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• Melanoma_TIL_Study_Exomes

  In this study, mutations present in a series of human melanomas (stage IV disease) will be determined, using autologous blood cells to obtain a reference genome. From each of teh samples that are analyzed, tumour-infiltrating T lymphocytes have also been isolated. This offers a unique opportunity to determine which (fraction of) mutations in human cancer leads to epitopes that are recognized by T cells. The resulting information is likely to be of value to understand how T cell activating drugs exert their action.

  Study EGAS00001000216

• Melanoma_Til_Study_RNAseq

  In this study, mutations present in a series of human melanomas (stage IV disease) will be determined, using autologous blood cells to obtain a reference genome. From each of the samples that are analyzed, tumour-infiltrating T lymphocytes have also been isolated. This offers a unique opportunity to determine which (fraction of) mutations in human cancer leads to epitopes that are recognized by T cells. The resulting information is likely to be of value to understand how T cell activating drugs exert their action.

  Study EGAS00001000251

• Identification of Genomic Markers of Cervical Dystonia and Subtypes

  As the third most common movement disorder, dystonias collectively affect more than 2 million people worldwide. Despite their high prevalence, their biological roots are largely unknown. Genetic influences are suggested in familial studies, however, no specific genetic variants are responsible for a significant proportion of identified cases. Previous genome-wide association studies of the dystonias were limited by smaller sample size and lack of coverage of rare variants. In this study, we use a high-throughput genomic approach to effectively investigate relationships between over genome-wide genetic variations and dystonias. We conduct targeted analyses of candidate genes, as well as agnostic searches for any genomic with the dystonias and subtypes in a large sample of dystonia patients available.

  Study phs001803

• Professors Colin Palmer and Ewan Pearson, from University of Dundee, are both members of the Access Group panel for the GoDARTS bioresource, which provided the data for the current study. The current Study used genotypes (EGAD00010000282) generated by the WTCCC2 (EGAS00000000121), on which both Colin and Ewan are also DAC panel members.

  Dac EGAC00001000504

• Glioblastoma stem cell lines WGS data

  WGS data for 20 Glioblastoma stem cell (GSC) lines and matched blood samples. Fastq files are available. For 10 GSC samples and the 10 matched blood samples the reads are on 3 fastq files per sample

  Dataset EGAD00001006488

• Celiac disease case-control North Indian Immunochip dataset

  Illumina Immunochip genotype data for coeliac disease and control samples of North Indian samples origin. Data is in PLINK binary format. Calling algorithm for genotypes is based on GenomeStudio (GenTrain), with manual clustering of selected variants.

  Study EGAS00001000849

• Effect_of_FAM50_knockout_on_the_transcriptome

  A knockout clone has been generated for both FAM50A and FAM50B; knockout of the other gene is then performed and the transcriptome is analysed to look at the effect of dual gene loss.

  Study EGAS00001004836

• Sudden Death in the Young Case Registry

  Knowledge gaps persist about the incidence of and risk factors for sudden death in the young (SDY). The SDY Case Registry is a collaborative effort between the National Institutes of Health, the Centers for Disease Control and Prevention, and the Michigan Public Health Institute. Its goals are to: (1) describe the incidence of SDY in the United States by using population-based surveillance: (2) compile data from SDY cases to create a resource of information and DNA samples for research; (3) encourage standardized approaches to investigation, autopsy, and categorization of SDY cases; (4) develop partnerships between local, state, and federal stakeholders toward a common goal of understanding and preventing SDY; and (5) support families who have lost loved ones to SDY by providing resources on bereavement and medical evaluation of surviving family members. Built on existing Child Death Review programs and as an expansion of the Sudden Unexpected Infant Death Case Registry, the SDY Case Registry achieves its goals by identifying SDY cases, providing guidance to medical examiners/coroners in conducting comprehensive autopsies, evaluating cases through child death review and an advanced review by clinical specialists, and classifying cases according to a standardized algorithm. The SDY Case Registry also includes a process to obtain informed consent from next-of-kin to save DNA for research, banking, and, in some cases, diagnostic genetic testing. The SDY Case Registry will provide valuable incidence data and will enhance understanding of the characteristics of SDY cases to inform the development of targeted prevention efforts. For cases where informed consent has been obtained for research genomic sequencing has been performed. On these cases genomic data, phenotype information and on a limited number of cases redacted autopsy reports will be available through dbGaP.

  Study phs003221

• Localised colon cancer WES study contaning WBCs, tissue and plasma samples at different time points

  Decision-making based on circulating tumor DNA (ctDNA) status following curative-intent surgery in stage II-III colon cancer (CC) is where the strongest clinical evidence lies. Commercial or academic assays are predominantly used to detect ctDNA, aiming to reveal minimal residual disease (MRD) and identify patients at high risk of recurrence. However, while current tests demonstrate exceptional specificity in detecting MRD among patients who later experience recurrence, their sensitivity is notably limited, particularly immediately after surgery when decisions regarding ACT are crucial. Additionally, up to 70% of patients with stage II-III colon cancer fail to clear ctDNA after standard adjuvant treatment (ACT) and subsequently experience recurrence. In this study, we performed whole exome sequencing (WES) of ctDNA at different timepoints in relapsed CC patients using two independent cohorts, alongside transcriptomic and proteomic analyses of metastases to gain a deeper understanding of progression mechanisms. An assay based on a tumor-agnostic approach from WES could enhance sensitivity in detecting MRD disease compared to current assays. Immune evasion appears to be the primary driver of progression in the localized CC setting, facilitated by a functional mutational burden at relapse. This suggests that immunotherapy could extend its efficacy to patients with microsatellite stability, broadening treatment options. Moreover, organoid modeling affirms the promising potential of targeted therapy to surpass conventional treatments in eradicating MRD.

  Study EGAS50000000204

• Perceptions, Prevalence, and Patterns of Cannabis Use among Cancer Patients in NCI-Designated Cancer Centers

  This study aimed to better understand the evolving landscape of cannabis use among patients undergoing cancer treatment across diverse geographic regions. It sought to characterize patterns of use, patient perceptions, and contextual influences such as legal status and provider engagement that affect cannabis use. Given the shifting legal environment, this study addresses a critical gap in the literature by providing data on how cancer patients integrate cannabis into their care. The available delivery methods of cannabis have also undergone dramatic changes and now include edibles, oils, tinctures, topicals, and inhaled forms. State-based policy changes are rapidly changing. Yet research on cannabis use by cancer patients across a variety of geographic settings remains limited. The extent of cannabis use, the perceived and real benefits and risks of use, potential interactions with cancer treatment and other medications, and impact on comorbid conditions are uncertain. Clinicians should be aware of the extent of use in order to assess potential drug-drug interactions, side effects, and contraindications; hence, an understanding of how cancer patients and clinicians engage in discussions about cannabis use is essential. Twelve NCI-designated cancer centers were awarded supplemental funding to conduct surveys assessing cannabis use among recently diagnosed cancer patients. Selected sites were in 8 states with varied legal status for medical and recreational cannabis use at the time of the survey. The 12 cancer centers independently received approval from their institutional review boards (IRB) and collected data from September 2021 to August 2023. Eligible participants were cancer patients or survivors who resided in their respective cancer center's catchment area. Cancer centers were responsible for sampling patients within their catchment area with the goal of 1,000 completed surveys. Ten out of 12 cancer centers drew probability samples of patients from patient lists defining their catchment area with some stratifying the sample in various ways including by cancer type, by sex, by race/ethnicity or by a combination of demographic variables.

  Study phs004046

• There are 66 pairs of LAML cases(complete genomics) in this project which belongs to LAML-CN.The library is constructed by the Completes Genomics protocol.

  There are 66 pairs of LAML cases(complete genomics) in this project which belongs to LAML-CN..The library is constructed by the Completes Genomics protocol.

  Dataset EGAD00001003310

• There are 22 pairs of LAML cases in this project which belongs to LAML-CN. The library is constructed by the Illumina protocol.

  There are 22 pairs of LAML cases in this project which belongs to LAML-CN.The library is constructed by the Illumina protocol.

  Dataset EGAD00001003317

• Programs, Origins, and Immunomodulatory Functions of Myeloid Cells in Gliomas

  Gliomas are challenging malignancies characterized by an immunosuppressive microenvironment filled with myeloid cells, whose roles in immune modulation are not fully understood. In this study, we utilized single-cell RNA sequencing (scRNA-seq) data from 85 primary human glioma tumors, related blood samples, and brain tumor organoid models. We found that nearly all glioma-associated myeloid cells express at least one of four distinct immunomodulatory activity programs. These programs include:1. Scavenger Immunosuppressive Program2. Complement Immunosuppressive Program3. Microglial Inflammatory Program4. Systemic Inflammatory ProgramAll four programs are found in both lower-grade and high-grade gliomas and are expressed across various myeloid cell types, whether derived from blood or resident origins. We validated the remarkable plasticity of myeloid cells by showing that the introduction of peripheral blood monocytes into glioma organoid models can induce the emergence of identities resembling microglia, macrophages, and dendritic cells, as well as all four immunomodulatory programs. Our study provides a valuable resource and a new framework for understanding the role of immunomodulatory myeloid cells in gliomas, laying the groundwork for developing effective immunotherapy strategies for glioma patients.

  Study phs003756

• Impact of Genetic Variation on Response to GO Therapy in COG-AML Trials AAML03P1 and AAML0531

  The 340 de novo Acute Myeloid Leukemia (AML) patients (ages 1 month to 21 years) were enrolled in COG-AAML03P1 (NCT00070174). Everyone received standard chemotherapy regimen of ara-C, daunorubicin and etoposide (ADE) with addition of one 3 mg/m2 dose of Gemtuzumab Ozogamicin (GO) in induction 1 as well as in intensification II phase. The 1022 de novo AML patients (ages 0–30 years) were enrolled in COG-AAML0531 (NCT01407757). They were randomly assigned to receive either the standard ADE regimen (ADE arm, n = 511) or with the addition of one 3 mg/m2 dose of GO, during induction I as well as intensification II phase (ADE+GO arm, n = 511). Detailed study design, treatment regimen, and clinical outcomes of these two trials have been previously published (Cooper TM, Franklin J, Gerbing RB, et al., PMID:21766293 and Gamis AS, Alonzo TA, Meshinchi S, et al., PMID:25092781). The current study used genomic DNA from 1,225 pediatric patients treated in these two trials with 470 patients treated with standard chemotherapy in COG-AAML0531 (ADE arm) and 755 patients treated with addition of GO to standard therapy in COG-AAML03P1 and COG-AAML0531 trials (ADE+GO arm). The 132 SNPs in 42 genes within DNA-damage repair (DDR) pathways or genes implicated in mediating calicheamicin were selected for genotyping. These SNPs were genotyped using the Sequenom platform at the Biomedical Genomics Center, University of Minnesota. All SNPs had a call rate of more than 0.98 and were in accordance with the Hardy–Weinberg equilibrium. These genotypes were used to test for association with clinical endpoints as defined in the COG-AAML03P1 and COG-AAML0531 trials.

  Study phs003490

• Genetic Basis of Cryptorchidism

  Non-syndromic cryptorchidism is a common malformation, but the genetic loci that increase susceptibility to cryptorchidism remain unknown. A genome-wide association study (GWAS) was completed to determine whether common allelic variants are associated with susceptibility to cryptorchidism. Two sets of discovery groups were genotyped. Group 1 (559 cases and 1772 controls) was genotyped with HumanHap550v1.0, HumanHap550v3.0 or Human610-quad v1.0. Group 2 (353 cases and 1149 controls) was genotyped with HumanOmniExpress-12v1 or HumanOmniExpress-12v1-1. The sample and marker QCs were performed separately using PLINK (v1.07; http://pngu.mgh.harvard.edu/purcell/plink/) and logistic regression analyses were performed with first and second multidimensional scaling (MDS) components as covariates.

  Study phs000986

• Multi-Ethnic Study of Atherosclerosis (Echocardiogram Image Repository)

  The Multi-Ethnic Study of Atherosclerosis (MESA) is a study of the characteristics of subclinical cardiovascular disease (disease detected non-invasively before it has produced clinical signs and symptoms) and the risk factors that predict progression to clinically overt cardiovascular disease or progression of the subclinical disease. MESA researchers study a diverse, population-based sample of 6,814 asymptomatic men and women aged 45-84. Thirty-eight percent of the recruited participants are white, 28 percent African-American, 22 percent Hispanic, and 12 percent Asian, predominantly of Chinese descent. Echocardiogram Image Repository includes Echocardiogram Images performed during MESA Exam 6 conducted between 2016 and 2018.

  Study phs003702

• Integration of Clinical and Molecular Biomarkers for Melanoma Survival (Berwick)

  The long-term goal of the InterMEL Program Project: Integration of Clinical and Molecular Biomarkers for Melanoma Survival is to identify molecular and clinical factors that predict survival of melanoma patients. Our overarching hypothesis is that we can identify factors in the primary melanoma tumor that will lead to more aggressive disease. Melanoma patients diagnosed at American Joint Committee on Cancer (AJCC) tumor, lymph nodes, and metastases (TNM) stages IIA/IIB/IIC/IIIA/IIIB/IIIC/IIID display highly variable clinical outcomes and responses to therapy. We wish to identify robust and reproducible biomarkers or sets of classifiers that distinguish patients likely to have poor prognosis. These biomarkers will help establish targets for adjuvant therapies for this set of patients before the tumors metastasize. Aim 1. Classify actionable somatic mutations, and copy number variations (CNVs) in relationship to melanoma survival. In Project 1, Targeted Sequencing and Clinicopathology to Evaluate Primary Melanoma Molecular Subtypes and Outcomes, we will profile 468 genes using the MSKIMPACT ™ assay and identify somatic mutations and CNVs associated with melanoma-specific survival, as well as their co-occurrence with other mutations, in 1,000 tumors from patients at AJCC TNM stages IIA-IIID: approximately 500 from patients who died with melanoma within five years and approximately 500 from individuals who have lived at least five years. We will also evaluate the joint effects of somatic mutations, CNVs and pathologic characteristics associated with good and poor outcomes. Aim 2. Identify primary melanoma DNA methylation profiles to evaluate subtypes and survival. Although it has been established that melanomas frequently have aberrant DNA methylation, it is unknown if DNA methylation in primary melanomas predicts outcome. In Project 2, Primary Melanoma DNA Methylation Profiling for Evaluating Subtypes and Survival, we will profile the same primary melanomas as in Project 1 with Illumina Infinium 850K methylation arrays. We expect to: identify and characterize DNA methylation-based melanoma subclasses; train, test and validate a CpG signature prognostic for survival from melanoma; determine whether this profile adds information to outcome prediction beyond AJCC TNM staging. This project is based on the hypothesis that DNA methylation in primary melanoma will define subgroups (including a poor-prognosis CIMP – ‘CpG island methylator phenotype' subtype) and that a CpG signature will be prognostic for melanoma survival. Aim 3. Define microRNA expression changes in relation to melanoma survival. MicroRNAs have been associated with poor prognosis in melanoma, as well as in other cancers. In Project 3, Prognostic and Functional Role of a Gene Expression Signature in Melanoma Patients, we hypothesize that altered miRNA expression, captured at the time of diagnosis, may contribute to the aggressive behavior of a subset of early stage primary melanomas. We will profile the same primary melanomas as in Projects 1 and 2 with a Nanostring assay. This project will define and validate a tissue-based microRNA signature in conducted to determine whether the prognostic miRNA signature, as well as other candidate genes emerging from other projects, contribute to melanoma survival. Aim 4. Integrate data from multiple platforms to identify melanoma subtypes and survival. Despite substantial literature on gene tumor mutation-, methylation- and gene expression-based prognostic and predictive signatures for melanoma, few such signatures are used in clinical practice. Project 4, Multiplatform Analysis of Melanoma Molecular Subtypes and Patient Survival Outcome, will use novel integrative clustering methods to identify molecular subtypes of melanoma jointly defined across these platforms.

  Study phs003099

• Rare SNPs in receptor tyrosine kinases are negative outcome predictors in multiple myeloma

  Multiple myeloma (MM) is a plasma cell disorder that is characterized by a great genetic heterogeneity. Recent next generation sequencing studies revealed an accumulation of tumor-associated mutations in receptor tyrosine kinases (RTKs) which may also contribute to the activation of survival pathways in MM. To investigate the clinical role of RTK-mutations in MM, we deep-sequenced the coding DNA-sequence of EGFR, EPHA2, ERBB3, IGF1R, NTRK1 and NTRK2 which were previously found to be mutated in MM, in 75 uniformly treated MM patients of the "Deutsche Studiengruppe Multiples Myelom". Subsequently, we correlated the detected mutations with common cytogenetic alterations and clinical parameters. We identified 11 novel non-synonymous SNVs or rare patient-specific SNPs, not listed in the SNP databases 1000 genomes and dbSNP, in 10 primary MM cases. The mutations predominantly affected the tyrosine-kinase and ligand-binding domains and no correlation with cytogenetic parameters was found. Interestingly, however, patients with RTK-mutations, specifically those with rare patient-specific SNPs, showed a significant lower overall, event-free and progression-free survival. This indicates that RTK SNVs and rare patient-specific RTK SNPs are of prognostic relevance and suggests that MM patients with RTK-mutations could potentially profit from treatment with RTK-inhibitors.

  Study EGAS00001001665

• SCANDARE HNSCC 3' Tag RNA-seq

  SCANDARE (NCT03017573) is a multicentric biobanking study, enrolling adult patients with newly diagnosed head and neck squamous cell carcinoma (HNSCC), triple negative breast cancer (TNBC), ovarian and cervical cancer. Tumor tissue and blood samples are collected at several time points during patient's journey, including at diagnosis, post-neoadjuvant chemotherapy in case of neoadjuvant treatment, at surgery, at recurrence and at disease progression following treatment initiated at recurrence. Since its launch in 2017 at Institut Curie, SCANDARE has enabled the longitudinal collection and preservation of samples for in-depth analyses. Here, we describe molecular alterations in 264 FFPE samples at baseline from 90 HNSCC patients using 3'-tag RNA-seq technology, with FASTQ files deposited in the dataset.

  Dataset EGAD50000001655

• Emirati Genome Project Population Variome (MAF Table)

  The Emirati Genome Project (EGP) Variome comprises allele frequency data derived from 43,608 individuals sequenced as part of the national genome program in the United Arab Emirates. Samples were processed at the M42 EGP Facility and sequenced to a minimum of 30x coverage using Illumina NovaSeq 6000 short-read technology. Variant calling and alignment were performed using the DRAGEN pipeline (v3.9) against the GRCh38 reference genome. This dataset contains a total of 421,605,069 short variants (SNVs and indels), stored in VCF format. Each variant is annotated with population-level metrics in the INFO field, including: AC (alternate allele count) AF (alternate allele frequency) RC (reference allele count) RF (reference allele frequency) For convenience, VCF files are split by chromosome (chr1–22, X, Y), compressed and indexed using bgzip and tabix.

  Dataset EGAD50000001558

• RNA-Seq of human longitudinal whole blood samples from PCR-positive and PCR-negative recent household contacts of COVID-19 index cases.

  Little is known about the transcriptomic profile of individuals who are exposed to SARS-CoV-2 yet resist becoming PCR positive. To investigate this, longitudinal whole-blood samples were taken (0, 7, 14, and 28 days after enrolment) from PCR positive and PCR negative SARS-CoV-2-naïve household contacts who were recently exposed to a COVID-19 index. Samples were also taken from pre- and post-pandemic unexposed controls. Total RNA was extracted from PAXgene tubes before undergoing poly(A) selection followed by globin and rRNA depletion. DNA libraries were constructed using the NEBNext® Ultra™ II Directional RNA Library Prep Kit for Illumina. All samples were then sequenced across 2 flowcells of an Illumina HiSeq 4000.

  Dataset EGAD50000000684

• untargeted whole genome sequencing - Evaluation and correction of GC biases in cell-free DNA at the fragment level

  These are aligned paired-end reads from Illumina NovaSeq 6000 whole-genome sequencing of 4 cfDNA samples extracted from blood plasma (plasma-Seq). Three samples from patients with breast cancer, prostate cancer, or colorectal cancer and one sample from a healthy individual were aligned to GRCh38 (GCA_000001405.15_GRCh38_no_alt_plus_hs38d1_analysis_set). The observed GC bias is different in each of these cfDNA samples which leads to different average GC content per sample. This bias is corrected using the GCparagon commandline tool.

  Dataset EGAD00001010100

• Tracking the evolution of esophageal squamous cell carcinoma under dynamic immune selection by multi-omics sequencing

  Intratumoral heterogeneity (ITH) has been linked to decreased efficacy of clinical treatments. However, although genomic ITH has been characterized in genetic, transcriptomic and epigenetic alterations are hallmarks of esophageal squamous cell carcinoma (ESCC), the extent to which these are heterogeneous in ESCC has not been explored in a unified framework. Further, the extent to which tumor-infiltrated T lymphocytes (TILs) are directed against cancer cells, but how the immune infiltration acts as a selective force to shape the clonal evolution of ESCC is unclear. In this study, we perform multi-omic sequencing on 186 samples from 36 primary ESCC patients. Through multi-omics analyses, it is discovered that genomic, epigenomic, and transcriptomic ITH are underpinned by ongoing chromosomal instability. Based on the RNA-seq data, we observe diverse levels of immune infiltrate across different tumor sites from the same tumor. We reveal genetic mechanisms of neoantigen evasion under distinct selection pressure from the diverse immune microenvironment. Overall, our work offers an avenue of dissecting the complex contribution of the multi-omics level to the ITH in ESCC and thereby enhances the development of clinical therapy.

  Dataset EGAD00001009482

• Nimblegen

  The aim of this project is to identify rare variants in the 1q region associated with type 2 diabetes. To this end 651 case samples and 651 control samples from six populations have been pooled (pool sizes range from 27-33 individuals), and are being sequenced. The hybridization solution being used captures the exons and UTRs of genes in the 1q region.

  Dataset EGAD00001000424

• Tubulointerstitial fibrosis is the histological hallmark of chronic kidney disease (CKD). Hypoxia and inflammation (i.e., interleukin (IL)-1β signalling) are independent mediators of tubulointerstitial fibrosis. However, the physiological response of human kidney tubular cells to IL-1β/IL-1RI signalling under the hypoxic conditions of CKD is poorly understood and remains a clinical imperative for therapeutic targeting. This study reports that hypoxia and IL-1β act in synergy to trigger cell cycle arrest/cellular senescence of ex vivo patient-derived primary proximal tubular epithelial cells (PTECs).

  Hypoxia and interleukin (IL)-1β are independent mediators of tubulointerstitial fibrosis, the histological hallmark of chronic kidney disease (CKD). Here, we examine how hypoxia and IL-1β act in synergy to augment maladaptive proximal tubular epithelial cell (PTEC) repair in human CKD. Ex vivo patient-derived PTECs were cultured under normoxic (21% O2) or hypoxic (1% O2) conditions in the absence or presence of IL-1β and examined for maladaptive repair signatures. Hypoxic PTECs incubated with IL-1β displayed a discrete transcriptomic profile distinct from PTECs cultured under hypoxia alone, IL-1β alone or under normoxia. Hypoxia+IL-1β-treated PTECs had 692 ‘unique’ differentially expressed genes (DEGs) compared to normoxic PTECs, with ‘cell cycle’ the most significantly enriched KEGG pathway based on ‘unique’ down-regulated DEGs (including CCNA2, CCNB1 and CCNB2). Hypoxia+IL-1β-treated PTECs displayed signatures of cellular senescence, with reduced proliferation, G2/M cell cycle arrest, elevated senescence-associated β-galactosidase (SA-β-gal) activity and increased production of pro-inflammatory/fibrotic senescence-associated secretory phenotype (SASP) factors compared to normoxic conditions. Treatment of Hypoxia+IL-1β-treated PTECs with either a senolytic drug combination, quercetin+dasatinib, or a type I IL-1 receptor (IL-1RI) neutralizing antibody attenuated senescent cell burden. Our data identify a mechanism whereby hypoxia in combination with IL-1β/IL-1RI signalling trigger PTEC senescence, providing novel therapeutic and diagnostic check-points for restoring tubular regeneration in human CKD.

  Study EGAS00001007904