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• High Sensitivity ctDNA Analysis Using a Novel Panel and NOIR-SS Technology for Monitoring Advanced Urothelial Carcinoma

  This dataset contains sequencing data generated by targeted amplicon analysis using the NOIR-SS method in 15 patients with advanced urothelial carcinoma. Formalin-fixed paraffin-embedded (FFPE) tumor tissues (15 samples) and plasma cfDNA (50 samples) were analyzed. Tumor tissues were subjected to targeted panel sequencing to identify mutations in TP53, FGFR3, TERT, and KRAS/HRAS. Plasma cfDNA was analyzed using a tumor-informed approach focusing on the mutations identified in matched tumor tissues. Sequencing was performed on the Ion PGM or Ion S5 XL platform. Raw sequencing data are provided in FASTQ format under controlled access.

  Study JGAS000836

• Research for candidate genes of splenic epidermoid cyst

  Splenic epidermoid cyst is a very rare benign tumor-like lesion filled with fluid or semi-fluid material. It occurs mostly in 2nd or 3rd decades of life with some female dominance. Most cases are asymptomatic and the clinical symptoms are dependent on the size of the cyst. Exome re-sequencing is an efficient strategy to selectively sequence the protein-coding regions of the genome, and has increasingly been used to identify novel genetic variants underlying Mendelian diseases. In this study, exome re-sequencing of 8 Japanese patients with splenic epidermoid cyst were conducted.

  Study JGAS000008

• Integrative understanding of human immune system by functional genomics and development of intervention strategies for the prevention of autoimmune diseases

  To elucidate the regulation of B cell recptor repertoire in B cell subsets and its contribution to autoimmune diseases, B cell subsets from 36 Systemic Lupus Erythematosus(SLE), 90 Systemic Sclerosis(SSc), 85 Myositis(IIM), 21 Mixed Connective Tissue Disease(MCTD), 18 Sjogren's syndrome(SjS), 27 Rheumatoid Arthritis(RA), 23 Behcet's disease(BD), 18 Adult Onset Still���s Disease(AOSD), 24 ANCA-associated Vasculitis(AAV), 16 Takayasu���s Arteritis(TAK) and 137 healthy controls(HC) were collected (Naive_B, USM_B, SM_B, DN_B, Plasmablast. RNA-seq and BCR-mapping was performed with each B cell subset samples.

  Study JGAS000485

• Multiomic characterization of clonotypic B cells

  DNA was purified using AMPure XP magnetic beads (Beckman Coulter [BC] Life Sciences, Indianapolis, IN) and its quality was evaluated in an Agilent 4200 Tapestation using the Genomic DNA ScreenTape system (Agilent, Santa Clara, CA). DNA was quantified using the Qubit System (Invitrogen). Extracted DNA from AL patients was fragmented to 200bp by a Covaris S220 ultrasonicator (Covaris, Woburn, MA) and used to generate and capture libraries following the manufacturer’s indications from Twist Bioscience’s Human Core Exome Enrichment Kit (Twist Bioscience). Extracted DNA from MM patients and HA was fragmented to an average size of 225 bp using a Covaris S220 ultrasonicator (Covaris, Woburn, MA) and subjected to DNA library construction using Chromium Genome Reagent Kit V2 for Exome Assays (10X Genomics). Target enrichment was performed with SureSelectXT Human All Exon V6 Capture Library (Agilent) or SureSelectXT2 Human All Exon V5+UTRs (Agilent), and sequence targets were captured and amplified in accordance with the manufacturer’s protocol. Final libraries were combined with standard Illumina sequencing primers and paired-end sequenced (150bp) on a HiSeq X platform (Illumina, CA) or in a NovaSeq 6000 (Illumina).

  Dataset EGAD50000002162

• Personalized Onco-Genomic Project for pediatric and adolescent patients in British Columbia

  This is an extension of the BC Cancer Agency's Personalized Onco-Genomics (POG) project to children and adolescents treated at BC Children's Hospital. The project provides access to whole genome and transcriptome sequencing, and integrated bioinformatics analyses, of relapsed, refractory or poor prognosis cancers with an aim to identify actionable variants that can inform clinical decision making.

  Study EGAS00001006967

• Hypertension delays viral clearance and exacerbates airway hyperinflammation in patients with COVID-19

  In Coronavirus Disease 2019 (COVID-19), hypertension and cardiovascular diseases are major risk factors for critical disease progression. However, the underlying reasons and the effect of the main anti-hypertensive therapies—angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs)—remain unclear. Combining clinical data (n = 144) and single-cell sequencing data of airway samples (n = 48) with in vitro experiments, we observed a distinct inflammatory predisposition of immune cells in patients with hypertension that correlated with critical disease progression. ACEI treatment associated with dampened COVID-19-related hyperinflammation and with increased cell intrinsic anti-viral responses, whereas ARB treatment related to enhanced epithelial–immune cell interactions. Macrophages and neutrophils of patients with hypertension, in particular under ARB treatment, exhibited higher expression of the pro-inflammatory cytokines CCL3 and CCL4 and the chemokine receptor CCR1. Although the limited size of our cohort does not allow us to establish clinical efficacy, our data suggest that the clinical benefits of ACEI treatment in patients with COVID-19 who have hypertension warrant further investigation.

  Dataset EGAD00001006828

• WES and RNA-seq of triple-negative breast cancers from the MyBrCa cohort

  The dataset contains a genomics characterization of 35 triple-negative Asian breast tumours from the Malaysian Breast Cancer cohort. This includes whole-exome sequencing of tumour tissue at 80X, whole-exome sequencing of matched normal (blood) tissue at 40X, and RNA-seq of tumour tissue at 40X coverage (>15 million reads). Whole-exome libraries were prepared using the Nextera Rapid Capture Exome Kit; exome capture was performed in pools of 3 and subjected to paired end 75 sequencing on a NovaSeq 6000 platform. RNA libraries were prepared using the TruSeq Stranded Total RNA HT kit with Ribo-Zero Gold as per manufacturer’s instructions and also subjected to paired end 75 sequencing on a NovaSeq 6000 platform. Uploaded bam files have been mapped to the hs37d5 human genome and processed using the standard GATK pipelines. Paired clinical, demographic, genotyping, and overall survival data for these patients are available from the associated publications or by request.

  Dataset EGAD00001009311

• Somatic mutation and clonal evolution normal breast tissue WGS

  Cancer is a genetic disease caused by an accumulation of mutations, however many of these mutations have been identified in pathologically normal tissue. We aim to use laser-capture microscopy (LCM) to sample individual clones from breast tissue to identify whether cancer-associated mutations appear in this normal tissue, assess the mutational burden present, and identify the mutational processes causing these mutations. We will sample from a wide age range of individuals (<20 to >70 years old) to determine whether these processes differ in pre- and post-menopausal women. We will also be comparing the tissue from healthy individuals (samples from breast reduction surgery) to those at elevated risk of breast cancer (mastectomy from BRCA1/2 patients) and those who have breast cancer (adjacent normal, distal normal, and tumour tissue from mastectomy). This will allow us to determine how these processes are different between these groups of individuals, and gain insight into the earliest stages of tumour development. . This dataset contains all the data available for this study on 2023-03-09.

  Dataset EGAD00001010123

• cfDNA analysis reveals relation of POLR1D amplification to bevacizumab resistance in colorectal cancer patients

  Bevacizumab is an approved anti-angiogenic drug for patients with metastasized colorectal cancer (mCRC) targeting VEGF. The survival benefit of anti-VEGF therapy in mCRC patients is limited to a few months and acquired resistance mechanisms are greatly unknown. Using plasma DNA, we studied the evolution of tumor genomes in a cohort of patients with mCRC (n=150) and observed a recurrent focal amplification (8.7% of cases) on chromosome 13q12.2. Analysis of TCGA data (n=619) suggested an association with later stages, which we confirmed by longitudinal plasma analyses. We defined the minimally amplified region and studied the mechanistic consequences of copy number gain of the involved genes. The amplification of one gene, POLR1D, impacted cell proliferation, resulting in upregulation of VEGFA, an important regulator of angiogenesis which has been implicated in the resistance to bevacizumab. In several patients, we observed the emergence of this 13q12.2 amplicon under bevacizumab treatment, which was invariably associated with evolution of therapy resistance. Hence, we describe a novel resistance mechanism against a widely applied treatment in mCRC patients which will impact clinical management .

  Dataset EGAD00001005761

• Somatic mutant selection is altered by prior NOTCH1 mutation in ageing esophageal epithelium

  Authors: Charlotte King1, Emilie Abbie1, Joanna C. Fowler1, Irina Abnizova1, Roshan K. Sood1, Swee Hoe Ong1, Michael W. J. Hall1,2, Faye Lynch-Williams3, Benjamin A. Hall4, Philip H. Jones1,2,5 Abstract: In cancer evolution, genome alterations often occur in a specific order, implying selection depends on the prior clonal genotype 1-3. It is unknown if similar constraints operate in normal epithelia. Here, we mapped mutations in normal mid-esophagus of aged UK subjects. Mutant NOTCH1 clones colonized most of the epithelium by age 60 and above 70 tissue was saturated with mutants under strong competitive selection. Mutant TP53 was more strongly selected in donors over 60 years of age. Samples predominantly mutant for NOTCH1 showed increased selection of NOTCH2 mutants and weaker selection of mutant TP53 compared with samples that were mostly NOTCH1 wild type. In mouse esophagus lacking Notch1 we observed strong selection of mutant Notch2 and other genes not selected in wild type esophagus. In normal ageing esophagus, the first driver mutation may change the trajectory of subsequent somatic evolution by altering mutant selection.

  Dataset EGAD00001015259

• Somatic mutant selection is altered by prior NOTCH1 mutation in ageing esophageal epithelium

  Authors: Charlotte King1, Emilie Abbie1, Joanna C. Fowler1, Irina Abnizova1, Roshan K. Sood1, Swee Hoe Ong1, Michael W. J. Hall1,2, Faye Lynch-Williams3, Benjamin A. Hall4, Philip H. Jones1,2,5 Abstract: In cancer evolution, genome alterations often occur in a specific order, implying selection depends on the prior clonal genotype 1-3. It is unknown if similar constraints operate in normal epithelia. Here, we mapped mutations in normal mid-esophagus of aged UK subjects. Mutant NOTCH1 clones colonized most of the epithelium by age 60 and above 70 tissue was saturated with mutants under strong competitive selection. Mutant TP53 was more strongly selected in donors over 60 years of age. Samples predominantly mutant for NOTCH1 showed increased selection of NOTCH2 mutants and weaker selection of mutant TP53 compared with samples that were mostly NOTCH1 wild type. In mouse esophagus lacking Notch1 we observed strong selection of mutant Notch2 and other genes not selected in wild type esophagus. In normal ageing esophagus, the first driver mutation may change the trajectory of subsequent somatic evolution by altering mutant selection.

  Dataset EGAD00001015260

• The Precision Medicine in Liver Cancer across an Asia-pacific NETwork (PLANET) - Intratumoural immune heterogeneity

  The clinical relevance of immune landscape intratumoural heterogeneity (immune-ITH) and its role in tumour evolution remain largely unexplored. Here, we uncover significant spatial and phenotypic immune–ITH from multiple tumour sectors and decipher its relationship with tumour evolution and disease progression in hepatocellular carcinomas (HCC). Immune–ITH is associated with tumour transcriptomic-ITH, mutational burden, and distinct immune microenvironments. Tumours with low immune–ITH experience higher immunoselective pressure and escape via loss of heterozygosity in human leukocyte antigens and immunoediting. Instead, the tumours with high immune-ITH evolve to a more immunosuppressive/exhausted microenvironment. This gradient of immune pressure along with immune-ITH represents a hallmark of tumour evolution, which is closely linked to the transcriptome-immune networks that contributes to disease progression and immune inactivation. Remarkably, high immune-ITH and its transcriptomic signature are predictive for worse clinical outcome in HCC patients. This in-depth investigation of ITH provides evidence on tumour-immune co-evolution along HCC progression.

  Dataset EGAD00001006570

• Alloreactive T-cell receptor (TCR) repertoire in kidney transplantation

  We analyzed the T-cell receptor (TCR) repertoires from twelve kidney transplant recipients. Six out of the twelve kidney transplant recipients experienced a cellular rejection after kidney transplantation. TCR repertoires of CD4+ and CD8+ positive T-cells were assessed prior to transplantation and after transplantation at time of allograft biopsy using RNA based T-cell receptor beta next generation sequencing (NGS). In addition, the pre-formed alloreactive TCR repertoire for each kidney transplant recipient was identified using mixed lymphocyte reaction and donor reactive T-cells were subjected to TCR beta sequencing. In two out of the six patients with cellular rejection the TCR repertoire of graft infiltrating T-cells was additionally captured. This dataset comprises a total of 98 samples. NGS TCR beta libraries of all samples were sequenced on an Illumina NextSeq 500 and raw sequencing data (in the form of fastq files) as well assembled clonotypes and their counts (in the form of clonotype tables) are provided.

  Dataset EGAD00001007695

• 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

• Neuroblastoma patient Total RNA Seq data

  Tumor Total RNA Seq data of primary neuroblastomas. This is an update of the „Berlin Neuroblastoma Dataset” (EGAS00001004022). This data was used for the analysis of circular RNA expression and regulation in neuroblastoma.

  Dataset EGAD00001008124

• Myeloid cell programming in patients with non-medullary thyroid carcinoma

  This dataset contains single-cell RNA sequencing data from patients with thyroid cancer (n=7), multinodal Goiter (n=3) and healthy individuals (n=5). Mononuclear cells were taken from both the peripheral blood and the bone marrow compartments. We used a pooled single-cell design where multiple individuals were pooled in a single sample for sequencing (NextSeq 500-V2) and later demultiplexed using their genotype data. Associated metadata contains information on the phenotypes per individual, the pooling design and the linkage between the supplied files and sequenced pools. Due to limitations from EGA in uploading single-cell data, the raw fastq files were processed as follows: (i) I1/I2/R1/R2 fast files were concatenated over the different lanes. (ii) Concatenated I1 and I2 files were interleaved, as were the concatenated R1 and R2 files to generate two fastq files per pool containing all the information. To interleave the fastq files, the BBmap tool bbmap/reformat.sh was used, which can also be used to de-interleave the files.

  Dataset EGAD00001008108

• T-cell reconstitution after reduced dose ATLG induction in kidney transplant patients

  We analyzed the T-cell receptor (TCR) repertoires from ten kidney transplant recipients. Five out of the ten kidney transplant recipients received ATLG while the other five recipients received basiliximab as induction therapy. TCR repertoires of CD4+ and CD8+ positive T-cells were assessed prior to transplantation and within the first month after transplantation as well as at three- and 12-months post-transplant. In addition, the pre-formed alloreactive TCR repertoire for each kidney transplant recipient was identified using mixed lymphocyte reaction and donor reactive T-cells were subjected to TCR beta sequencing. This dataset comprises a total of 106 samples. NGS TCR beta libraries of all samples were sequenced on an Illumina NextSeq 500 and raw sequencing data (in the form of fastq files) as well assembled clonotypes and their counts (in the form of clonotype tables) are provided.

  Dataset EGAD00001008478

• Transcriptome analysis for intrahepatic cholangiocarcinoma

  Intrahepatic cholangiocarcinomas (iCCs) are characterized by their rarity, difficulty in diagnosis, and overall poor prognosis. We performed comprehensive transcriptomic characterization of treatment-naive iCC. Whole transcriptome analyses identified two prognostic subtypes, concordant with previous reports.The findings could assist in patient stratification with iCCs and in developing rational therapeutic strategies.

  Dataset EGAD00001008544

• Assessment of epigenetic variation in human iPS cells-Medip

  n order to progress human induced pluripotent stem cells (hiPSCs) towards the clinic, several outstanding questions must be addressed. It is possible to reprogram different somatic cell types into hiPSCs and from studies in the mouse, it appears that an epigenetic memory of the starting cell type is carried over to hiPSCs. However a comprehensive comparative study of the characteristics of these hiPSCs has been missing from the literature. Importantly studies which aimed to address these aspects of hiPSCs have used cells from different patients. In order to avoid this important confounding variable and to keep the genetic background constant, tissue samples were procured from the patients and reprogrammed to iPS cells. The methylation status of these iPS cells will be compared. Protocol: Primary cell cultures were generated and reprogrammed to iPS cells. DNA was extracted and immunoprecipitated using anti-methyl cytosine and anti-hydroxymethyl cytosine antibodies. 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/

  Dataset EGAD00001000827

• Organoid Derivation Project: WGS (2023-06-22)

  Sequencing of tissue samples and their derived organoids from oesophageal, pancreatic and colorectal cancer patients. . This dataset contains all the data available for this study on 2023-06-22.

  Dataset EGAD00001011090

• Dataset for other_cancer-RNA

  Rare cancer sequencing data of 95 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008847

• Southern African Prostate Cancer Study (SAPCS) Ethnic Disparity

  The cohort (n=130) consists of prostate cancer patients from South Africa (n=123) and Brazil (n=7). For each patient, a pair of blood and tumour samples were collected. The sequencing data was mapped to hg38 reference. Blood BAMs are named with “-B” as suffix and tumour BAMs are named with “-T” as suffix.

  Dataset EGAD00001009067

• The mutational landscape of human somatic and germline cells

  During the course of a lifetime normal human cells accumulate mutations. Here, using multiple samples from the same individuals we compared the mutational landscape in 29 anatomical structures from soma and the germline. Two ubiquitous mutational signatures, SBS1 and SBS5/40, accounted for the majority of acquired mutations in most cell types but their absolute and relative contributions varied substantially. SBS18, potentially reflecting oxidative damage, and several additional signatures attributed to exogenous and endogenous exposures contributed mutations to subsets of cell types. The mutation rate was lowest in spermatogonia, the stem cell from which sperm are generated and from which most genetic variation in the human population is thought to originate. This was due to low rates of ubiquitous mutation processes and may be partially attributable to a low cell division rate of basal spermatogonia. The results provide important insights into how mutational processes affect the soma and germline.

  Dataset EGAD00001006641

• Somatic mutant selection is altered by prior NOTCH1 mutation in ageing esophageal epithelium

  Authors: Charlotte King1, Emilie Abbie1, Joanna C. Fowler1, Irina Abnizova1, Roshan K. Sood1, Swee Hoe Ong1, Michael W. J. Hall1,2, Faye Lynch-Williams3, Benjamin A. Hall4, Philip H. Jones1,2,5 Abstract: In cancer evolution, genome alterations often occur in a specific order, implying selection depends on the prior clonal genotype 1-3. It is unknown if similar constraints operate in normal epithelia. Here, we mapped mutations in normal mid-esophagus of aged UK subjects. Mutant NOTCH1 clones colonized most of the epithelium by age 60 and above 70 tissue was saturated with mutants under strong competitive selection. Mutant TP53 was more strongly selected in donors over 60 years of age. Samples predominantly mutant for NOTCH1 showed increased selection of NOTCH2 mutants and weaker selection of mutant TP53 compared with samples that were mostly NOTCH1 wild type. In mouse esophagus lacking Notch1 we observed strong selection of mutant Notch2 and other genes not selected in wild type esophagus. In normal ageing esophagus, the first driver mutation may change the trajectory of subsequent somatic evolution by altering mutant selection.

  Dataset EGAD00001015257

• CBD-RAW-SC-GEX: 10X Single-Cell Gene Expression

  Raw Illumina sequencing data and CellRanger BAM output files. For further information regarding this dataset, please contact Stephen Sansom at contact@combat.ox.ac.uk.

  Dataset EGAD00001008007