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• Sequencing data for Hepatoblastoma samples

  This dataset contains DNA sequencing data for twelve hepatoblastoma tumor samples, four of which have matched normals. Nine of the samples also have RNA sequencing data from the tumor sample. The dataset comprises six samples from patient tissues and six from cell lines; see metadata for details.

  Dataset EGAD00001006621

• Genome-wide genotype data for 1,433 ni-Vanuatu

  Here, we generated genome-wide genotype data for 1,433 contemporary ni-Vanuatu and assessed their fine-scale genetic structure, in order to address central questions about the settlement of western Remote Oceania.

  Study EGAS00001005910

• Genomic determination for Homologous Recombination Deficiency (HRD) by shallow Whole Genome Sequencing (sWGS)

  Genomic determination for Homologous Recombination Deficiency (HRD) by shallow Whole Genome Sequencing (sWGS) with shallowHRD (PMID : 32315385) on 55 triple-negative breast cancer Patient Derived-Xenograft (PDX) treated with platinum.

  Study EGAS00001005926

• Learning from the thymic human cell atlas for T cell engineering: Paediatric RNA (2025-10-02)

  T cells are central to adaptive immunity and thus crucial for understanding and treating human disease. While extensively studied in model organisms, translating this knowledge to humans can sometimes be limited by their rapid cross-species evolution and diverse . This dataset contains all the data available for this study on 2026-03-10.

  Dataset EGAD00001015720

• Exome and RNA sequencing data for Diffuse Large B Cell Lymphomas

  Exome sequencing data for 1001 DLBCL patients and RNA sequencing data for 775 DLBCL patients

  Dataset EGAD00001003600

• PCR-free shallow whole genome sequencing for chromosomal copy number detection from plasma of cancer patients is an efficient alternative to the conventional PCR-based approach

  Somatic copy number alterations (SCNAs) can be detected in tumor cell-free DNA (cfDNA) by shallow whole genome sequencing (sWGS). Polymerase chain reaction (PCR) is typically included in library preparations, but a PCR-free method could be an effective alternative for research and diagnostics. Peripheral blood samples (n=22) were collected in EDTA-containing tubes from non-small cell lung cancer patients (n=10) and healthy donors (n=12). PCR and PCR-free library preparations underwent sWGS and the following metrics were compared: mapping quality, proportion of duplicate reads, genome coverage, sequencing read length and copy number profiles. The PCR-free method was further evaluated on archived plasma samples (n=33) of varying pre-analytical quality collected in EDTA or lithium heparin tubes. Archived samples were from acute myeloid leukaemia (n=15) and B-cell lymphoma (n=18) patients. The percentage of unique reads was significantly higher for the 22 samples analysed by PCR-free (95.7%) compared to PCR (84%). PCR-free libraries from 33 archived samples produced data of a comparable quality, with 95.4% unique reads. All other evaluated metrics were highly comparable for PCR and PCR-free library preparations. We conclude that SCNA detection can be performed by PCR-free sWGS on cfDNA from cancer patients and is feasible for diagnostic and archival plasma collected in EDTA- or lithium heparin-containing tubes. Our results pave the way for an automated cfDNA workflow for cancer plasma samples.

  Study EGAS00001004692

• NIH Roadmap Epigenomics Program - Broad Institute

  For the NIH Roadmap Epigenomics project, we applied ChlP-Seq, HTBS and WGBS pipelines to generate comprehensive high-resolution maps of chromatin state and DNA methylation for 100 diverse cell types. Cell types were selected for their biological and medical importance, and for their potential to maximize the comprehensiveness of acquired epigenomic data. They include human ES cells, ES-derived cells, mesenchymal stem cells, reprogrammed stem cells and primary tissues. Comprehensive characterization of epigenetic marks ("the epigenome") is a critical step towards a global understanding of the human genome in health and disease. In this study we provide unprecedented views of the human epigenetic landscape and its variation across cell states, which offer fundamental insight into the functions and interrelationships of epigenetic marks, and provide a framework for future studies of normal and diseased epigenomes. The Roadmap Epigenomics Broad cohort is utilized in the following dbGaP sub-study. To view molecular data and derived variables collected in this sub-study, please click on the following sub-study below or in the "Sub-studies" box located on the right hand side of this top-level study page phs000700 the Roadmap Epigenomics Broad cohort. phs000610 RM_Epigenomics_Broad_Alz

  Study phs000700

• Cholesterol and Pharmacogenetics (CAP) Study

  The Cholesterol and Pharmacogenetics Study was a 6-week open label, non-randomized study of 40mg/day simvastatin treatment in 335 black and 609 white (944 total) men and women. Plasma lipids and lipoproteins were measured on two occasions prior to treatment and at 4 and 6 weeks of treatment. The study was designed to test for genetic associations with baseline measurements and changes in response to simvastatin treatment. Whole genome genotyping was performed on 592 white CAP study participants in two stages. In Stage 1, 304 were genotyped for 314,621 SNPs to tag for common genomic variation. In Stage 2, 290 participants were genotyped, including 280 who were genotyped for 620,901 SNPs. Two samples were excluded due to gender discrepancies. More recently, CAP self-reported black participants were genotyped on Illumina Omni2.5Exome chips. PolyA-selected strand-specific RNA-seq libraries were generated in several batches from lymphoblastoid cell lines (LCLs) derived from 268 white and 165 black CAP participants. The LCLs were exposed to sham buffer (control) or 2 uM activated simvastatin for 24 hours, producing a total of 866 100/101 bp paired end RNA-seq libraries sequenced on Illumina HiSeq 2000 machines.

  Study phs000481

• Pharmacogenomics of HIV Therapy - Atazanavir Bilirubin-related Side Effects

  This is an evaluation of genetic associations with atazanavir (ATV) discontinuation for bilirubin-related causes within 12 months of treatment. Patients were treated at an HIV primary care clinic in Nashville TN from 1998 to 2012. A previously known SNP in UGT1A1 (rs887829) was used to define metabolizer genotypes (extensive, intermediate, slow metabolizer). Over 500,000 SNPs from genome-wide genotyping were used to define MDS (Multidimensional Scaling) coordinates to account for population stratification. Patients were defined as cases if they discontinued ATV for bilirubin-related causes within 12 months of treatment, otherwise they were defined as controls if they did not stop treatment. Among 321 evaluable patients, 15 (4.6%) had bilirubin-related atazanavir discontinuation within 12 months. Homozygosity for rs887829 T/T was present in 28.1% of black, 21.4% of Hispanic, and 8.6% of white patients. Among all patients the hazard ratio (HR) for bilirubin-related discontinuation with T/T versus C/C genotype was 7.3 (95% C.I.: 1.7 to 31.5; p = 0.007). Among 152 white patients the HR was 14.4 (95% CI: 2.6 to 78.7; p = 0.002), but among 153 black patients the HR was 0.8 (95% C.I. 0.05 to 12.7; p = 0.87).

  Study phs001484

• Cohort-Based Genome-Wide Association Study of Glioma (GliomaScan)

  We conducted a new independent GWAS of adult glioma using 1,856 cases and 4,955 controls from 14 cohort studies belonging to the Cohort Consortium, 3 case-control studies, and 1 population-based case only study. Cases were newly diagnosed glioma [ICDO-3 codes 9380-9480 or equivalent], and controls were cancer-free at the time of glioma diagnosis. We found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to higher grade tumors being captured in the cohort studies. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.

  Study phs000652