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• WGS Fastq files from the CPC-Gene project in support of PRAD-CA, DCC Release 26

  PRAD-CA, DCC Release 26 : This dataset contains fastq files with Whole genome sequencing data for the CPC-Gene Project. Data from each sample was generated using multiple whole genome libraries and sequenced across multiple runs

  Dataset EGAD00001003706

• Melanoma multi site metastases

  These are caveman, pindel and sequenza calls for the metastatic melanoma exomes within this study.

  Dataset EGAD00001005487

• Low-pass nanopore whole genome sequencing of brain tumors

  Dataset EGAD00001003382

• Normal pancreas cells cohort

  Mixed exocrine and purified ductal and de-differentiated acinar human cells obtained from normal pancreases. Ductal and de-differentiatedacinar cells where isolated by FACS after 4 days culture of the exocrine mixed population

  Dataset EGAD00010002007

• Exome-wide mutation analysis of cell-free DNA to simultaneously monitor the full spectrum of cancer treatment outcomes

  Purpose: Cell-free DNA (cfDNA) offers a non-invasive approach to monitor cancer. Here we develop a method using whole-exome sequencing (WES) of cfDNA for simultaneously monitoring the full spectrum of cancer treatment outcomes, including MRD, recurrence, evolution, and second primary cancers. Experimental Design: Three simulation datasets were generated from 26 cancer patients to benchmark the detection performance of MRD/recurrence and second primary cancers. For further validation, cfDNA samples (n=76) from cancer patients (n=35) with six different cancer types were used for performance validation during various treatments.Results: We present a cfDNA-based cancer monitoring method, named cfTrack. Taking advantage of the broad genome coverage of WES data, cfTrack can sensitively detect MRD and cancer recurrence by integrating signals across known clonal tumor mutations of a patient. In addition, cfTrack detects tumor evolution and second primary cancers by de novo identifying emerging tumor mutations. A series of machine learning and statistical denoising techniques are applied to enhance the detection power. On the simulation data, cfTrack achieved an average AUC of 99% on the validation dataset and 100% on the independent dataset in detecting recurrence in samples with tumor fraction ≥0.05%. In addition, cfTrack yielded an average AUC of 88% in detecting second primary cancers in samples with tumor fraction ≥0.2%. On real data, cfTrack accurately monitors tumor evolution during treatment, which cannot be accomplished by previous methods.Conclusion: Our results demonstrated that cfTrack can sensitively and specifically monitor the full spectrum of cancer treatment outcomes using exome-wide mutation analysis of cfDNA.

  Study EGAS00001005906

• Molecular Genetics of Histiocytic Sarcoma

  This is a comprehensive genomic analysis of a rare set of histiocytic sarcomas from the consult service of the Hematopathology section of the Laboratory of Pathology, NCI, NIH. The study identifies two distinct groupings of these tumors based on the site of disease, their mutational spectrum, and proliferation signature.

  Study phs001748

• Transcriptome of CD4+ T cells and CD8+ T cells in glioblastoma multiforme

  Patients included in this study were over 18 years of age and had a histology-confirmed diagnosis of glioblastoma multiforme (GBM). Exclusion criteria were the previous administration of any anti-tumor therapy including radiation therapy. All patients gave written informed consent. The study was approved by the local ethics committee (TUM Medical school) and conducted following the Declaration of Helsinki. During resection of the tumors, tumor tissue and tissue from normal appearing brain within the operative channel was collected. Blood was drawn during the surgical procedure. Single cell suspensions were prepared from the tumor tissue, the normal appearing brain, and the blood. CD4+ T cells and CD8+ T cells were sorted by flow cytometry. Only patients with a complete set of specimens (CD4+ tumor infiltrating lymphocytes (TIL), CD8+ TIL, CD4+ T cells from normal appearing brain, CD8+ T cells from normal appearing brain, blood-derived CD4+ and CD8+ T cells) containing a minimum of 1000 cells in each sorted sample were further analyzed (n=9). Total RNA was isolated from sorted cell populations using the RNAeasy Plus micro kit (Qiagen, 74034). Quality and integrity of total RNA was controlled on a Bioanalyzer 2100 (Agilent Technologies). Library preparation for bulk-sequencing of poly(A)-RNA was done as described previously (Parekh et al., 2016). Briefly, barcoded cDNA of each sample was generated with a Maxima RT polymerase (ThermoFisher Scientific, EP0742) using oligo-dT primer containing barcodes, unique molecular identifiers (UMIs) and an adaptor. Ends of the cDNAs were extended by a template switch oligo (TSO) and full-length cDNA was amplified with primers binding to the TSO-site and the adaptor. NEB UltraII FS kit was used to fragment cDNA. After end repair and A-tailing, a TruSeq adapter was ligated and 3'-end-fragments were finally amplified using primers with Illumina P5 and P7 overhangs. In comparison to previous descriptions (Parekh et al., 2016), the P5 and P7 sites were exchanged to allow sequencing of the cDNA in read 1 and barcodes and UMIs in read 2 to achieve a better cluster recognition. The library was sequenced on a NextSeq 500 (Illumina) with 59 cycles for the cDNA in read 1 and 16 cycles for the barcodes and UMIs in read 2. Data were processed using the published Drop-seq pipeline (v1.0) to generate sample- and gene-wise UMI tables (Macosko et al., 2015). Reference genome (GRCh38) was used for alignment. Transcript and gene definitions were used according to the Genecode Annotation Version 35.

  Study EGAS50000000156

• De novo metastatic prostate cancer cohort

  Fastq files from RNA sequencing of normal and tumor samples from 16 patients from the de novo metastatic prostate cancer cohort.

  Dataset EGAD50000002381

• 10X Genomics WGS data of de novo assembly individual EGYPT

  10x Genomics linked read data used in variant phasing and de novo assembly scaffolding for the EGYPT individual (mapped against GRCh38).

  Dataset EGAD00001006035

• STAMPEED: Northern Finland Birth Cohort 1966 (NFBC1966)

  The Northern Finland Birth Cohorts program (NFBC) was initiated in the 1960s in the two northernmost provinces of Finland to study risk factors involved in pre-term birth and intrauterine growth retardation, and the consequences of these early adverse events on subsequent morbidity and mortality. The uniqueness of NBFCs is that the data of the cohorts were obtained from early fetal life (including maternal health during pregnancy) to adulthood. The NFBC1966 includes 12,058 live births to mothers in the two northern-most provinces of Finland. Two decades later, a second cohort of 9432 births was obtained (NFBC1986). In NFBC1966 pregnancies were followed prospectively from the first antenatal contact (10-16th week). After birth, the offspring were examined and then again underwent clinical evaluation at ages 1y, 7y, 14-16y and 31y. At each visit, a wide range of phenotypic, lifestyle and demographic data were gathered by questionnaires and clinical examinations. For the most part, NFBC1986 has undergone similar evaluations to NFBC1966. Linkage to national registries includes hospitalization, deaths, education, medication, pensions, and provides up-to-date demographic and clinical information for members of both cohorts. DNA samples were obtained from 5,923 subjects from NFBC1966 and 6688 subjects from NFBC1986. Data coverage, 96% of all births in 1966 and 99% in 1986, is highly representative for the whole population. The NFBC program comprises more than 20 different projects coordinated by the Center of Lifecourse Disease studies in Northern Finland (COLD) at Oulu University. The prospective data collected from the NFBCs form a unique resource, allowing the study of disease emergence, and of the importance of genetic, biological, social and behavioral risk factors. The genome-wide association (GWA) study sponsored through the STAMPEED program of NHLBI employed genomic DNA samples previously collected by the NFBC1966 study and stored in the DNA repository of the National Institute for Health and Welfare, Finland. This NHLBI sponsored RO1 project aimed to identify genetic variants contributing to metabolic and cardiovascular diseases (CVD). In addition to de-identified genome wide genotypic data, a selected list of phenotypic data related to CVD including weight, height, BMI, HDL, LDL, total cholesterol, triglyceride, glucose, insulin and fasting status, are also available in dbGaP. A summary of the GWAS for the NFBC1966 cardiovascular risk traits can be found in Sabatti et al., Nature Genetics 41: 35-46, 2009, PMID: 19060910. The version 2 release of this study contains sequence data from seventeen loci associated with levels of triglyceride, HDL-C, LDL-C, total cholesterol, fasting plasma glucose, and fasting plasma insulin (Kathiresan et al. 2008, Willer et al. 2008, Sabatti et al. 2009, Dupuis et al. 2010, Teslovich et al. 2010). At each locus, protein-coding regions and 5' and 3' untranslated regions of genes nearest to single nucleotide polymorphisms showing genome-wide significant association with metabolic syndrome-related traits, were sequenced. Targeted Illumina sequencing of 78 genes (~270kb) using 150bp probes was performed on 4943 subjects of the Northern Finland Birth Cohort 1966 (NFBC1966). Whole exome sequencing on the Illumina platform was carried out on 586 of those participants. The sequencing study is part of a larger project that is funded by the National Human Genome Research Institute's Allelic Spectrum in Common Disease Initiative, and comprises sequence data from more than 7000 individuals in two Finnish cohorts: NFBC1966 and the Finland-United States Investigation of NIDDM Genetics (FUSION) study.

  Study phs000276

• HGSOC genome-wide SNP (project ITH)

  SNP array genotyping of multi-site HGSOC samples

  Dataset EGAD00010002482

• Melanoma multi site metastases

  These are caveman, pindel, battenberg and brass calls for index patients' metastatic melanoma genomes within this study.

  Dataset EGAD00001005483

• Meningioma Exome

  Meningioma Exome

  Dataset EGAD00001000099

• Patient Microbiome and Surgical Site Infection in Spine Surgery

  Single center, prospective cohort study on the contribution of the preoperative patient microbiome and resistome to surgical site infection (SSI) and resistance to surgical antibiotic prophylaxis in spine surgery. The samples in this entry comprise a subset of patients for whom paired preoperative microbiome samples and postoperative wound culture isolates were obtained. These samples were analyzed by Illumina-based sequencing of metagenomic libraries enriched for the SSI pathogen of interest using the GenCap-Seq methodology (PMID: 36121157) to identify instances of endogenous infection with strains present in the preoperative microbiome.

  Study phs003358

• Joslin Study on the Genetics of Type 2 Diabetes

  Between 1993 and 2003, families were recruited in the Joslin Study on the Genetics of Type 2 Diabetes for the presence of an autosomal dominant mode of inheritance of diabetes. Recruiting and screening of families occurred through probands who were receiving medical care at the Joslin Clinic (Boston, MA). Screening of families included 1) a proband and at least one sibling with type 2 diabetes, 2) diabetes occurring in at least three generations, 3) diabetes inherited on one side of the prospective family. Probands had to have a diabetes diagnosis between the age range from 10 to 60 years. Demographic data, clinical data, and family history were collected from participating family members, along with blood and urine samples. This study includes genetic and phenotypic data from one family examined in Simeone, Wilkerson, et. al. (NPJ Genomic Medicine 2022, PMID: 35869090). Genotype data for 14 family members and whole genome sequencing data for 6 individuals were generated with the goal of identifying a potential genetic cause of disease in this family. To de-identify this family and protect confidentiality, information on sex in phenotype data and variants identified in X, Y, and MT chromosomes have been removed in compliance with IRB guidelines.

  Study phs002959

• RNA-seq of tumor samples from clear cell renal cell carcinoma patients included in the Translational Program of the NIVOREN GETUG-AFU-26 trial

  Study on RNA-seq data from tumor tissue samples of primary tumors of advanced clear cell renal cell carcinoma patients enrolled in the NIVOREN GETUG-AFU-26 trial who consented to and participated in the translational program. The goal of this study was to assess previously published gene expression signatures and evaluate their association with the benefit and/or resistance to nivolumab, as well as their association with circulating soluble factors.

  Study EGAS50000001057

• RNA-seq after drug perturbation of primary lymphoma samples

  3'-end low-depth RNA sequencing data from 108 patients with chronic lymphocytic leukemia and 8 patients with lymphoma. Each primary patient sample was treated in vitro with DMSO as a control and with up to ten small-molecule inhibitors (ibrutinib, duvelisib, everolimus, trametinib, nutlin-3a, I-BET762, MK2206, selinexor, compound 26, and a combination of ibrutinib and compound 26). Sequencing was performed on the Illumina HiSeq4000. The dataset contains FASTQ files.

  Dataset EGAD50000002166

• Metastatic Prostate Follow Up 2

  Validation/deeper sequencing for metastatic prostate cancer samples

  Dataset EGAD00001000989

• Assessment of Complex Chromosomal Changes in De-Identified Cell Lines

  In this study, we obtained DNA from the Coriell Repository from individuals with complex chromosomal changes. The database ("Chromosome Abnormalities") of these de-identified samples contains 1,366 individuals as per https://www.coriell.org/1/NIGMS. We started with 16 individuals in this pilot study that we will hopefully expand out in a potential large NIH grant using information derived in this pilot study. De-identified samples were sequenced using internal funding from Washington University in St. Louis. A description of the sequencing we did on these individuals is provided in our medRxiv preprint at https://www.medrxiv.org/content/10.1101/2025.03.28.25324850v1.

  Study phs004000

• AML Proteogenomic Landscape Whole-transcriptome RNA-Sequencing

  Whole transcriptome RNA-sequencing of purified bone marrow blasts of 136 de novo, treatment naive AML patients. For further details, we refer to the manuscript "The Proteogenomic Landscape of AML" by Jayavelu, Wolf, Buettner et al. mRNA extraction and whole transcriptome sequencing For transcriptome analysis the TruSeq Total Stranded RNA kit was used, starting with 250ng of total RNA, to generate RNA libraries following the manufacturer’s recommendations (Illumina, San Diego, CA, USA). 100bp paired-end reads were sequenced on the NovaSeq 6000 (Illumina) with a median of 57 mio. reads per sample. RNA Data Analysis Data quality control was performed with FastQC v0.11.9. Reads were aligned to the human reference genome (Ensembl GRCh38 release 82) using STAR v2.6.1. Gene count tables were generated while mapping, using Gencode v31 annotations. All downstream analyses were carried out using R v4.0 and BioConductor v3.12 (Huber et al., 2015; R Core Team, 2020). Size-factor based normalization was performed using DESeq2 v1.28.1(Love et al., 2014).

  Dataset EGAD00001008484

• Possible DNA damage after paternal exposure to ionizing radiation in radar technicians

  Effects of accidental and prolonged radiation exposure on the human germline remain a topic of medical interest. Transgenerational signatures of ionizing radiation exposure are primarily implicated to be clustered de-novo mutations (cDNMs, multiple de-novo mutations within 20bp). We sequenced the whole genome of 110 children from 70 families (Radar cohort). The father in this cohort were exposed to 0-353mSv of ionizing radiation and serve as exposed samples.

  Study EGAS00001007321

• Biallelic tumor suppressor loss and DNA repair defects in de novo small cell prostate cancer

  Small cell prostatic carcinoma (SCPC) is an aggressive pathology that is managed similar to small cell lung cancer. SCPC can evolve from prostatic adenocarcinoma in response to androgen deprivation therapy but in rare cases is present at initial cancer diagnosis. The molecular etiology of de novo SCPC is incompletely understood due to the scarcity of tumor tissue and the brief life expectancy of patients. Through a retrospective search of our regional oncology pharmacy database, we identified 18 patients diagnosed with de novo SCPC between 2004 and 2017. Ten patients had pure SCPC pathology and the remainder had some admixed adenocarcinoma foci, but all were treated with first line platinum-based chemotherapy. Median overall survival was 28 months. We performed targeted DNA sequencing, whole exome sequencing and mRNA profiling on formalin-fixed paraffin embedded archival tumor tissue. We observed frequent biallelic deletion and/or mutation of tumor suppressors TP53, RB1 and PTEN, similar to treatment related SCPC. Indeed, at the RNA level pure de novo SCPC closely resembled treatment-related SCPC. However, five patients had biallelic loss of DNA repair genes including BRCA1, BRCA2, ATM and MSH2/6: potentially underlying the high genomic instability of this rare disease variant. Two patients with pure de novo SCPC harbored ETS gene rearrangements to androgen-driven promoters, consistent with evolution of de novo SCPC from an androgen-driven ancestor. Overall, our results reveal a highly aggressive molecular landscape underlies this unusual pathologic variant, and propose opportunities for targeted therapy strategies in a disease with few treatment options.

  Study EGAS00001003007

• Ongoing Replication Stress Tolerance and Clonal T Cell Responses Distinguish Liver and Lung Recurrence and Patient Outcomes in Pancreatic Ductal Adenocarcinoma

  Patients with metastatic pancreatic ductal adenocarcinoma (PDAC) survive longer when disease spreads to the lung but not to the liver. We generated overlapping, multi-omic datasets to identify molecular and cellular features that distinguish patients whose disease develops liver metastasis (liver cohort) from those whose disease progression results in lung metastasis without liver metastases (lung cohort). Lung cohort patients generally survived longer than liver cohort patients, independent of tumor subtype. We developed a pORG gene signature that distinguishes primary tumors in the liver and lung cohorts. We identified ongoing replication stress (RS) response pathways in high pORG/liver cohort tumors, while low pORG/lung cohort tumors had greater densities of lymphocytes and shared T cell clonal responses. Our study demonstrates that liver-avid PDAC is associated with tolerance to ongoing RS, limited tumor immunity, and less favorable outcomes; whereas low RS, lung-avid/liver-averse tumors are associated with active tumor immunity that may account for favorable outcomes. As expected, we found high frequencies of KRAS, TP53, CDKN2A, and SMAD4 gene alterations in our tumor samples. High pORG activity (GSVA scores) in our primary tumors appear to be positively correlated with alteration frequencies in both TP53 and CDKN2A. We did not see a correlation with alterations in KRAS as almost all the tumor samples have KRAS alterations. From a de-identified dataset of 1,873 patients diagnosed with and/or treated for PDAC at our institution between 2004 and 2020, we identified 422 patients for which we had specimens with sequencing data (N=374) and/or specific evidence of disease metastasis site(s) from the OHSU cancer registry or disease-relevant computed tomography (CT) scans to allow cohort classification. Note that our study includes RNA-Seq, DNA-Seq panel, and TCR-Seq (T-cell Receptor Sequencing) data, but that this dbGaP submission just includes the patients/samples with RNA-Seq and/or DNA-Seq panel data. Therefore, this submission includes 290 samples from 278 patients. TCR sequence data is available on the Adaptive Biotechnologies platform. Clinical course timepoints, patient demographics, stage, grade, nodal involvement, resection margins, and angiolymphatic invasion were provided as deidentified data by the OHSU cancer registry with quality control data verification in a subset by pathologists (BB and TM). We reviewed all available computed tomography (CT) scans for all patients with primary tumor resection dates recorded by the cancer registrar, with tumor samples analyzed by RNA-seq, DNA-seq, or TCR-seq, and/or with additional information indicating metastatic spread (e.g., metastatic samples received for related studies). We abstracted the site of all lesions proven to be metastatic by biopsy and/or that clearly increased in size during progression or decreased in size during treatment as long as a radiologist described the lesion as “likely”, “suspicious for”, “concerning for”, or “favor” metastasis. Clinical imaging was reviewed by a radiologist (AG) to validate patient assignments to the liver, lung, and neither liver nor lung (other recurrence site) cohorts. Time to recurrence was calculated from the earliest of either the recurrence date provided by the OHSU cancer registry, or the date of earliest lesion abstracted from CT reports. The subject attributes reported in this submission were up to date at the time of our data freeze, which occurred July 2021.

  Study phs003597

• CPC-GENE Prostate Cancer Heterogeneity Study

  Raw sequence data, fastq format

  Dataset EGAD00001002885

• DAC Admixture histories of São Tomé e Príncipe

  Contacts: Paul Verdu +33144057317 paul.verdu@mnhn.fr CNRS-MNHN-Université de Paris UMR7206 Eco-anthropology Jorge M. Rocha jrocha@cibio.up.pt CIBIO Short description The Data Access Committee for acess to genotype and sample information used in the article "Nested admixture during and after the Trans-Atlantic Slave Trade in the island of Sao Tome" by Ciccarella M et al.2025 ensures that data-access requests comply with the Informed Consent provided by donors, and with ethical and deontological guidelines with respect to privacy. Research sampling protocols followed the Declaration of Helsinki guidelines and written informed consent was obtained from all volunteer participants involved in the sampling in São Tomé e Príncipe. The study of the São Tomé e Príncipe sample was undertaken with the support and permission of the Provincial Government of the Ministry of Health of the Democratic Republic of São Tomé e Príncipe, and the Provincial Government of Príncipe. Research sampling protocols also followed the French laws of scientific research deontology (Loi n° 2016-483 du 20 avril 2016) and were approved by the French ethics committees and CNIL (Declaration n°1972648).

  Dac EGAC50000000437