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• Ovarian Cancer Organoid Biobank

  WGS of ovarian cancer organoids, tumor samples and blood references. Ovarian cancer (OC) is a heterogeneous disease usually diagnosed at a late stage. Experimental in vitro models that faithfully capture the hallmarks and tumor heterogeneity of OC are limited and hard to establish. We present a novel protocol that enables efficient derivation and long-term expansion of OC organoids. Utilizing this protocol, we have established 56 organoid lines from 32 patients, representing the spectrum of ovarian neoplasms, including non-malignant borderline tumors, as well as mucinous, clear-cell, endometrioid, low- and high-grade serous carcinomas. OC organoids recapitulate histological and genomic features of the pertinent lesion from which they were derived, illustrating intra- and inter-patient heterogeneity, and can be genetically modified. We show that OC organoids can be used for drug screening assays and capture different tumor subtype responses to the gold standard platinum-based chemotherapy, including acquisition of chemoresistance in recurrent disease. Finally, OC organoids can be xenografted, enabling in vivo drug sensitivity assays. Taken together, this demonstrates their potential application for research and personalized medicine.

  Dataset EGAD00001004387

• Genome and transcriptome sequence data from a metastatic carcinoma to paraspinal mass with primary unknown patient

  Genome and transcriptome sequence data from a metastatic carcinoma to paraspinal mass with primary unknown patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001004693

• Partner independent fusion gene detection by multiplexed CRISPR Cas9 enrichment and long read Nanopore sequencing (FUDGE)

  Targeted long-read nanopore sequencing. Abstract: Fusion genes are hallmarks of various cancer types and important determinants for diagnosis, prognosis and treatment. Fusion gene partner choice and breakpoint-position promiscuity restricts diagnostic detection, even for known and recurrent configurations. To accurately and impartially identify fusions, we developed FUDGE: FUsion Detection from Gene Enrichment. FUDGE couples target-selected and strand-specific CRISPR/Cas9 activity for fusion gene driver enrichment - without prior knowledge of fusion partner or breakpoint-location – to long-read Nanopore sequencing with the bioinformatics pipeline NanoFG. FUDGE has flexible target-loci choices and enables multiplexed enrichment for simultaneous analysis of several genes in multiple samples in one sequencing run. We observe on-average 665 fold breakpoint-site enrichment and identify nucleotide resolution fusion breakpoints - within two days. The assay identifies cancer cell line and tumor sample fusions irrespective of partner gene or breakpoint-position. FUDGE is a rapid and versatile fusion detection assay, providing unparalleled opportunity for diagnostic pan-cancer fusion detection.

  Dataset EGAD00001006111

• Whole blood RNA-sequencing of covid-19 patients and healthy controls

  This dataset contains whole blood transcriptome data generated from 93 patients with COVID-19 across a range of severities and 23 healthy controls. All patients were PCR positive for SARS-CoV-2 and disease severity ranged from asymptomatic to severe disease requiring ventilation. Individuals without symptoms, or with mild symptoms, were recruited from routine screening of healthcare workers, while COVID-19 patients were recruited at or soon after admission to Addenbrooke’s or Royal Papworth hospitals. Blood samples were taken at recruitment and then again four weeks later. Further details of the cohort and the generation of the RNA-Sequencing data can be obtained from Bergamaschi, L. et al. Longitudinal analysis reveals that delayed bystander CD8+ T cell activation and early immune pathology distinguish severe COVID-19 from mild disease. Immunity 54, 1257-1275 e8 (2021).

  Dataset EGAD00001007776

• MutWP5: CRUK Mutographs of Cancer: Lung: PD43291_Novaseq (WG)

  Sequencing of LCM-derived microbiopsies from explanted lung from COPD 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 mutaiton burden in different portions of the lung. Whole-genome sequencing will be conducted on samples identified as promising from the initial targeted data. Results from this poriton 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 2023-03-08.

  Dataset EGAD00001010111

• RNAseq of GEPARSIXTO

  294 formalin-fixed paraffin-embedded (FFPE) tissue samples were sent to the UNC Lineberger Comprehensive Cancer Center Translational Genomics Lab (TGL) for RNA isolation using the Maxwell 16 MDx Instrument (Promega AS3000) and the Maxwell 16 LEV RNA FFPE Kit (Promega AS1260) following the manufacturer’s protocol (Promega 9FB167). 279 total RNA sequencing libraries were prepared at TGL using a Bravo Automated Liquid-Handling Platform (Agilent G5562A) and the TruSeq Stranded Total RNA Library Prep Gold Kit (Illumina 20020599) following the manufacturer’s protocol (Illumina 1000000040499). RNAseq library quality and quantity were measured using a TapeStation 4200 (Agilent G2991AA) and Qubit 3.0 fluorometer (Life Technologies Q33216), pooled at equal molar ratios, and denatured following the manufacturer’s protocol (Illumina 1000000106351). 271 total RNA sequencing libraries were sequenced at TGL on NovaSeq 6000 (Illumina 20012850) S4 flow cells (Illumina 20028313) following the manufacturer’s protocol (Illumina 1000000019358) using a 2x50 bp paired-end configuration and pool sizes of 91 libraries to target a read depth of 110 million clusters per library on average.

  Dataset EGAD00001010201

• Genome and transcriptome sequence data from a metastatic cancer to the breast patient

  Genome and transcriptome sequence data from a metastatic cancer to the breast patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001010959

• Genomic evolution and natural history of myeloproliferative neoplasms on therapy - triple-negative-ET

  Philadelphia-negative myeloproliferative neoplasms are chronic blood neoplasms. Treatments control blood counts but disease can progress to myelofibrosis or acute myeloid leukaemia. We performed longitudinal whole-genome and targeted sequencing in 30 patients, integrating clonal dynamics with 7,986 blood counts and clinical histories. Distinct evolutionary patterns distinguished stable from progressive disease, with leukaemic transformation arising via TP53 loss, stepwise driver mutation acquisition within complex clones, or emergence of independent leukaemic clones. In contrast, stable disease showed long-term clonal equilibrium without new drivers. Phylogenetic analysis using 203 whole-genomes of haematopoietic colonies revealed age-appropriate polyclonal haematopoiesis in triple-negative essential thrombocythaemia and germline predisposition to thrombocytosis, supporting non-neoplastic origins. Therapy-associated mutagenesis was observed, including C>G mutations following azacitidine and characteristic T>A/T>G after hydroxycarbamide exposure in blood cells, although not in skin where UV damage predominated. These findings demonstrate progression is genomically encoded years in advance and support serial monitoring and further study of treatment-related mutagenesis.

  Dataset EGAD00001016066

• Genomic evolution and natural history of myeloproliferative neoplasms on therapy - MPN_bulk

  Philadelphia-negative myeloproliferative neoplasms are chronic blood neoplasms. Treatments control blood counts but disease can progress to myelofibrosis or acute myeloid leukaemia. We performed longitudinal whole-genome and targeted sequencing in 30 patients, integrating clonal dynamics with 7,986 blood counts and clinical histories. Distinct evolutionary patterns distinguished stable from progressive disease, with leukaemic transformation arising via TP53 loss, stepwise driver mutation acquisition within complex clones, or emergence of independent leukaemic clones. In contrast, stable disease showed long-term clonal equilibrium without new drivers. Phylogenetic analysis using 203 whole-genomes of haematopoietic colonies revealed age-appropriate polyclonal haematopoiesis in triple-negative essential thrombocythaemia and germline predisposition to thrombocytosis, supporting non-neoplastic origins. Therapy-associated mutagenesis was observed, including C>G mutations following azacitidine and characteristic T>A/T>G after hydroxycarbamide exposure in blood cells, although not in skin where UV damage predominated. These findings demonstrate progression is genomically encoded years in advance and support serial monitoring and further study of treatment-related mutagenesis.

  Dataset EGAD00001016067

• Single-cell profiling of neoantigen-specific T cells in lung cancers treated with neoadjuvant PD-1 blockade

  We study the expression profile of MANA-specific T cells, we used the MANA functional expansion of specific T cells (MANAFEST) assay in neoadjuvant anti-PD-1-treated lung cancers and applied their T cell receptor’s (TCR) complementarity-determining region 3 (CDR3) as a “barcode” to track and analyze their transcriptional programs in the tumor microenvironment using single cell TCR sequencing coupled with single cell RNA sequencing. We revealed distinct phenotype for MANA- and virus-specific clones in TIL and adjacent normal lung, regardless of response. MANA-specific T cells show features that drive the differences between responders and non-responders.

  Study EGAS00001005343

• Sequential single-cell transcriptional and protein marker profiling reveals TIGIT as a marker of CD19 CAR-T cell dysfunction in patients with non-Hodgkin’s lymphoma

  Employed single cell RNA sequencing and protein surface marker profiling of serialCAR-T cell samples from patients with non-Hodgkin’s lymphoma (NHL) to reveal CAR-T cell evolution, identify biomarkers of response, and test for evidence of exhaustion inCAR-T cells of poor responders. At the transcriptional and protein levels, we note the evolution of CAR-T cells toward a non-proliferative, highly-differentiated, andexhausted state that is enriched in CAR-T cells of patients with poor response.Furthermore, we identified the checkpoint receptor TIGIT as a novel prognosticbiomarker and potential driver of CAR-T cell exhaustion.

  Study EGAS00001005356

• Genome-Wide Analysis of Diffuse Large B-Cell Lymphoma (De Novo and Derived from the High Grade Transformation of Follicular Lymphoma)

  Version 1. Diffuse Large B-cell Lymphoma (DLBCL) represents the most common form of B-cell non-Hodgkin Lymphoma (B-NHL), accounting for ~30% of the de novo diagnoses and also arising as a frequent clinical evolution of Follicular Lymphoma (FL). The molecular pathogenesis of DLBCL is associated with multiple genetic lesions that in part distinctly segregate with individual phenotypic subtypes, suggesting the involvement of distinct oncogenic pathways. However, the lesions identified so far likely represent only a fraction of those necessary for malignant transformation. In order to characterize the entire set of structural alterations present in the DLBCL genome, we have integrated next generation whole exome sequencing analysis of 6 DLBCL cases and genome-wide high-density SNP array analysis of 72 DLBCL cases. We report here that FL and DLBCL harbor frequent structural alterations inactivating CREBBP and, more rarely, EP300, two highly related histone and non-histone acetyltransferases (HATs) that act as transcriptional co-activators in multiple signaling pathways. Overall, ~37% of DLBCL and 36% of FL cases display genomic deletions and/or somatic point mutations that remove or inactivate the HAT coding domain of these two genes. These lesions commonly affect a single allele, suggesting that reduction in HAT dosage is important for lymphomagenesis. We demonstrate specific defects in the acetylation-mediated inactivation of the BCL6 oncoprotein and activation of the p53 tumor suppressor. These results identify CREBBP/EP300 mutations as a major pathogenic mechanism shared by common forms of B-NHL, and have direct implications for the use of drugs targeting acetylation/deacetylation mechanisms. Version 2. Follicular lymphoma (FL) is an indolent, but incurable disease that, in 30-40% of cases, undergoes transformation to an aggressive diffuse large B cell lymphoma (DLBCL). The history of clonal evolution and the mechanisms that underlie transformation to DLBCL (tFL) remain largely unknown. Using whole exome sequencing and copy number analysis of 39 tFL patients, including 12 with paired sequential FL/tFL biopsies, we show that, in most cases, FL and tFL arise by divergent evolution from a common mutated precursor cell through the acquisition of distinct genetic lesions. Mutations in epigenetic modifiers (e.g., MLL2, CREBBP, EZH2, ARID1A) and anti-apoptotic genes (BCL2, FAS) were observed in 93% (36/39) and 78% (30/39) of cases, respectively, and were invariably shared between the two disease phases, suggesting an early acquisition in the common mutated precursor. Conversely, the development of tFL is associated with deregulation of genes involved in the control of cell proliferation, cell cycle progression and DNA damage responses (CDKN2A/2B, MYC, TP53), as well as with an aberrant activity of the somatic hypermutation mechanism. Finally, we show that the genomic profile of tFL shares significant similarities with that of germinal center B-cell type de novo DLBCL, but also displays unique combinations of altered genes that may explain the dismal clinical course of tFL.Version 3. This version includes thirty-five additional de novo DLBCL samples, newly diagnosed, and their paired normal DNA from previously untreated patients, which were analyzed by whole exome sequencing (n=27T and 25N), whole genome sequencing (8T and 10N), and/or targeted HLA-next generation sequencing (n=26T/N pairs) in order to identify genetic alterations associated with loss of surface MHC-II expression.

  Study phs000328

• Recurrent DNMT3B gene rearrangements are associated with unfavorable outcome in dicentric (9;20)-positive pediatric BCP-ALL

  The dicentric chromosome dic(9;20)(p11∼13;q11), occurs in 2% of pediatric acute lymphoblastic leukemia (ALL) cases. However, the prognostic significance of the dic(9;20) alterations and the mechanism in which these alterations drive leukemogenesis remains elusive. Our study describes the demographic, clinical, prognostic, and molecular characteristics of the dic(9;20)-positive ALL in a cohort of 57 pediatric BCP-ALL patients. Targeted RNA-seq and Array CGH analysis unraveled heterogeneous breakpoints on chromosomes 9 and 20 and frequent deletions of the IKZF1 gene. Together with the intrinsic susceptibility for deletions in CDKN2A, CDKN2B, and PAX5 genes in the dic(9;20)-positive ALL, these patients are eligible for treatment escalation in the AIEOP-BFM ALL 2017 clinical study. Survival analysis revealed poor 5-year event-free survival (pEFS) of 69% in dic(9;20)-positive ALL cases, compared to BCP-ALL patients enrolled in modern treatment studies. Strikingly, we identified six dic(9;20)-positive cases with rearrangements involving the DNMT3B gene, and poor 5-year pEFS of 25% (SE = 20%), compared to 79% (SE = 9%) for the remaining cohort (P = 0.011). Despite the loss of the methyltransferase domain of the DNMT3B gene in most cases with DNMT3B rearrangements, we did not observe major changes in the global methylation patterns. Differential gene expression analysis of DNMT3B-rearranged ALL unraveled a dysregulation of genes involved in hematopoiesis, lymphocyte maturation, and the PI3K/AKT signaling pathway. After confirmation in an independent cohort, DNMT3B-rearranged ALL cases should be considered high-risk for relapse and treated accordingly. We provide clinical data sets of Array CGH, targeted RNA-seq, total RNA-seq, whole genome bisulfite (WGBS) and whole genome DNA sequencing (WGS) obtained from bone marrow (BM) or peripheral blood (PB) mononuclear cells of 57 pediatric patients with dicentric chromosome dic(9;20) positive Acute lymphocytic leukemia (ALL), from which in 6 cases DNMT3B gene rearrangement was identified. This data is complemented by total RNA-seq and WGBS of samples from 4 additional ALL patients with a t(12;21) translocation and ETV6-RUNX1 gene fusion. DNA was isolated from BM or PB lymphocytes using Qiagen QIAamp DNA Blood Midi Kit to perform i) Array CGH of 58 dic(9;20) positive samples by hybridizing 500ng DNA using a Agilent 400K SurePrint G3 Custom CGH Human Genome Microarray (e-Array design 84704) ii) WGBS of 6 DNMT3B rearrangement positive samples and 4 ETV6-RUNX1 positive samples using Tecan TrueMethyl oxBS-Seq module for library preparation and Illumina NovaSeq 6000 platform to run 2x151 cycles iii) WGS of DNMT3B rearrangement positive samples using Illumina Lotus DNA Library Prep Kit followed by sequencing running 2x160 cycles on an Illumina NovaSeq 6000 platform. RNA was isolated from PB lymphocytes using the PerkinElmer Chemagic 360 instrument, followed by i) targeted RNA-seq of 56 dic(9;20) positive samples prepared using Illumina TruSight RNA Pan-Cancer Panel and sequenced on an Illumina MiSeq platform running 2x75 cycles ii) total RNA-seq of 6 DNMT3B rearrangement positive samples and 4 ETV6-RUNX1 positive samples utilizing TruSeq Stranded Total RNA Library Prep Gold kit and running 2x100 cycles on an Illumina NovaSeq 6000 platform.

  Study EGAS00001007383

• Multimodal epigenetic sequencing analysis of cell-free DNA identifies biomarkers for ALS diagnosis and progression

  The role of the epigenome in age-related neurodegenerative disorders remains understudied. Here, we analyzed circulating cell-free DNA (cfDNA) from blood to detect methylation changes as a liquid-biopsy for Amyotrophic Lateral Sclerosis (ALS). Our study included 20 patients with sporadic ALS, 10 patients with C9orf72-associated ALS, 10 asymptomatic carriers of the C9orf72 repeat expansion mutation, and 21 non-disease controls.

  Dac EGAC50000000739

• Altered Blood and Keratinocyte microRNA/transfer RNA Fragment Profiles Related to Fibromyalgia Syndrome and its Severity

  We provide small RNA transcriptome signatures of whole blood and cultured keratinocytes, which separate FMS patients from healthy controls. This opens new perspectives for FMS diagnostics, symptom monitoring, and clinical management.

  Study EGAS50000000638

• Transcriptome of periadrenal and subcutaneous fat in patients with hyperaldosteronism in comparison to patients with non-functional adenomas

  This study analyzed subcutaneous fat (SCF) and periadrenal fat (PAF) from patients with aldosterone-producing adenomas (APAs) and, as controls, non-functional adrenal adenomas (NFA) (SCF, n = 7; PAF, n = 5).

  Study EGAS50000001095

• G3BP2-KIT drives leukemia amenable to kinase inhibition in Ph-like ALL

  We describe a patient with Ph-like ALL, in which leukemic cells harbored an in-frame fusion between the GTPase-activating protein (SH3 domain)-binding protein 2 (G3BP2) and the KIT proto-oncogene.

  Study EGAS00001005181

• Predictors of Immune Checkpoint Blockade Response in dMMR Colorectal Cancer Using an Integrated Immune-Enhanced Multi-Omics Platform

  To identify candidate tumor- and immune-related biomarkers associated with clinical outcomes following anti–PD-1 therapy in dMMR colorectal cancer, we conducted a comprehensive genomic profiling using ImmunoID NeXT platform, including whole exome, whole transcriptome and TCR/BCR sequencing.

  Dataset EGAD50000002504

• 10X single-cell Multiome (RNA+ATAC) of cord blood-derived HSPC

  10X genomics chromium single-cell ATAC+RNA (Multiome) was use to prepare single-nucleus RNA- and ATAC-seq libraries, sequenced on an Illumina NovaSeq 6000 platform. BAM files are provided. Samples from 4 donors were sequenced after sorting for primitive HSPCs in 2 libraries, each with cells from 1 male and 1 female CB.

  Dataset EGAD50000002327

• Multi-platform genome sequencing of families with rare disease

  This dataset contains genome sequencing data from 51 individuals from 19 different family trios/quads with rare disease who consented to data sharing. PacBio Revio HiFi data (FASTQ, unaligned or aligned BAM) are available for 48 samples, and Illumina NovaSeq 6000 FASTQ data are available for 13 samples (1 trio without HiFi data, plus 10 affected probands with corresponding HiFi data).

  Dataset EGAD50000002109

• Differentiation-associated ISG expression of NK cells in chronic viral hepatitis

  Little is known about the effects of ISGs on NK cell responses in chronic viral hepatitis. Here, we determined the expression, regulation and function of ISGs in NK cells with respect to phenotype and function, we performed high-throughput single cell RNA sequencing of circulating CD3-CD56+ NK cells from healthy donors (HD) and patients with chronic HBV or HCV infections.

  Dataset EGAD50000001623

• Whole exome sequence of human XXY fibroblasts

  This dataset contains Whole exome sequence generated using human skin fibroblast sample (ID 419281) from Klinefelter XXY syndrome patient fibroblasts. These fibroblasts were used to generate autosomally isogenic human iPSCs. The sample DNA was collected using commercial kit and Human All Exon v5 capture paired library was sequenced using Illumina HiSeq device. The fastq file (ID 493224) and analysis (ID 3209) bam files have been deposited.

  Dataset EGAD50000001362

• 10Xchromium 3' RNA-seq of 21 samples from human embryonic heart

  21 samples were taken from human embryonic heart of PCW 5.5-14 of a total of 13 fetuses. Samples were subject to 10Xgenomics chromium single cell 3' sequencing version 2 or 3. Data was analyzed using STARSolo version 2.7.10a, using human genome GRCh38.p12 and transcript annotations from ENSEMBL release 93 from reference package GRCh38-3.0.0 as available from 10Xgenomics.

  Dataset EGAD50000001499

• M116 DNA Methylation Array

  DNA samples were quantified with Qubit BR kit on a Qubit2.0 fluorimeter (ThermoFisher Scientific), and integrity was checked using agarose gel electrophoresis. DNA from samples passing the quality control was bisulfite-converted using the EZ DNA Methylation-Gold™ Kit (Zymo Research, Cat. D5005) following the manufacturer's instructions. Then, bisulfite-converted DNA was hybridized into the Methylation EPICv1.0 BeadChip (Illumina) array interrogating > 850,000 CpG sites according to manufacturer's instructions

  Dataset EGAD50000001678

• Transcriptome data of periadrenal and subcutaneous fat in patients with hyperaldosteronism in comparison to patients with non-functional adenomas

  We analyzed subcutaneous adipose tissue (scAT) and periadrenal adipose tissue (paAT) from patients with Aldosterone-Producing Adenomas (APA) and, as controls, non-functional adrenal adenomas (NFA). RNA sequencing and immunohistochemistry of AT was performed (IHC, only on scAT). IHC markers included adipokines (leptin, adiponectin) and transcription factors (eg, c-jun, CaMKII)

  Dataset EGAD50000001590