for "cancer rna-seq"

in 20.39 milliseconds.

• RNA-sequencing of human skin samples obtained from SSc patients and healthy controls.

  Patient information SSc patients were recruited at the Department of Rheumatology of the Leiden University Medical Center (Leiden, The Netherlands). All patients met the American Rheumatism Association classification criteria for SSc (Subcommittee for scleroderma criteria 1980), and were classified according to LeRoy and Medsger criteria as either limited or diffuse cutaneous disease (LeRoy EC, Black C, Fleischmajer R, Jablonska S, Krieg T, Medsger TA Jr, Rowell N 1988). Institutional review board approval and written informed consent was obtained before patients entered this study. Two 4 mm skin biopsies were taken from a standardized location on the most proximal part of the lower arm, distal from the elbow. In 10 patients the skin biopsy came from a clinically affected area and in 4 patients the skin was locally unaffected. One sample was used for RNA sequencing and one sample was used for immunohistochemistry. Skin biopsies from healthy individuals were commercially sourced (Tissue Solutions, UK) and collected from donors undergoing skin resection surgery and after informed consent. To match the healthy skin with patients as much as possible, skin biopsies from healthy controls were also taken from a similar position (the under-arm (for 4 controls) and leg (for 2 controls)). Healthy skin donors were selected to match the age and sex of the SSc patient cohort. Biopsies from patients and controls were equally treated and were both stored at -80°C until RNA isolation was performed. RNA from frozen skin biopsies was isolated using RNeasy kit from fibrous tissue (Qiagen, the Netherlands). RNA quantity was determined by using SimplyNano 2000 and quality was assessed on Tapestation (Agilent, the Netherlands). All samples included in the study had a RIN score above 7.0. Transcriptome characterisation and analysis RNA sequencing was performed using polyA selection and a stranded protocol using Ion Torrent next generation sequencing technology (Service XS, The Netherlands). The Ion PI Template OT2 200 Kit v3 and Ion PI Sequencing 200 Kit v3 were used according to the manufacturer’s instructions. 20 samples were run on 11 PI chips. PI chip analyses, base calling and quality checks were performed using the Torrent Server Suite. An average of 42 million 100 bp reads was generated per sample. Following quality control, reads were aligned to the human genome (Homo sapiens GRh38.78) using Bowtie2 and STAR (Dobin et al. 2013; Langmead and Salzberg 2012). Reads were first aligned with STAR. For the unmapped reads from STAR, a second alignment step was performed using bowtie2 (local very sensitive options)

  Dataset EGAD00001003832

• Glioblastoma epigenome profiling identifies SOX10 as a master regulator of molecular tumour subtype

  Glioblastoma in adult patients are classified into four subtypes, IDH, MES, RTK I, and RTK II, based on DNA methylation and RNA expression data. Tumour subtype transitions commonly occur during the treatment of glioblastoma patients, and transitions to the mesenchymal (MES) subtype have been associated with therapy resistance and adverse prognosis. Here, we generate DNA methylome and histone modification data of glioblastoma primary tumours and show that glioblastoma subtypes differ by their enhancer landscapes. Using Core Regulatory Circuitry analysis of H3K27ac data, and independent analysis of RNA-derived gene regulatory networks, we identified 38 subtype master regulators whose cell type-specific activities we mapped in single-cell RNA sequencing data. These analyses identified the chromatin modifier SRY-Box 10 (SOX10) as a master regulator in tumours of the RTK I subtype. In functional studies we demonstrate that SOX10 loss causes a transition of RTK I tumour cells to a mesenchymal cellular state by altering the accessibility of enhancer-rich chromatin regions and their occupancy by Bromodomain Containing 4 (BRD4), a dynamic constituent of super-enhancers. Treatment with the BRD4 inhibitor JQ1 blocked this transition. These data demonstrate the fundamental role of enhancer chromatin remodelling and master regulator activity in the establishment, maintenance and plasticity of glioblastoma cellular states. We also make our data publically browsable at https://dkfz-b060.github.io/gb_browse/

  Study EGAS00001003953

• RNA Editing Exome

  Exome sequencing data for tumor and matched normal samples of the EGAS00001000495 project.

  Dataset EGAD00001000626

• RNA Editing AZIN1 amplicon sequencing

  AZIN1 amplicon sequencing data of the EGAS00001000495 project.

  Dataset EGAD00001000708

• Saliba Lab Data Access Committee

  DAC for data generated by Saliba Lab at Helmholtz institute for RNA-based Infection Research, Würzburg, Germany

  Dac EGAC50000000152

• UTUC RNAseq data

  RNA sequencing of upper urinary tract urothelial carcinoma

  Dataset EGAD00001007667

• Mapping the Evolution of T Cell States During Response and Resistance to Adoptive Cellular Therapy

  We investigated single T cell transcriptional states that define donor lymphocyte infusion (DLI) response and resistance from cryopreserved bone marrow mononuclear cells from 15 patients with relapsed chronic myeloid leukemia (CML) after allogeneic hematopoietic stem cell transplant. By integrating bulk ATAC-seq data from sorted T cell populations from these bone marrow samples, we also defined gene regulatory networks that underlay these clusters.

  Study phs002877

• DAC for a single-cell multi-omic atlas of nodal B-cell non-Hodgkin lymphomas

  Nodal B-cell non-Hodgkin lymphomas (B-NHL) are a clinically diverse set of cancers thought to originate from distinct stages of B-cell maturation. To characterize intratumor heterogeneity across B-NHL entities, we performed CITE-Seq (cellular indexing of transcriptomes and epitopes) on 51 lymph node samples including mantle cell lymphoma (MCL, n = 8), follicular lymphoma (FL, n = 12), germinal center (GCB, n = 5) or activated B-cell (non-GCB/ABC, n = 7) diffuse large B-cell lymphoma (DLBCL) and marginal zone lymphoma (MZL, n = 11) tumors, in addition to non-malignant reactive lymph nodes (rLN, n = 8). We also performed 5 prime scRNA-seq with immune receptor profiling for 11 of these samples (2 rLN, 2 MCL, 3 FL, 2 DLBCL, and 2 MZL).

  Dac EGAC50000000226

• SUM-seq data for Primary T-cells differentiated to helper subtypes

  Briefly, naive CD4+ T cells were isolated from PBMCs obtained from buffy coats from three healthy human donors, and differentiated into Th0, iTreg, Th2, Th1, Th17, and IFN-β-activated subsets. This allowed us to study the differentiation of naive CD4+ T cells into distinct helper subsets under the influence of a specific cytokine environment. Following 5 days of differentiation, T cells were left unstimulated or re-stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin to assess their functional responses. Thus, this SUM-seq experiment consisted of 36 multiplexed conditions (3 donors x 6 stimulations x with/without re-stimulation). Single-cell chromatin accessibility and gene expression data is provided as demultiplexed fastq files.

  Dataset EGAD50000001204

• cfMeDIP-seq for 18 patients with pleural mesothelioma

  The dataset contains cfMeDIP-sequencing data (bam files) for 18 plasma samples from pleural mesothelioma patients. The libraries were prepared according to the published protocol (Shen, S. Y., Burgener, J. M., Bratman, S. V. & De Carvalho, D. D. Preparation of cfMeDIP- seq libraries for methylome profiling of plasma cell-free DNA. Nat. Protoc. 14, 2749–2780 (2019)). Whole genome sequencing (WGS) was performed for pre-made libraries on NovaSeq X Plus with a 150 paired-end strategy. Low-quality reads and adapters were removed with Trim Galore version 0.6.6 (https://www.bioinformatics.babraham.ac.uk/projects/trim_galore). The trimmed reads were aligned to hg38 with Bowtie2 version 2.3.4.3. SAMTools version 1.9 was used to convert the SAM alignment files to BAM files, sort and index reads, and remove duplicates.

  Dataset EGAD50000002126