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• Defining and Overcoming Intrinsic T Cell Dysfunction to Enable Pediatric Immunotherapy

  T-cells from 71 children and young adults with B-cell malignancies on trial to receive anti-CD19 CAR T-cell therapy were analyzed. These T-cells represent the pre-manufacture T-cells that were subsequently used for CAR T manufacture. Bulk RNA-Seq was performed on sorted T-cell subsets for all patients, in addition to CITE-Seq and single-cell ATAC-Seq on a subset of 6 patients. The primary clinical outcome was duration of B-cell aplasia, a surrogate measure of functional CAR T-cell persistence. From these data, molecular signatures associated with long and short-term CAR T-cell persistence were identified. This data submission includes bulk RNA-Seq, CITE-Seq, and single-cell ATAC-Seq data from this study.

  Study phs002323

• Sequence-Based Analysis of Human Breast Tumors

  The goal of this study is to study gene expression patterns in tumors, normal tissues, and cell lines.

  Study phs000676

• scCRISPRi/a-seq Control and IFN treated iPS derived human GPC/OPCs

  Datasets consists of 2 batches of human glial progenitors (iPS), cells were sequenced as controls and IFN treated. Using the 10Genomics platform from the samples 2 libraries were built forgene expression libraries (scRNA-seq) and captured guides sequencing library (gRNA) on a set of Multiple Sclerosis associated SNPs. Batch one includes KRAB and P300 perturbed cells in 2 rounds sequenced RNA libraries for Ctrl and IFN and 1 round of capture guides for Ctrl and IFN. Batch 2 includes 1 round of both RNA expresison library and captures guides for KRAB and P300 perturbations in Ctrl and IFN treated cells.

  Dataset EGAD50000002053

• Exome sequencing of a Novel Primary T Cell Immunodeficiency Kindred (2019-08-19)

  Primary T cell immunodeficiency disorders have a heterogeneous genetic basis. This study will focus on one case characterised by severe T cell lymphopenia in the index case. We aim to sequence the complete exomes of this individual, her three unaffected siblings and parents in an effort to identify the causative genetic mutation responsible for this disorder. We will perform exome capture using Agilent SureSelect system, followed by sequencing on the HiSeq platform. Our study has the potential to uncover genes important for T cell development and novel therapeutic strategies to treat T cell immunodeficiencies. . This dataset contains all the data available for this study on 2019-08-19.

  Dataset EGAD00001005263

• MYOSEQ

  The MYOSEQ project focuses on the application of next generation sequencing, in particular whole exome sequencing (WES), in a large cohort of patients with unexplained limb‐girdle weakness (LGW). Focusing on undiagnosed patients with a clearly defined clinical phenotype enables increased diagnostic rates for known genes (in particular Pompe disease, GNE related pathologies and other known LGMD subtypes) in this cohort, while the use of WES provides scope both for new gene discovery and for additional research into disease modifiers and genotype‐phenotype correlation with substantial cost effectiveness. The LGW patient cohort was collated by Newcastle University in collaboration with clinical centers across Europe. The sequencing was performed at the Broad Institute and jointly analyzed with Newcastle University.

  Dataset EGAD00001006158

• Functional Enhancer Elements Drive Subclass-Selective Expression From Mouse to Human Neocortex

  A complete epigenomic map of human brain cell types will be necessary to fully understand their genetic regulation, and to create the next generation of non-species-restricted genetic tools for their functional characterization. Here we performed both bulk and single-nucleus ATAC-seq studies of fresh human neocortical samples excised during neurosurgery, in order to discover the functional genomic elements that discriminate cell types. This dataset contains 78 bulk layer-dissected ATAC-seq samples, and 3660 single-nucleus ATAC-seq samples from fresh acutely isolated human neurosurgical samples. Furthermore, from these data we identified and validated several enhancers for use in AAV context. We also provide validation single cell RNA-seq for 456 human acutely labeled neurosurgical neurons labeled by 3 unique enhancer-AAV vectors, and single cell RNA-seq for 1483 mouse neurons labeled in vivo by 11 unique enhancer-AAV vectors. Together these datasets provide high-resolution maps of single human neocortical cell types, as well as proof of the functional utility of the genomic elements discovered. As a whole these data will be important to furnish the next generation of cell type-specific functional tools and therapies in neuroscience.  

  Study phs002292

• Whole Genome Bisulfite Sequencing of Circulating Cell-Free (CCF) DNA and its Cellular Contributors

  Background: Circulating cell free (ccf) fetal DNA has enabled non-invasive prenatal fetal aneuploidy testing without direct discrimination of the genetically distinct maternal and fetal DNA. Current testing may be improved by specifically enriching the sample material for fetal DNA. DNA methylation may allow for such a separation of DNA and thus support additional clinical opportunities; however, this depends on knowledge of the methylomes of ccf DNA and its cellular contributors. Results: Whole genome bisulfite sequencing was performed on a set of unmatched samples including ccf DNA from 8 non-pregnant (NP) and 7 pregnant female donors and genomic DNA from 7 buffy coat and 5 placenta samples. We found CpG cytosines within longer fragments were more likely to be methylated, linking DNA methylation and fragment size in ccf DNA. Comparison of the methylomes of placenta and NP ccf DNA revealed many of the 51,259 identified differentially methylated regions (DMRs) were located in domains exhibiting consistent placenta hypomethylation across millions of consecutive bases, regions we termed placenta hypomethylated domains. DMRs identified when comparing placenta to NP ccf DNA were recapitulated in pregnant ccf DNA, confirming the ability to detect differential methylation in ccf DNA mixtures. Conclusions: We generated methylome maps for four sample types at single base resolution, identified a link between DNA methylation and fragment length in ccf DNA, identified DMRs between sample groups, and uncovered the presence of megabase-size placenta hypomethylated domains. Furthermore, we anticipate these results to provide a foundation to which future studies using discriminatory DNA methylation may be compared.

  Study phs000846

• LLDeep DAG2+ scRNA-seq in PBMCs

  Single cell transcriptomics of PBMCs of 47 donors from the Lifelines Deep cohort (general population, Northern part of the Netherlands). Cells of five or six different donors were pooled together in one sample pool, resulting in eight different sample pools. In total, 28.855 cells were captured and their transcriptomes were sequenced to an average depth of 74k. Genotype data was available for each donor, which allowed us to use the Demuxlet method that uses variable SNPs between the pooled individuals to determine which cell belongs to which individual. Since genotype information is lacking of 2 individuals, the transcriptome of only 45 individuals could be retrieved.

  Dataset EGAD00010001315

• Single cell RNA-sequencing of tissues from NSCLC patients treated with chemoimmunotherapy

  The goal of this study is to characterize immune cell populations by single cell RNA-sequencing (scRNA-seq) in tumor and uninvolved normal tissues from non-small cell lung cancer (NSCLC) patients with resectable non-small cell lung cancer and who received neoadjuvant chemoimmunotherapy. scRNA-seq was performed on seven pairs of tumor and normal tissues as well as one lymph node (LN) sample. Data set includes pair-end fastq files for single cell RNA sequencing of 7 neo-immuno patients. (Total 15 samples and 50 runs).

  Dataset EGAD00001009778

• Renal habitat WXS

  This project is correlating the molecular profiling of renal tumours with multiparametric and 13C-MRI including by 13C-MRSI. . This dataset contains all the data available for this study on 2023-03-09.

  Dataset EGAD00001010125

• DAC for "CUT&RUN-sequencing identifies PTK7 as a direct Wnt target in patient-derived colorectal cancer organoids"

  Dac EGAC00001003592

• MutWP5: CRUK Mutographs of Cancer: Lung: PD38234 (Targeted) (2020-01-29)

  Sequencing of LCM-derived microbiopsies from explanted lung from pulmonary fibrosis patient. Goal to assess the mutational burden, spectrum, and clonal dynamics within the tissue. Deep sampling throughout multiple regions of the lung will determine whether there are differences in smoking-related mutation burden in different portions of the lung. Targeted sequencing will be conducted on samples to identify drivers of interest and clonality of the samples, well-performing samples will be sent for subsequent whole-genome sequencing. Results from this portion of the study will be compared to other individuals with smoking-related diseases (COPD, pulmonary fibrosis, lung cancer), and normal, non-smoking lungs. . This dataset contains all the data available for this study on 2020-01-29.

  Dataset EGAD00001005925

• A Genome-Wide Association Study of CALGB 90401: Randomized, Double-Blind, Placebo-Controlled Phase III Trial Comparing Docetaxel and Prednisone with or without Bevacizumab in Men with Metastatic Castration-Resistant Prostate Cancer

  The Cancer and Leukemia Group B (CALGB) 90401 trial compared docetaxel and prednisone with or without bevacizumab in men with metastatic castration-resistant prostate cancer. A genome-wide association study using clinical outcomes and toxicities was conducted on the basis of data from CALGB patients who provided consent for pharmacogenomic studies and usable DNA

  Study phs001002

• HLA-A*3101 and Carbamazepine-Induced Hypersensitivity Reactions in Europeans

  Based on the prior knowledge of involvement of the human leukocyte antigen locus in Han Chinese patients with carbamazepine-induced Stevens-Johnson syndrome, we imputed the HLA types for each case and control subject from the array of SNPs in the Human610-Quad GWAS platform (NCBI Build 36.1). We then performed a genome-wide association test which included the imputed HLA alleles as markers.

  Study EGAS00000000036

• A single-cell transcriptional gradient in human cutaneous memory T cells restricts Th17/Tc17 identity

  We identified a gradated transcriptional program of coordinately regulated inflammation-suppressive genes in psoriatic resident memory T cells. This dataset includes bulk RNA-seq for CRISPR-based deactivation of two core components of this inflammation-suppressive program, ZFP36L2 and ZFP36, in human PBMCs. It also includes scRNA-seq of cutaneous immune cells from psoriasis patients before and during therapeutic IL-23 blockade.

  Study EGAS00001006716

• Spatially confined sub-tumor microenvironments in pancreatic cancer

  Intratumoral heterogeneity is a critical frontier in understanding how the tumor microenvironment (TME) propels malignant progression. Here, we deconvolute the human pancreatic TME through large-scale integration of histology-guided regional multiOMICs with clinical data and patient-derived preclinical models. We discover subTMEs, histologically definable tissue states anchored in fibroblast plasticity, with regional relationships to tumor immunity, subtypes, differentiation, and treatment response. Reactive subTMEs rich in complex but functionally coordinated fibroblast communities were immune-hot and inhabited by aggressive tumor cell phenotypes. The matrix-rich deserted subTMEs harbored less activated fibroblasts and tumor- suppressive features yet were markedly chemoprotective and enriched upon chemotherapy. SubTMEs originated in fibroblast differentiation trajectories and transitory states were notable both in single cell transcriptomics and in situ. The intratumoral co-occurrence of subTMEs produced patient-specific phenotypic and computationally predictable heterogeneity tightly linked to malignant biology. Therefore, heterogeneity within the plentiful, notorious pancreatic TME is not random but marks fundamental tissue organizational units.

  Dataset EGAD00001008155

• DLBCL NGS Genomic Datasets of non-China cohort from Phoenix Clinical Trial

  Study biopsies (n=773; 189 cases as China cohort and 584 cases as non-China cohort) underwent whole exome sequencing or targeted gene panel DNA sequencing and RNA sequencing, allowing the identification of somatic mutations. Tumors were assigned to DLBCL genetic subtypes as the MCD (n=110), BN2 (n=47) or N1 (n=28) using the LymphGen algorithm based on their somatically mutated genes. In younger patients (age≤60), ibrutinib plus R-CHOP was associated with a 100% event free survival (EFS) at 3-years in the MCD and N1 groups, whereas R-CHOP alone was associated with a 3-year EFS of 42.9% (p=0.01) and 50% (p=0.016) in the MCD and N1 groups, respectively. This analysis showed a benefit of ibrutinib with R-CHOP chemotherapy in particular genetic subtypes, providing mechanistic support for its survival benefit in younger patients with non-GCB DLBCL. The EGA collects RNA-Seq and NuGene targeted sequencing datasets of 584 cases for non-China cohort.

  Study EGAS00001005554

• Distinct evolutionary trajectories of primary high grade serous ovarian cancers revealed through spatial mutational profiling

  High-grade serous ovarian cancer (HGSC) is characterized by poor outcome, often attributed to emergence of treatment-resistant sub-clones. We sought to measure the degree of genomic diversity within primary, untreated HGSC to examine the natural state of tumor evolution prior to therapy. We performed exome sequencing, copy number analysis, targeted amplicon deep sequencing and gene expression profiling on thirty-one spatially and temporally separated HGSC tumor specimens (six patients) including ovarian masses, distant metastases, and fallopian tube lesions. We found widespread intra-tumoral variation in mutation, copy number, and gene expression profiles, with key driver alterations in genes present in only a subset of samples (e.g. PIK3CA, CTNNB1, NF1). On average, only 51.5% of mutations were present in every sample of a given case (range: 10.2% to 91.4%), with TP53 as the only somatic mutation consistently present in all samples. Complex segmental aneuploidies, such as whole genome doubling, were present in a subset of samples from the same individual, with divergent copy number changes segregating independently of point mutation acquisition. Reconstruction of evolutionary histories showed one patient with mixed HGSC and endometrioid histology with common etiologic origin in the fallopian tube and subsequent selection of different driver mutations in the histologically distinct samples. In this patient, we observed mixed cell populations in the early fallopian tube lesion, indicating diversity arises at early stages of tumorigenesis. Our results reveal that HGSC exhibit highly individual evolutionary trajectories and diverse genomic tapestries prior to therapy, exposing an essential biological characteristic to inform future design of personalized therapeutic solutions and investigation of drug resistance mechanisms.

  Study EGAS00001000547

• Amplicon Sequencing for 'Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma'

  BAMs from deep sequencing using a custom panel for the study 'Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma'

  Dataset EGAD00001015012

• SCI-MAP: Single Cell Microgel embedded iPS-cells to map molecular variability of cell differentiation using a systems biology approach.

  In the SCI-MAP project we will map cell states encountered across a previously established 49 day in vitro chondrogenic differentiation protocol. We do this to optimise the differentiation process for therapeutic and in vitro modelling ends. We collect epigenetic open chromatin and phenotypic transcriptome data to determine cell states and so performed single nucleus sequencing in two modalities: RNA- and ATAC-sequencing. Data was collected in a time series experiment at 7 points: Days 0, 3, 6, 8, 14, 21, and 49, starting with the first pilot data from day 21 (D21).

  Study EGAS50000001041

• Multi-omic analyses from a randomized phase II study of epigenetic priming followed by nivolumab in previously treated metastatic non-small cell lung cancer

  Emergence of resistance to immune checkpoint blockade (ICB) mandates the development of strategies for ICB sensitization. We aimed to understand the effects of epigenetic priming in re-shaping the tumor microenvironment, together with molecular drivers of therapeutic response of epigenetic therapy followed by ICB in non-small cell lung cancer (NSCLC; NCT01928576). This was done through a multi-omic approach encompassing both genomic and transcriptomic analyses. Findings suggest that epigenetic therapy may reshape the tumor microenvironment towards a more inflamed phenotype and prime responses to immunotherapy.

  Study EGAS50000000913

• ATACseq - Notch Signaling Maintains a Progenitor-Like Subclass of Hepatocellular Carcinoma

  To assess how Notch inhibition impacts chromatin accessibility and how chromatin changes relate to HNF4A and CEBPA activities, we performed Assay-for-Transposase-Accessible-Chromatin (ATAC) sequencing of LIV78 tumors, 72 hours after treatment with NOTCH2 blocking or control antibodies. Our TF activity and chromatin analyses thus lead to a model in which Notch inhibition leads to increased expression of CEBPA, thus enabling CEBPA to partner with HNF4A to jointly drive transcriptional programs and the underlying chromatin rearrangements that promote differentiation of progenitor-like tumor cells to a mature hepatocyte fate incompatible with tumor growth and maintenance.

  Study EGAS50000000516

• Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia

  In this study, we demonstrate that aberrant expression of SLAMF6 on acute myeloid leukemia (AML) cells serves as a novel immune escape mechanism that can be inhibited by antibodies against the SLAMF6 dimerization site. This constitutes a novel mechanism of checkpoint inhibition, which paves the way for immunotherapy in AML and other SLAMF6-expressing cancers. This study utilizes single cell sequencing data from the AML cell line HNT-34 co-cultured with normal T cells, with and without antibody targeting SLAMF6, as well as single cell data of 38 primary AML samples.

  Study EGAS50000001085

• Whole exome sequencing of cell-free DNA reveals temporo-spatial heterogeneity and identifies treatment-resistant clones in neuroblastoma

  Background: Neuroblastoma (NB) displays important clinical and genetic heterogeneity, with emergence of new mutations at tumor progression. Patients and Methods: To study clonal evolution during treatment and follow-up, an innovative method based on circulating cell-free DNA (cfDNA) analysis by whole exome sequencing (WES) paired with target sequencing was realized in sequential liquid biopsy samples of 19 NB patients. Results: WES of the primary tumor and cfDNA at diagnosis showed overlap of Single Nucleotide Variants (SNVs) and Copy Number Alterations (CNAs), with 41% and 93% of all detected alterations common to the primary NB and cfDNA. CfDNA WES at a second time point indicated a mean of 22 new SNVs for patients with progressive disease. Relapse-specific alterations included genes of the MAPK pathway and targeted the protein kinase A signaling pathway. Deep coverage target sequencing of intermediate timepoints during treatment and follow-up identified distinct subclones. For 17 seemingly relapse-specific SNVs detected by sequencing detected these alterations in minor subclones, with relapse-emerging SNVs targeting genes of neuritogenesis and cell cycle. Furthermore a persisting, resistant clone with concomitant disappearance of other clones was identified by a mutation in the ubiquitin protein ligase HERC2. Conclusion: Modelisation of mutated allele fractions in cfDNA indicated distinct patterns of clonal evolution, with either a minor, treatment-resistant clone expanding to a major clone at relapse, or minor clones collaborating towards tumor progression. Identification of treatment-resistant clones will enable development of more efficient treatment strategies.cfDNA WES at relapse but not tumor or cfDNA WES at diagnosis, deep coverage target.

  Study EGAS00001002705

• PopCol 16S gut microbiome sequencing

  PopCol is a cohort study in Stockholm, Sweden that includes a data-rich set of individuals with data available from bowel symptoms questionnaires, gastroenterology visits and biospecimens (genotype and 16S sequencing from blood and stool samples, respectively). Genotyping was carried out using the Illumina HumanOmniExpressExome-8v1 arrays at the SciLifeLab NGI facility in Uppsala, Sweden. Fecal DNA was extracted from samples kept at -80°C using Qiagen 5 QIAamp DNA Stool Mini Kits and analyzed using 16S rRNA gene amplicon sequencing (in the V1-V2 hypervariable region). This was performed on the Illumina MiSeq platform at the Institute of Clinical Molecular Biology (IKMB) in Kiel, Germany. Of these, six PopCol participants were PPI users and 12 used antibiotics. The study was approved by the local Committee of Research Ethics (Forskningskommitté Syd) at Karolinska Institutet, Stockholm, in November 2001. Written informed consent was obtained from all participants

  Dataset EGAD00001007071