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• Development of a fully human glioblastoma-in-brain-spheroid model for accelerated translational research

  In glioblastoma (GBM) the intricate interplay between tumor cells and the surrounding microenvironment plays a crucial role in tumor progression, invasion, and therapeutic resistance. So far, studying these interactions in a controlled and representative model system has been challenging. Here, we report the development of hGliCS, a human glioma-cortical spheroid model that allows the elucidation of the biology of GBM cells and their interactions with a human-specific brain-like microenvironment and neurons. GBM cells efficiently invade the cortical spheroids, forming a well-connected network of communicating cells. The heterogeneous cellular states of the GBM cells within this model closely resembled findings previously observed in glioblastoma patients and in mouse xenografts. We observed a transition from predominantly mesenchymal-like cells to heterotopic states with a high diversity. In contrast to the substantial changes observed in the tumor cell population, the impact of the GBM cells on the neurons was minimal. We further demonstrate the suitability of hGliCS to test compounds targeting tumor-specific neurobiological features.

  Study EGAS50000000757

• WGS of T-cell and NK-cell lymphoma for ICGC (NKTL-SG)

  Lymphomas are malignancies originating from the lymphatic system and there is a worldwide significant increase in incidences of this cancer. Lymphomas can be further classified into 2 categories namely Hodgkin’s (HL), and Non-Hodgkin’s lymphoma (NHL). The latter can be divided further into B, T and NK cell NHL. Peripheral T-cell lymphoma (PTCL) and Natural Killer/ T-cell lymphoma (NKTL) arise from mature T lymphocytes and NK cells. The more common subtypes include NKTL, PTCL not-otherwise-specified (PTCL-NOS), systemic anaplastic large cell lymphoma (ALCL), follicular PTCL (F-PTCL), angioimmunoblastic T-cell lymphoma (AITL) and enteropathy-associated T-cell lymphoma (EATL). Whole genome analyses on T-cell and NK-cell lymphoma samples from various countries to gain a better understanding of the pathogenesis and biology of these tumors. The comprehensive profiling and comparison among patients from various countries with different etiopathogenesis will hopefully facilitate the elucidation of key pathways and underlying molecular mechanisms driving these cancers, opening up novel therapeutic strategies in the future.

  Study EGAS00001002398

• The cellular immune and airway epithelial profile throughout childhood and in response to COVID-19 at multi-omic single cell level.

  Single-cell data gene expression data set (5’Chromium 10X) of healthy paediatric volunteers, and paediatric and adult COVID-19 patients. Gene expression was determined from samples of nasal, tracheal and bronchial brushings and blood (PBMCs). In addition to gene expression, PBMC’s were assayed by CITE-seq. A subset of samples have VDJ sequencing data for T cell receptors (TCR) and B cell receptors (BCR).

  Dataset EGAD00001007718

• Deep whole genome ctDNA chronology of treatment-resistant prostate cancer

  Circulating tumor DNA (ctDNA) in blood plasma is an emerging tool for clinical cancer genotyping and longitudinal disease monitoring. We performed deep whole-genome sequencing of serial plasma and synchronous metastases in patients with aggressive prostate cancer. We comprehensively assess all classes of genomic alterations and demonstrate that ctDNA harbors multiple dominant populations whose evolutionary histories frequently indicate whole-genome doubling and shifts in mutational processes. Although tissue and ctDNA showed concordant clonally-expanded cancer driver alterations, each individual metastasis contributed only a minor share of total ctDNA. By comparing serial ctDNA before and after clinical progression on potent androgen receptor (AR) pathway inhibitors, we reveal population restructuring converging solely on AR augmentation as the dominant genomic driver of acquired treatment-resistance. Finally we leverage nucleosome footprints in ctDNA to infer mRNA abundance in synchronously biopsied metastases, including treatment-induced changes in AR pathway transcriptional activity.

  Dataset EGAD00001008460

• Dataset for hepatopancreaticobiliary_malignancy-RNA

  Rare cancer sequencing data of 119 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008863

• Genomic Advances in Sepsis (GAinS): RNA-seq

  Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. This cohort comprises a subset of patients enrolled in the Genomic Advances in Sepsis (GAinS) study, an established biobank of adult sepsis patients. Patients with sepsis due to community acquired pneumonia or faecal peritonitis were recruited from 34 hospitals across the UK from 2005-2018, with samples for functional genomics and detailed clinical information collected on the first, third and/or fifth day following ICU admission. RNA was extracted from leukocytes isolated at the bedside using LeukoLOCK kits. We have previously identified sepsis response signatures (SRSs), transcriptomic endotypes that are associated with differential early mortality (Davenport et al, Lancet Respir Med, 2016; Burnham et al, AJRCCM, 2017) and response to treatment in a clinical trial (Antcliffe et al, AJRCCM, 2018). We generated RNA sequencing data on 903 samples, including 134 samples repeated from our previously released microarray data. Libraries were prepared using NEB Ultra II Library Prep kits (Illumina) and sequenced on a NovaSeq 6000. Reads were aligned to the reference genome (GRCh38) using STAR and gene counts quantified using featureCounts (annotation Ensembl v99). Counts were TMM-normalised and log-transformed. Following QC, processed data were available on 864 samples from 667 unique patients.

  Dataset EGAD00001008730

• cell-free DNA Whole Genome Sequencing of 3784 samples on MGI and Illumina platform

  The dataset of Integrative modeling of tumor genomes and epigenomes for enhanced cancer diagnosis by cell-free DNA includes 3784 whole genome sequencing bam files on the MGI and Illumina platform. The analyzed samples include plasma samples from normal individuals and patients with cancer.

  Dataset EGAD00001009335

• Palindromic Amplification of The ERBB2 Oncogene in HER2-Positive Breast Cancer

  DNA Inverted Repeats as an At-risk Motif for Palindromic Gene Amplificatio defines oncogene amplification that is configured as a series of inverted duplications (palindromic gene amplification). There are several, recurrently amplified oncogenes throughout the human genome. However, it remains unclear whether this recurrent amplification is solely a manifestation of increased fitness resulting from random amplification mechanisms, or if genomic locus-specific amplification mechanism plays a role. In this study, we show that the ERBB2 oncogene at 17q12 is susceptible to palindromic gene amplification in HER2-positive breast tumors. We investigated eight tumors in this study, of which five tumors were HER2-positive, and three tumors were HER2-negative. HER2-status was determined by clinical FISH tests. We applied three genomic approaches to investigate the amplification mechanism: (1) copy number analysis by array-CGH on the Affymetrix SNP6.0 platform (8 files), (2) sequencing of DNA libraries enriched with tumor-derived palindromic DNA (Genome-wide Analysis of Palindrome Formation, GAPF-seq) (8 files) and (3) unbiased whole genome sequencing (WGS) (1 file). These molecular data is made available in the dbGaP. Genomic studies using tumor DNA was approved under the Internal Institutional Review Board at the Cleveland Clinic (IRB07-136: EXEMPT: Chromosome Breakage and DNA Palindrome Formation). Specimens were obtained and methods were carried out under the auspices of IRB 7881 (Evaluation of Genetic and Molecular Markers in Patients with Breast Cancer). All patients consented to allow their cancer specimens to be used by researchers in an anonymized fashion. The consent form indicates that publication will take place without identifiers to protect the identity of any specific individual. We observed significant and enrichment of palindromic DNA within amplified ERBB2 genomic segments in four out of five HER2-positive tumors. None of three HER2-negative tumors showed such enrichment. Palindromic DNA was particularly enriched at amplification peaks and boundaries between amplified and normal copy-number regions. Thus, palindromic gene amplification shaped the amplified ERBB2 locus. The moderate enrichment of palindromic DNA throughout the amplified segments leads us to propose that the ERBB2 locus is amplified through a mechanism that repeatedly generates palindromic DNA, such as Breakage-Fusion-Bridge cycles. Our results reveal a potential interaction between local genomic environments and gene amplification mechanisms. This study is published under the title "Palindromic amplification of the ERBB2 oncogene in primary HER2-positive breast tumors" (PMID:28211519).

  Study phs001261

• Genetics of Human Inherited Retinal Diseases (GHIRD)

  The goal of this project is to identify novel mutations and genes involved in human retinal disorders, a stated priority of the National Eye Institute. To accomplish this, additional genes whose mutations cause inherited retinal diseases (IRD) will be identified by combining targeted gene panel sequencing, whole exome sequencing, and whole genome sequencing. We have collected about 1050 patient families around the world. In this proposal, we will identify the underlying mutations in these patients using a combination of targeted gene panel sequencing, whole exome sequencing, whole genome sequencing, bioinformatics, statistics, and functional studies. Genes targeted for gene panel sequencing are: ABCA4; ASIC2; JAG1; ABCC6; ARL3; ATP1B2; BBS1; BBS2; BBS4; OPN1SW; CAPN5; C21orf2; CA4; CACNA1F; CDH3; CHM; ERCC8; CLCN2; CLCN3; CLCN7; TPP1; CLN3; CLN5; CNGB1; CNGA1; CNGA3; COL2A1; COL9A1; COL11A1; CRX; VCAN; CTSD; TIMM8A; DMD; CLN8; ERCC6; EFEMP1; OPN1MW; GNAT1; GNAT2; GNGT1; GRM6; GUCA1A; GUCA1B; GUCY2F; GUCY2D; HARS; CFH; HK1; IDH3B; IMPDH1; IMPG1; KCNJ13; KIF11; LRP5; MAK; MITF; TRPM1; MTTP; MVK; MYO7A; NDP; NEK2; NEUROD1; NPHP1; NRL; OAT; OPA1; OTX2; PAX2; PAX6; PDCL; PCYT1A; PDE6A; PDE6C; PDE6G; PDE6H; PDE6B; PEX1; PEX6; PEX7; PEX10; PEX12; PEX13; PEX14; PFDN5; PGK1; PHYH; PIN1; PLA2G5; PPT1; PRKCZ; PEX19; PEX2; PEX5; RB1; RBP3; RBP4; OPN1LW; RDH5; PRPH2; RGR; RHO; GRK1; RLBP1; ROM1; RP9; RP1; RP2; RPGR; RPE65; RS1; SAG; ATXN7; CCL2; SLC6A6; ELOVL4; TEAD1; NR2F1; TIMP3; NR2E1; TTPA; TUB; TULP1; UCHL3; USH2A; CLRN1; VLDLR; BEST1; WFS1; ALMS1; MKKS; FZD4; OFD1; PEX3; CTSF; GBF1; ADAM9; RGS9; PEX11B; PROM1; UNC119; PRPF4; PRPF3; AIFM1; SLC24A1; LRAT; ASIC3; RAB28; PEX16; ITM2B; SLC4A7; IQCB1; CROCC; IFT140; DHX38; MFN2; NR2E3; USH1C; TOPORS; MERTK; FBLN5; CIB2; PRPF8; SDCCAG8; IFT27; TREX1; RRAS2; CEP164; ATF6; TRIM32; RIMS1; SNRNP200; CLUAP1; EMC1; ZNF423; TTLL5; AGTPBP1; RPGRIP1L; CRB1; TSPAN12; ARL2BP; AIPL1; PRPF6; FSCN2; ABHD12; PRPF31; TCTN3; IFT172; CNNM4; NPHP3; INVS; BBS9; FLVCR1; RDH8; IMPG2; WDPCP; RDH11; TMEM216; TMEM138; LZTFL1; CNGB3; AHI1; MKS1; CLN6; BBS7; POMGNT1; PEX26; SPATA7; KIZ; KLHL7; INPP5E; MDM1; CABP4; RPGRIP1; MCOLN1; CC2D2A; KIAA1549; SLC7A14; WDR19; NYX; CDH23; SEMA4A; MPP5; NMNAT1; TMEM237; PCDH15; C5orf42; GNPTAB; TMEM231; TCTN1; SRD5A3; BBS10; ZNF408; TTC21B; CSPP1; LPCAT1; DHDDS; PDZD7; PANK2; CEP290; OPA3; DNAJC5; PITPNM3; MFRP; HMCN1; ADGRV1; ARL6; FAM161A; TMEM126A; GNPTG; GJA10; RAX2; TUBGCP6; TMEM67; ACBD5; C12orf65; CDHR1; BBIP1; REEP6; CACNA2D4; RP1L1; CEP41; C1QTNF5; NXNL1; TTC8; USH1G; BBS5; ZNF513; RDH12; SLC38A8; C8orf37; VPS13B; NXNL2; BBS12; ADGRA3; LCA5; KCNV2; ADAMTS18; ARL13B; ATOH7; MFSD8; NPHP4; CCDC66; CYP4V2; CRB2; RD3; LRIT3; EYS; KIF7; CERKL; RGS9BP; C2orf71; GDF6; DTHD1; GPR179; CISD2; CCR2; PRCD; WHRN; ADGRA3. The current dbGaP study release makes available all sequencing-derived vcf data of study participants.

  Study phs001517

• CCDG CVD: VIRGO - Variation in Recover-Role of Gender on Outcomes of Young Acute Myocardial Infarction (AMI) Patients

  The VIRGO study is a four year research project funded by the NHLBI to study young women and men with heart attacks. A total of 2,000 women who are 18 - 55 years of age and a smaller comparison group of 1,000 similarly aged men will be enrolled in this multi-site observational study from approximately 120 different hospitals across the country. Young women have a much greater risk of dying after an acute myocardial infarction (AMI) than similarly aged men. Their mortality risk is markedly higher than that of young men, and limited data on young minority women suggest that they may have the highest risk of any young subgroup. Findings from the small number of published studies of young women with ischemic heart disease suggest that the biology, epidemiology, care, and outcomes of this group are distinct from those of men. To date, there have been no large studies of this population, even as the death toll is comparable to that from breast cancer in this country. This study will help researchers identify key factors that influence recovery from a heart attack and potentially improve the care and outcomes of young women and men with AMI. Specific Aims: To investigate the excess risk in young women with AMI and to identify key demographic, clinical, metabolic, psychosocial, health care delivery, and biological determinants of prognosis, we propose a national, prospective, observational study of 2,000 women who are 55 years or younger with AMI and a smaller comparison group of 1,000 men. Our prior work and preliminary studies indicate that the sex differences are most prominent in this age group and suggest that by 1 year after discharge, there are substantial sex differences in outcomes. We will also develop risk stratification tools that will help clinicians to identify young women with the highest and lowest risk. Specific Aim 1: Determine sex differences in outcomes following AMI. Specific Aim 2: Determine sex differences in the prevalence and prognostic importance of demographic, clinical, and psychosocial risk factors. Specific Aim 3:Determine sex differences in quality of care. Specific Aim 4: Determine sex differences in the prevalence and prognostic importance of selected biochemical biomarkers following AMI. These samples have been whole genome sequenced as part of the NHGRI's Center for Common Disease Genetics at the Broad Institute.

  Study phs001259