Search Results - EGA European Genome-Phenome Archive

Whole Genome Sequences of 18th century African descended individuals from Charleston, South Carolina.

This study presents Whole Genome Sequencing results from the Anson Street African Burial Ground Project, which is a community-based initiative aimed at understanding the histories of 37 Ancestors in Charleston, South Carolina. Here we report fastq files for all 37 Ancestors. DNA was extracted at the University of Tennessee-Knoxville following Dabney et al. 2013, and dual index libraries prepared using a modified NEBNext Ultra II kit with partial USER enzyme digestion. Libraries were then enriched for human genomic DNA (MyBaits) and sequenced on Illumina Platforms.

Dataset EGAD00001009643

Test dataset with ligh-weight files

This is a test dataset derived from public data of the 1000 Genomes Project. Its purpose is not to allow for any inference about cohort data or results, but to aid bioinformaticians in the technical development and testing of tools, as well as data consumers in learning how to access information. This dataset consists of 3 pairs of light-weight (sliced) files: BAM + BAI, CRAM + CRAI and VCF + TBI. These files can be downloaded directly through the EGA-download-client PyEGA3 (https://github.com/EGA-archive/ega-download-client). For any further questions, please contact the DAC (Helpdesk - email: helpdesk [at] ega-archive [dot] org).

Dataset EGAD00001009826

Tumour sample for patient SA533

Whole genome sequencing of tumour sample for triple negative breast cancer patient SA533

Dataset EGAD00001009517

Tumour sample for patient SA409

Whole genome sequencing of tumour sample for triple negative breast cancer patient SA409

Dataset EGAD00001009518

Tumour sample for patient SA420

Whole genome sequencing of tumour sample for triple negative breast cancer patient SA420

Dataset EGAD00001009519

Tumour sample for patient SA296

Whole genome sequencing of tumour sample for triple negative breast cancer patient SA296

Dataset EGAD00001009520

Tumour sample for patient SA597

Whole genome sequencing of tumour sample for triple negative breast cancer patient SA597

Dataset EGAD00001009521

Biomarker analysis and treatment dynamics following preoperative ipilimumab plus nivolumab in locally advanced urothelial cancer from the phase 1B NABUCCO study

In the current analysis of the full NABUCCO trial population (cohorts 1 and 2), we aimed to explore both potential biomarkers for response to combination ICB, as well as treatment dynamics to gain a better understanding of the effects of ICB on the urothelial cancer tumor microenvironment (TME).

Study EGAS50000001781

Whole Transcriptome Analysis + AbSeq + Sample Tag Multiplexing

Multiomics data for a cohort of 20 COVID-19 patients (10 patients mild, 3 patients moderate, 4 patients severe, 3 patients critical) obtained from peripheral blood mononuclear cells (PBMCs) from longitudinally sampled at hospital admission, discharge, and 1 month thereafter. The data has been obtained a multiwell-based single-cell technology (BD Rhapsody) that includes the analysis of PBMCs' whole transcriptome and a set of 52 surface proteins. The samples of the different patients at different collection times were labelled using a cell hashing strategy with the BD Single-Cell Multiplexing Kit (6 samples for each run).

Dataset EGAD00001011318

Elucidating the heterogeneity of immunotherapy response and immune-related toxicities by longitudinal ctDNA and immune cell compartment tracking in lung cancer

The dataset for the study Elucidating the heterogeneity of immunotherapy response and immune-related toxicities by longitudinal ctDNA and immune cell compartment tracking in lung cancer includes 207 bam files from hybrid capture targeted error-correction next-generation sequencing (TEC-Seq) from plasma cell-free DNA and matched white blood cell DNA from 30 individuals with non-small cell lung cancer, alongside 46 bam files from whole exome sequencing of tumor and matched normal DNA for 21 individuals with non-small cell lung cancer who received immunotherapy-containing regimens.

Dataset EGAD00001011991

AWI-GEN 2 Phenotype Dataset

Core phentoype data for AWI-Gen Phase 2 Microbiome Project for 1824 samples.

Dataset EGAD00001015440

Phased whole genome sequencing of 10 melanoma samples

We have sequenced 10 melanoma samples using 10X linked reads technology to obtain phased whole genome sequence data. Using this data, we created diploid personalized genomes for each sample and aligned functional genomics data obtained from the same samples in order to find allele specific events (such as allele-specific binding and allele-specific chromatin accessibility).

Study EGAS00001004136

Whole genome sequencing libraries from the study "Histological Transformation and Progression in Follicular Lymphoma: a Clonal Evolution Study".

Whole genome sequencing libraries from the study "Histological Transformation and Progression in Follicular Lymphoma: a Clonal Evolution Study". These are libraries from 41 patients. Specifically: 15 transformed follicular lymphoma (TFL), 6 early progressers (PFL), and 20 non-early progressers (NPFL). For TFL and PFL patients, trios consisting of diagnostic (T1), transformed/progressed (T2) and a matching normal are available (n = 63 libaries in total). For NPFL patients, a tumor-normal pair are available (n = 40 libraries).

Dataset EGAD00001002897

Gut metagenome/FR 2002

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 EGAS00001005038

Somatic copy number alterations profiling in non-small cell lung cancer and their correlation with clinical efficacy in first-line treatment

Genomic data from FFPE tumor samples of patients with non-small cell lung cancer (NSCLC), profiled by shallow whole-genome sequencing (sWGS). The study aimed to characterize somatic copy number alterations (SCNAs) and SCNA burden to assess their clinical relevance for patient stratification across different first-line treatments.

Study EGAS50000001619

The British Autozygosity Populations BioResource (2018-06-06)

This data set contains whole exome sequences of individuals with self-stated parental relatedness from the East London Genes & Health cohort. Rare frequency functional variants in these healthy individuals will be studied with respect to the genetic health of the participants and loss-of-function analysis of human genes. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ . This dataset contains all the data available for this study on 2018-06-06.

Dataset EGAD00001004150

Sequencing data for Maturity-Onset Diabetes of the Young (MODY) patients in south India

We performed whole genome, whole or targeted exome sequencing for 289 individuals from India. This included 152 clinically diagnosed MODY and 137 control samples. Whole genome libraries were constructed using TruSeqNano DNA Library Preparation Kit (Illumina, CA) and sequenced on Illumina HiSeq2500 (Illumina, CA). The whole exome analysis was performed using Agilent SureSelect (Santa Clara, CA) Human All Exome kit v5 (50 Mb). Exome capture libraries were sequenced on HiSeq 2500 (Illumina, CA). Targeted exome sequencing was performed using custom probes corresponding to 1965 genes implicated in pancreatic cell biology and/or diabetes.

Dataset EGAD00001003919

Clonal expansion of mutated cell population in bladder urothelium (2018-08-03)

1cm biospies of from patients undergoing bladder cystectomy will be collected. The underlying muscle and stroma will be removed and the remaining epithelia dissected into small sequential areas which will be sent for ultra-deep exome sequencing using a panel of known cancer and viral genes. Sequence analysis using similar methods to Martincorena I et al (Science 2015, 348:880) will provide an idea of the somatic mutational landscape in these patient samples. Individual patient muscle samples will also be sequenced as a reference. . This dataset contains all the data available for this study on 2018-08-03.

Dataset EGAD00001004274

High-Coverage Whole-Exome Sequencing Identifies Candidate Genes for Suicide in Victims with Major Depressive Disorder

In this study, we applied an Illumina HighSeq platform-based high-coverage WES technique, which, in addition to the exons, allows the determination of 5′- and 3′-UTRs, promoters to a certain length, along with off-target sequences, such as introns, intergenic regions and infecting viruses. Brains from suicide victims (n = 23; 15 males and eight female) who had suffered from major depressive disorder and from control participants (n = 21; 14 males and seven females) who had died from other causes were used for whole-exome sequencing. Alignment files in bam format were uploaded.

Dataset EGAD00001004082

BLUEPRINT release August 2014, RNA-Seq for CD34-negative, CD41-positive, CD42-positive megakaryocyte cell

RNA-Seq data for 4 CD34-negative, CD41-positive, CD42-positive megakaryocyte cell sample(s). 22 run(s), 4 experiment(s), 4 alignment(s). Part of BLUEPRINT release August 2014. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_rnaseq_analysis_crg_20140811

Dataset EGAD00001000903

Deep sequencing of melanoma for driver mutations

Dataset EGAD00001001445

Whole genome sequence of third generation family member (SFHS)

Previously we performed deep WGS on 6 parents and 13 children from 3 large families from the Scottish Family Health Study to identify de novo mutations. This prelim is cover the additional sequencing of one grandchild from one of these three families. The inclusion of a third generation individual will provide additional experimental validation for the de novo mutations found in the initial trio. As in the previous study, the DNA will be WGS to a depth of approximately 25X to achieve this purpose.These data can only be used for the investigation of the genetic causes of the reported clinical phenotypes in these patients

Dataset EGAD00001001454

PRDM9 loss of function follow up from Born-in-Bradford Autozygosity sequencing

In the autozygosity exome sequencing of Born-in-Bradford samples of Pakistani origin there is a mother who is homozygous for an apparent truncating stop codon in PRDM9, the gene responsible for localising recombination during meiosis. We plan to deep sequence mother and child with X10, and physically phase the mother with PacBio sequencing. We will use this data to identify recombination locations, and test whether these are consistent with the known fine scale recombination map. Data Access is controlled by the Wellcome Trust Sanger Institute DAC and the Born In Bradford Executive Group.

Dataset EGAD00001001686

BLUEPRINT release January 2015, RNA-Seq for CD34-negative, CD41-positive, CD42-positive megakaryocyte cell

RNA-Seq data for 5 CD34-negative, CD41-positive, CD42-positive megakaryocyte cell sample(s). 23 run(s), 5 experiment(s), 5 alignment(s). Part of BLUEPRINT release January 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_rnaseq_analysis_crg_20140811

Dataset EGAD00001001165

BLUEPRINT release August 2015, RNA-Seq for CD34-negative, CD41-positive, CD42-positive megakaryocyte cell, on genome GRCh38

RNA-Seq data for 5 CD34-negative, CD41-positive, CD42-positive megakaryocyte cell sample(s). 23 run(s), 5 experiment(s), 5 alignment(s) on human genome GRCh38. Part of BLUEPRINT release August 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20150820/homo_sapiens/README_rnaseq_analysis_crg_20150820

Dataset EGAD00001001534

ENU-LS-411N-TripleTherapy

BRAF V600E colorectal cancers do not respond to the only currently FDA approved targeted therapy for CRC. There is currently a trial underway in the UK recruiting V600E CRC patients for treatment with a triple therapy combination of Cetuximab, Trametinib and Dabrafenib. We have mutagenized a pool of V600E CRC cell lines and treated with this triple therapy to select out drug resistant clones. We will now sequence these drug resistant clones with the aim of identifying common point mutations engendering resistance to this new therapy.

Dataset EGAD00001002051

BLUEPRINT release August 2016, RNA-Seq for CD34-negative, CD41-positive, CD42-positive megakaryocyte cell, on genome GRCh38

RNA-Seq data for 6 CD34-negative, CD41-positive, CD42-positive megakaryocyte cell sample(s). 24 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_rnaseq_analysis_crg_20160816

Dataset EGAD00001002339

Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cell types, (RNA-Seq for CD4-positive, alpha-beta T cell, on genome GRCh37)

RNA-Seq data for 212 CD4-positive, alpha-beta T cell sample(s). 212 run(s), 212 experiment(s), 212 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_rnaseq_analysis_sanger_20160816

Dataset EGAD00001002671

Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cell types, (ChIP-Seq for CD14-positive, CD16-negative classical monocyte, on genome GRCh37)

ChIP-Seq data for 172 CD14-positive, CD16-negative classical monocyte sample(s). 572 run(s), 345 experiment(s), 340 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_chipseq_analysis_ebi_20160816

Dataset EGAD00001002672

Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cell types, (ChIP-Seq for CD4-positive, alpha-beta T cell, on genome GRCh37)

ChIP-Seq data for 154 CD4-positive, alpha-beta T cell sample(s). 355 run(s), 265 experiment(s), 250 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_chipseq_analysis_ebi_20160816

Dataset EGAD00001002673

Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cell types, (RNA-Seq for CD14-positive, CD16-negative classical monocyte, on genome GRCh37)

RNA-Seq data for 197 CD14-positive, CD16-negative classical monocyte sample(s). 197 run(s), 197 experiment(s), 197 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_rnaseq_analysis_sanger_20160816

Dataset EGAD00001002674

Single cell resolution of human CNV body map (2019-10-02)

12 tissues from the warm autopsy are selected for this project. Using 10X Chromium technology we will generate ~1000 single cell/nulei genomic libraries per tissue. Each tissue will be whole genome sequenced (~2 lanes per 1000 cells) on hiseq X10. per single cell we will generate CNV profile and we investigate the level of genomic heterogenity with in tissue and across different tissues. . This dataset contains all the data available for this study on 2019-10-02.

Dataset EGAD00001005372

Systematic comparative analysis of single-nucleotide variant detection methods from single-cell RNA sequencing data

In this study, we performed systematic comparative analysis of seven widely-used SNV-calling methods, including SAMtools, the GATK Best Practices pipeline, CTAT, FreeBayes, MuTect2, Strelka2 and VarScan2, on both simulated and real single-cell RNA-seq datasets. We generated SMART-seq2 data for 70 CD45- single cells, which were derived from two colorectal cancer patients (P0411 and P0413). The average sequencing depths of these cells were 1.4 million reads per cell. We also generated tumor and adjacent normal bulk WES data, as well as tumor bulk RNA-seq data for these patients.

Dataset EGAD00001005373

NHLBI TOPMed: The Jackson Heart Study (JHS)

Since there is a greater prevalence of cardiovascular disease among African Americans, the purpose of the Jackson Heart Study (JHS) is to explore the reasons for this disparity and to uncover new approaches to reduce it. The JHS is a large, community-based, observational study whose 5306 participants were recruited from among the non-institutionalized African-American adults from urban and rural areas of the three counties (Hinds, Madison, and Rankin) that make up the Jackson, MS, metropolitan statistical area (MSA). Jackson is the capital of Mississippi, the state with the largest percentage (36.3%) of African Americans in the United States. The JHS design included participants from the Jackson ARIC study who had originally been recruited through random selection from a drivers' license registry. Approximately six months before the JHS was to begin, an amendment to the federal Driver's Privacy Protection Act was passed that changed the level of consent for public release of personal information from driver's license lists from an "opt out" to an "opt in" basis. The Mississippi Highway Patrol was no longer able to release a complete listing of all persons with driver's licenses or state identification cards, which prevented its use in the JHS. New JHS participants were chosen randomly from the Accudata America commercial listing, which provides householder name, address, zip code, phone number (if available), age group in decades, and family components. The Accudata list was deemed to provide the most complete count of households for individuals aged 55 years and older in the Jackson MSA. A structured volunteer sample was also included in which demographic cells for recruitment were designed to mirror the eligible population. Enrollment was opened to volunteers who met census-derived age, sex, and socioeconomic status (SES) eligibility criteria for the Jackson MSA. In addition, a family component was included in the JHS. The sampling frame for the family study was a participant in any one of the ARlC, random, or volunteer samples whose family size met eligibility requirements. Eligibility included having at least two full siblings and four first degree relatives (parents, siblings, children over the age of 21) who lived in the Jackson MSA and who were willing to participate in the study. No upper age limit was placed on the family sample. Known contact information was obtained during the baseline clinic examination from the index family member with a verbal pedigree format to identify name(s), age(s), address (es), and telephone number(s). Recruitment was limited to persons 35-84 years old except in the family cohort, where those 21 years old and above were eligible. Only persons who otherwise met study criteria but were deemed to be physically or mentally incompetent by trained recruiters were excluded from study eligibility.1 1 Wyatt SB, Diekelmann N, Henderson F, Andrew ME, Billingsley G, Felder SH et al. A community-driven model of research participation: the Jackson Heart Study Participant Recruitment and Retention Study. Ethn Dis 2003; 13(4):438-455 (PMID: 14632263).

Study phs000964

INCLUDE: The Epidemiology of Transient Leukemia in Newborns with Down Syndrome

The INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Project is an NIH-wide collaboration that seeks to improve health and quality-of-life for people with Down syndrome. The INCLUDE Project Data Coordinating Center and partners created the INCLUDE Data Hub, a centralized data resource that allows access to large-scale clinical and multi-omics datasets specific to Down syndrome and supports collaborative, cloud-based analysis to accelerate scientific discoveries related to Down syndrome and its co-occurring conditions.Down syndrome (DS) is associated with a remarkably high risk of childhood acute myeloid leukemia (AML), with an approximately 500-fold increased risk of the rare subtype acute megakaryoblastic leukemia. Though largely treatable, a proportion of myeloid leukemia in DS (ML-DS) patients relapse with dismal survival. ML-DS is preceded by a preleukemia, transient abnormal myelopoiesis (TAM), which presents clinically at birth and is driven by somatic truncating mutations in the erythro-megakaryocytic transcription factor gene GATA1. Up to 15% of DS newborns have TAM, and this can be fatal in up to 20% of cases. A further 10-15% of newborns with DS harbor subclonal GATA1 mutations with clinically silent disease (i.e., Silent TAM). Of the DS newborns with either TAM or Silent TAM (i.e., transient leukemia), up to 15% will acquire additional somatic mutations and progress to ML-DS. We predict that germline variation modifies the risk of developing somatic truncating GATA1 mutations, the first step towards ML-DS, however this has yet to be examined. To address this, the main aim of this X01 study is to perform the first genetic association study of GATA1 mutations in DS, through whole-genome sequencing (WGS) of 470 DS newborns in the Oxford Down Syndrome Cohort Study (ODSCS). Targeted sequencing of GATA1 has already been performed in the 470 DS newborns in the ODSCS, with 130 (28%) confirmed to harbor a somatic truncating GATA1 mutation. We will perform a genome-wide association study (GWAS) of GATA1 mutations to assess genetic variation genome-wide, in particular focusing on variants in candidate genes on the trisomic chromosome 21, RUNX1, ERG, ETS2, and DYRK1A, which have previously been associated with upregulation of GATA1. We will also carry out a chromosome X-wide association study (XWAS) to investigate genetic variation at the GATA1 gene, which resides on chromosome X. WGS data will also enable us to assess the potential role of copy number variation in the risk of transient leukemia in DS. Discovering genetic risk factors for GATA1 mutations in DS may reveal targets for new targeted therapies for TAM, and also inform the etiology of ML-DS as well as AML in the non-DS population. Finally, the ODSCS includes rich phenotypic data for the 470 DS newborns, including clinical diagnosis of TAM and other hematologic complications, complete blood counts, maternal pregnancy complications, and information on congenital heart disease and other birth defects. Thus, whole genome sequencing data in DS newborns from the ODSCS will provide a rich resource for the DS research community.

Study phs002982

The Role of E2F4 in Controlling Resistance to Irinotecan (CPT-11) in Human Colon Cancer

This study reports the results of RNA sequencing (RNA-seq) experiments performed on three isogenic clones of the human HT29 colon cancer cell line, genetically engineered to achieve the selective inactivation of the adenovirus early 2 (E2) gene transcription factor 4 (E2F4) protein, a key functional component of the multimeric transcriptional repression complex known as the dimerization partner (DP), retinoblastoma-like (RB-like), E2F and multi-vulva class B (MuvB) complex (DREAM). In previous studies, we identified E2F4 as a key regulator of colorectal cancer (CRC) resistance to irinotecan (CPT-11), a cytotoxic agent that stands at the backbone of multiple chemotherapy regimens for the treatment of metastatic CRCs. The molecular mechanisms linking E2F4 to irinotecan resistance, however, remain poorly understood. The present study was designed to identify which genes are under the transcriptional control of E2F4, either at baseline or following exposure to SN38 (i.e., the active metabolite of irinotecan, generated in vivo by biotransformation in the liver) in order to clarify the role played by E2F4 in shaping colon cancer resistance to chemotherapy. The cell line used for this study (HT29) is aneuploid and contains three copies of the E2F4 gene, because of a trisomy of chromosome 16, where the E2F4 gene is located (Kawai et al., Genes, Chromosomes & Cancer, 34:1-8, 2002; PMID: 11921276). HT29 cells were infected with lentivirus vectors encoding for CRISPR/Cas9 constructs designed to selectively inactivate the E2F4 gene, using three distinct guide-RNAs (gRNAs), each targeting a different sequence within the proximal exons of the E2F4 gene (exon 1, exon 2). Lentivirus-infected cells were sub-cloned by single-cell fluorescence-activated cell sorting (FACS), based on the differential expression of a fluorescent reporter (EGFP) expressed in tandem with the gRNAs. Isogenic clones (EGFP+) were then screened to identify those with a tri-allelic knock-out, as revealed by both genetic sequencing of the E2F4 gene (revealing the presence of three distinct frameshift mutations) and Western blot (revealing complete loss of E2F4 protein expression). The study includes twelve (n=12) RNA-seq experiments, representative of 3 experimental replicates (i.e., three distinct isogenic clones of the HT29 cell line, each displaying complete loss of E2F4 expression) and 3 negative controls (i.e., three independent preparations of the parent HT29 cell line, infected with a lentivirus vector encoding for a non-targeting gRNA) exposed to 2 distinct in vitro cell culture conditions: a) treatment with SN38 resuspended in dimethyl sulfoxide (DMSO); or b) treatment with DMSO alone (negative control). The in vitro treatment regimen used for SN38 (32 nM, 24 hours) was designed so that the exposure to SN38 experienced in vitro by HT29 cells would mirror the exposure to SN38 experienced in vivo by malignant tissues, as measured, for example, in metastatic CRC patients receiving a standard dose of irinotecan (180 mg/m2) administered by intravenous infusion over 90 minutes (Deyme et al., Cancer Chemotherapy and Pharmacology, 88:247-258, 2021; PMID: 33912999).

Study phs003560

Weighing Risks and Benefits of Laparoscopic Anti-Reflux Surgery in Patients With Idiopathic Pulmonary Fibrosis (WRAP-IPF-BioLINCC)

Data Access NOTE: Please refer to the "Authorized Access" section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: To determine if the reduction of abnormal gastro-esophageal reflux (GER) with laparoscopic anti-reflux surgery will slow the progression of idiopathic pulmonary fibrosis (IPF) as measured by forced vital capacity (FVC).Background: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown cause and increasing prevalence in the United States. Aside from lung transplantation, which approximately only 1% of participants will receive, there is no FDA-approved therapy. Abnormal acid gastro-esophageal reflux (GER) has been well described in participants with IPF and is thought to play a role in the progression of the disease. The several retrospective cohort studies that have assessed the association of anti-acid therapies for GER with clinical outcomes in IPF have had inconsistent results.Participants: A total of 58 participants were enrolled.Design: The WRAP-IPF trial was a multicenter, unblinded randomized clinical trial with participants randomized to either laparoscopic anti-reflux surgery or no surgery. Participants in the no-surgery group had the option of receiving laparoscopic anti-reflux surgery from 24 weeks after randomization if their clinician deemed it medically necessary. Medications for acid GER were allowed in both groups if the clinician felt it was necessary.Participants were followed up from time of randomization to 52 weeks. All participants had study visits at baseline, 12, 24, 36, and 48 weeks, during which spirometry, 6-min walk testing, and participant-related outcome assessments were done. Participants in the surgery group had clinical visits for preoperative evaluation, laparoscopic anti-reflux surgery, and postoperative management as clinically indicated. Surgery participants additionally underwent repeat 24-hour pH testing at 24 weeks to assess the efficacy of the surgery. All participants were contacted by telephone for safety assessments at weeks 4, 8, 16, 20, 28, 32, 40, 44, and 52. All participants completed an exploratory questionnaire on reflux symptoms at baseline and 48 weeks. The primary endpoint was change in FVC from randomization (baseline) to 48 weeks. Secondary endpoints included acute exacerbation, non-elective hospitalization (both all-cause and respiratory-related), death, change in cough severity, change in dyspnea severity, change in health-related quality of life, change in 6-min walk distance, and time to selected event-driven composite endpoints of disease progression. Conclusions: In participants with IPF and abnormal acid GER, laparoscopic anti-reflux surgery is safe and well tolerated but did not significantly slow the rate of FVC decline. Further research is needed, particularly with a larger study in order to achieve sufficient statistical power, regarding the possible benefits of anti-reflux surgery in this population.Raghu G, Pellegrini CA, Yow E, et al. Laparoscopic anti-reflux surgery for the treatment of idiopathic pulmonary fibrosis (WRAP-IPF): a multicentre, randomised, controlled phase 2 trial. Reference: Raghu, et al., 2018; PMID: 30100404.

Study phs003968

HIV Viremic Non-Progressors (VNPs) and HIV Progressors Data Access Committee

Data Access Committe for the project: Analyzing exome sequencing in HIV Viremic Non-Progressors (VNPs) and HIV Progressors

Dac EGAC50000000062

A Risk Score Incorporating Low Pass Whole Genome Sequencing of Cell Free DNA from Patients Receiving CD19 CAR T-Cell Therapy for Large B-Cell Lymphoma

Study EGAS00001006308

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