14983 results for "cancer studies using rna-seq"

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• Gene expression by RNAseq in bronchial biopsies of asthmatics, asthma in remission and healthy subjects

  The study focus was differential expression in bronchial biopsies between persistent asthma, asthma in remission and healthy controls using RNAseq. There were 184 samples that passed QC. RNA samples were processed using the TruSeq Stranded Total RNA Sample Preparation Kit (Illumina, San Diego, CA), using an automated procedure in a Caliper Sciclone NGS Workstation (PerkinElmer, Waltham, MA). In this procedure, all cytoplasmic and mitochondria rRNA was removed (RiboZero Gold kit). The obtained cDNA fragment libraries were loaded in pools of multiple samples unto an Illumina HiSeq2500 sequencer using default parameters for paired-end sequencing (2 × 100 bp). Data are available as 221 pairs of FASTQ-files. Note that several samples are associated with multiple sequence runs.

  Dataset EGAD00001005112

• Prime-seq of human term placenta-derived trophoblast organoids

  To study the one of the mechanisms through which obesity could affect placental cells, we used a novel microfluidic organs-on-a-chip device fabricated for co-culturing adipose spheroids and trophoblast organoids. The organoids were derived from the term placenta of a over-weight women. The adipose spheorids were derived from the white adipose tissue of a woman. And we sequenced the RNAs from the trophoblast organoids. The RNA extracted were subjective to Prime-seq library preparation protocol and being sequenced on Illumina NovaSeq 6000 at Novogene.

  Study EGAS50000000833

• RNA sequencing analysis of lymphoblastoid cell lines with wildtype or defective Epstein-Barr virus

  Lymphoblastoid cell lines established using either wildtype or BALF5-deficient Epstein-Barr virus were analyzed by RNA sequencing.

  Dataset EGAD00001004297

• Transcriptome - MBD4-deficient AML

  Transcriptome sequencing for WEHI-AML-1 and WEHI-AML-2. RNA libraries were generated using the Illumina TruSeq RNA Sample Preparation Kit v2 and sequenced on an Illumina HiSeq2500.

  Dataset EGAD00001003569

• English Longitudinal Study of Ageing Genome-wide genotyping using the Illumina HumanOmni2.5-8

  These data are for a Genome Wide Association Study (GWAS) in the English Longitudinal Study of Ageing (ELSA, www.ifs.org.uk/elsa), building on the existing ELSA DNA Repository (EDNAR). This will establish a valuable resource for UK and international scientists, giving them access to GWAS genotyping data. Phenotype data, available on request, includes measures of personality, attitudes, behaviours as well as detailed social and economic outcomes; high quality biomarkers and other intermediate phenotypes; a range of more distal phenotypes, such as direct assessments of health (for example, hypertension, diabetes, muscle strength and cognitive function), and the opportunity to analyse existing biological samples for additional biomarkers, including metabolomic studies. Importantly, this resource would be matched with a near identical resource established in the United States for the Health and Retirement Study (HRS), giving the potential for high quality replication studies and comparative analyses.

  Study EGAS00001001036

• Transcriptome of CD4+ T cells and CD8+ T cells in glioblastoma multiforme

  Patients included in this study were over 18 years of age and had a histology-confirmed diagnosis of glioblastoma multiforme (GBM). Exclusion criteria were the previous administration of any anti-tumor therapy including radiation therapy. All patients gave written informed consent. The study was approved by the local ethics committee (TUM Medical school) and conducted following the Declaration of Helsinki. During resection of the tumors, tumor tissue and tissue from normal appearing brain within the operative channel was collected. Blood was drawn during the surgical procedure. Single cell suspensions were prepared from the tumor tissue, the normal appearing brain, and the blood. CD4+ T cells and CD8+ T cells were sorted by flow cytometry. Only patients with a complete set of specimens (CD4+ tumor infiltrating lymphocytes (TIL), CD8+ TIL, CD4+ T cells from normal appearing brain, CD8+ T cells from normal appearing brain, blood-derived CD4+ and CD8+ T cells) containing a minimum of 1000 cells in each sorted sample were further analyzed (n=9). Total RNA was isolated from sorted cell populations using the RNAeasy Plus micro kit (Qiagen, 74034). Quality and integrity of total RNA was controlled on a Bioanalyzer 2100 (Agilent Technologies). Library preparation for bulk-sequencing of poly(A)-RNA was done as described previously (Parekh et al., 2016). Briefly, barcoded cDNA of each sample was generated with a Maxima RT polymerase (ThermoFisher Scientific, EP0742) using oligo-dT primer containing barcodes, unique molecular identifiers (UMIs) and an adaptor. Ends of the cDNAs were extended by a template switch oligo (TSO) and full-length cDNA was amplified with primers binding to the TSO-site and the adaptor. NEB UltraII FS kit was used to fragment cDNA. After end repair and A-tailing, a TruSeq adapter was ligated and 3'-end-fragments were finally amplified using primers with Illumina P5 and P7 overhangs. In comparison to previous descriptions (Parekh et al., 2016), the P5 and P7 sites were exchanged to allow sequencing of the cDNA in read 1 and barcodes and UMIs in read 2 to achieve a better cluster recognition. The library was sequenced on a NextSeq 500 (Illumina) with 59 cycles for the cDNA in read 1 and 16 cycles for the barcodes and UMIs in read 2. Data were processed using the published Drop-seq pipeline (v1.0) to generate sample- and gene-wise UMI tables (Macosko et al., 2015). Reference genome (GRCh38) was used for alignment. Transcript and gene definitions were used according to the Genecode Annotation Version 35.

  Dataset EGAD50000000226

• Oral Microbiome in Esophageal Adenocarcinoma

  The purpose of our study was to assess the influence of oral microbiota on the development of esophageal cancer. Our preliminary case-control studies reported a global alteration of foregut microbiome in esophageal adenocarcinoma with the strongest changes found in the oral microbiome. We hypothesise that commensal oral bacteria are capable of activating or degrading carcinogens in cigarette smoke and therefore may contribute to esophageal carcinogenesis. We conducted a prospective study nested in two large US cohorts, to determine whether oral microbiota are associated with subsequent esophageal adenocarcinoma.

  Study phs001527

• Pharmacogenomic Analysis of Microtubule Targeting Agent Response and Toxicity

  Microtubule targeting agents are commonly prescribed for early and metastatic breast cancer and other solid tumors. However, interindividual variability in microtubule targeting drug response and toxicity can cause limited therapeutic benefit and impact quality of life. In the present study, genome-wide analyses were performed to investigate how genetic factors can be used to increase prediction of treatment response and toxicity, identify genes or gene pathways associated with chemotherapy-induced neurotoxicity, and inform further in vitro studies that may help isolate differences in response and toxicity of microtubule targeting agents.

  Study phs002060

• Research for drug discovery and elucidation of pathophysiology using disease-specific iPS cells

  We investigated roles of KRAS on stemness maintenance and differentiation propensity in the context of induced pluripotent stem cells (iPSCs) using isogenic KRAS mutant (G13C/WT) and wild-type (WT/WT) iPSCs from the same RAS-associated autoimmune lymphoproliferative syndrome-like disease (RALD) patients. Exome-seq analysis was conducted to compare gene profiles of WT/WT and G13C/WT iPS cells. We have not found any differences of gene mutation in the two genotypes.

  Study JGAS000136

• Single nucleus and spatial transcriptomic characterization of prostate cancer versus normal controls

  10x Genomics Visium and Chromium platforms were used for spatial and single-nuclei RNA-sequencing, respectively. Cohort consisted of 8 prostate cancer patients (8 prostate cancer + 8 paired non-malignant control samples, fresh-frozen)

  Study EGAS50000001143

• Targeting the DNA Repair Pathway in Ewing Sarcoma

  Ewing’s Sarcoma is a bone and soft tissue tumor that primarily affects adolescents and young adults. With current therapies, 70% of patients with localized disease survive but survival for metastatic and recurrent disease is poor. Whole genome sequencing of 19 Ewing’s Sarcoma tumors showed that STAG2 was mutated in 10% (2/19) of the tumors and STAG2 protein was absent in 14% (13/106) tumors by immunohistochemical staining. Previous studies have shown that glioblastoma cells lacking STAG2 are more sensitive to poly-ADP ribose polymerase (PARP) inhibitors. We found that Ewing’s Sarcoma cell lines are sensitive to PARP inhibitors irrespective of STAG2 protein expression. Ewing Sarcoma cell lines are defective in double strand DNA break repair. PARP inhibitor cytotoxicity in Ewing’s Sarcoma cells was potentiated 10-1,000 fold by DNA damaging agents (irinotecan and temozolomide). To extend these studies in vivo, we developed an orthotopic Ewing’s Sarcoma mouse model and performed pharmacokinetic and pharmacodynamic studies with three different PARP inhibitors (BMN-673, olaparib and veliparib) in clinical development for pediatric cancer. Those data were used to design preclinical phase I studies to identify tolerable drug combinations for pilot efficacy testing (preclinical phase II). Based on the results of the preclinical phase I/II data, we performed a double blind, randomized, placebo controlled preclinical phase III trial with 274 mice in 15 treatment groups. Irinotecan administered in a low-dose protracted schedule optimized for pediatric patients was an effective DNA damaging agent to combine with olaparib and BMN-673 and was better tolerated than combinations with temozolomide. Combining olaparib or BMN-673 with irinotecan and temozolomide gave complete and durable responses in over 80% of the mice.

  Study EGAS00001000839

• Revealing active mutational processes in tumours using DigiPico/MutLX at unprecedented accuracy

  Active mutational processes in a tumor result in genetic micro-heterogeneity that can determine the tumor’s evolutionary trajectory. Identification of these processes by studying micro-heterogeneity can unveil novel aspects of tumor evolution with potential therapeutic implications. Such studies, however, are inherently problematic because of the discovery of excessive false positive mutations. Here we report the optimization and validation of a robust whole genome sequencing and analysis pipeline (DigiPico/MutLX) that virtually eliminates false positive results. Using our method, we identified, for the first time, a sub-clonal local hyper-mutation (kataegis) event in a recurrent ovarian carcinoma, which was unidentifiable from the bulk WGS data of the same tumor. Overall, we propose DigiPico/MutLX method as a powerful framework for the reliable study of genetic micro-heterogeneity in tumor and normal tissues.

  Study EGAS00001003555

• Cambridge COVID-19 Single-cell PBMC

  Single-cell multi-omic profiling of healthy controls, asymptomatic and hosptial-admitted COVID19 patients recruited from Addenbrookes and Royal Papworth hospitals, in collaboration with the NIHR Cambridge Bioresource. Data represent RNA-seq, surface protein measurements (CITE-seq) of 192 antibody targets, along with VDJ-seq profiling of single T cell and B cell receptors. Samples are pooled, with 4 donors per pool. Germ-line genotypes are provided (VCF) to aid demultiplexing of single-cell and assignment to specific patient donor samples.

  Dataset EGAD00001007867

• MuTHER_adipose_tissue_small_RNA_expression

  We investigate the naturally occurring variation of small RNA expression in conjunction with genetic and gene expression variation. We shall assess the variation in subabdominal fat tissue small RNA levels in 168 unrelated MuTHER individuals. Using gene expression data from the same samples, we can survey how much the small RNA expression contributes to the variance in gene expression profiles. We can also take advantage of the high density genotyping data on these samples to identify genetic associations of small RNA expression levels, and the downstream effect of the genetic variants in small RNA sequence. Previous small RNA sequencing efforts have also extended the repertoire of small RNAs, and we hope to potentially find additional small RNAs active in adipose tissue biology. Altogether, the project should provide an exciting view into small RNA biology in humans, and lead to development of new methodology for analysis of molecular phenotype data.

  Study EGAS00001000212

• p200503_fn2

  RNA-Sequencing data of Fusobacterium nucleatum (Fna 71) treated CRC patient derived (CAF180, CAF181) and CAF05 cancer associated fibroblasts (CAFs).

  Study EGAS50000001121

• MutWP6__CRUK_Grand_Challenge_Mutographs_of_Cancer__oncology_agents

  he Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Within Mutographs, work lead by the Sanger Institute will investigate whether detection of somatic mutations and mutational signatures in circulating white blood cells can be developed into a practical, generic system for surveying and monitoring multiple different endogenous and exogenous exposures, providing an ‘observatory’ on somatic mutational processes in humans. Whole genome sequences are generated at the Wellcome Sanger Institute (Illumina HiSeqX). Somatic mutational signatures are subsequently extracted by non-negative matrix factorisation methods. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development.

  Study EGAS00001004125