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• Indonesian Genome Diversity Project 3

  Term and condition for Indonesian Diversity Project v3. 254 Low Coverage genome from Wallacean and West Papuan, Indonesia

  Dac EGAC50000000312

• DAC for Hematological toxicity following CAR-T cells injection

  Data access committee to have access to Hematological toxicity following CAR-T cells injection

  Dac EGAC50000000490

• Cardiac fibroblast DAC

  DAC for reviewing requests to access data on cardiac fibroblasts as described by Aguado-Alvaro et al (Nature Communications, 2025)

  Dac EGAC50000000479

• BCR-HGBCL-DH-BCL2 project DAC

  Data Access Committee for high-grade B cell lymphomas MYC-BCL2 datasets

  Dac EGAC50000000500

• Small Intestine Adenocarcinoma Subtyping Data Access Committee

  DAC created for the Molecular classification of small intestinal adenocarcinomas Study in Amsterdam UMC.

  Dac EGAC50000000663

• Genome-wide DNA Methylation Analysis Reveals a Unique Methylation Pattern for Pleural Mesothelioma Compared to Healthy Pleura and Other Lung Diseases

  Study EGAS00001007783

• Exome sequencing VCF files for glioma progression

  Exome sequencing VCF files describing mutations during glioma progression.

  Dataset EGAD00001001887

• Whole genome sequencing data of ccRCCs

  Whole genome sequencing data of ccRCCs were utilized for somatic variations calling.

  Dataset EGAD00001004588

• RNAseq data

  RNAseq data for 10 patients: 10 tumors and 10 cell lines

  Dataset EGAD00001002691

• Brain mets discovery cohort variant calls

  These are the variant calls for the 50 brain tumour samples in the discovery cohort.

  Dataset EGAD00001005982

• Biomarker Data Subset

  This dataset contains data for CBC counts and absolute protein abundance measurements from ELISA experiments.

  Dataset EGAD00001011163

• Phylogenetic reconstruction of breast cancer

  This dataset contains the fastq files used for this study

  Dataset EGAD00001006121

• Genetic Progression of Head and Neck Squamous Cell Carcinoma

  These data are tumor/normal-matched exome sequencing results on 45 participants (median age of 58.6 years) treated for squamous cell carcinoma of the oropharynx at Mass Eye and Ear (MEE; Boston, MA, USA). Some tumors had two portions sequenced separately. All research complied with all relevant ethical regulations. Human subject research on patients at MEE was approved by the MEE Human Studies Committee under protocol HSC 11-024H, with informed consent obtained from participants. Participants were not compensated. Clinical data, including HPV status, were abstracted from patient records. Sequencing and clinical data were combined with TCGA data on 486 cases of head and neck squamous cell carcinoma (HNSCC). The PhylogicNDT suite of genomic analysis tools was used to infer the relative timing of genetic events during tumor progression for major molecularly defined classes of HNSCC: HNSCC negative for human papillomavirus (HPV), HPV-associated HNSCC, and HPV-negative HNSCC involving mutations in CASP8, NSD1, and NOTCH1. The timing of the development of whole-genome somatic events leading to tetraploidy or triploidy and to increased measures of intratumor genetic heterogeneity was determined. Associations of heterogeneity measures with clinical outcomes were assessed. The analysis identified genes with early mutations that likely play roles in HPV-tumor initiation (FBXW7, NOTCH1, CASP8, FAT1, NSD1, HRAS, EP300, CREBBP, KMT2D). Genes with mutations at later median relative timing (PK3CA, NFE2L2, HLA-A, SPEN, and KMT2C) were more likely to be important for progressing to later stages of the disease. Gain of chromosome arm 3q and loss of arm 11q were found to occur more frequent in HPV+ HNSCC cases. A high prevalence of 3p and 17p loss were also observed in HPV+ HNSCC cases.

  Study phs003139

• Identifying Novel Small RNA Biomarkers Unique to Patients with Gastric Cancer

  The biomarker development study consisted of two parts: discovery and validation. The first part was the discovery and verification phase of biomarkers using two different platforms: transcriptomic and miRNA. The salivary transcriptomes of 63 GC samples and 31 non-GC controls were profiled using Affymetrix HG U133+2.0 microarrays (Affymetrix, Santa Clara, CA). The identified exRNA candidates were verified by quantitative real-time PCR (RT-qPCR) using all 94 of the original samples. In the discovery phase for the miRNA biomarkers, 10 early-stage GC samples and 10 non-GC controls were selected. The salivary miRNAs of these samples (n=20) were profiled using the TaqMan MicroRNA Array (Applied Biosystems, Foster City, CA). MicroRNA candidates were verified using TaqMan miRNA Assay (Thermo Scientific, Grand Island, NY). The second part of the study was to validate these verified exRNA biomarker candidates with exRNA samples extracted from an independent cohort of 100 GC and 100 non-GC saliva samples. The cohort was not balanced for demographics on gender and smoking history but more accurately reflected the diagnostic setting where our proposed final model could be implemented. Reprinted from "Li F, Yoshizawa MJ, Kim K, Kanjanapangka J, Grogan T, Wang X, Elashoff D, Ishikawa S, Chia D, Liao W, Akin D, Yan X, Lee M, Choi R, Kim S, Kang S, Bae J, Sohn T, Lee J, Choi M, Min B, Lee J, Kim J, Kim Y, Kim S, Wong D. (2018) Development and Validation of Salivary Extracellular RNA Biomarkers for Noninvasive Detection of Gastric Cancer. Clin Chem. PMID: 30097497 DOI: 10.1373/clinchem.2018.290569", with permission from American Association for Clinical Chemistry (United States).

  Study phs001767

• The Role of Germline Mutation and Parental Age in Autism Spectrum Disorders

  <p>We will apply whole genome sequencing of trio families to determine how patterns of germline mutation throughout the genome determine risk for Autism Spectrum Disorder (ASD). We will investigate the nature intrinsic hypermutability and the extrinsic forces, such as paternal age, that influence rates of germline mutation. We will accomplish these goals through the following specific aims: Specific Aim 1 will characterize germline de novo mutations (DNMs) by whole genome sequencing in families. These studies will identify and validate ~8,000 de novo point mutations and structural variants in trios and controls to determine the parent of origin of DNMs. Specific Aim 2 will identify hot spots for germline mutation based on the regional density of DNMs in the genome, and determine the effects of DNA sequence features on rates of mutation. We will determine the association of mutation hotspots with ASD in the discovery sample and in genomic datasets from an independent sample of 2700 cases and 2700 controls. Specific Aim 3 will characterize the effects of extrinsic factors, including parental age and environment, on genome-wide rates of mutation. We will quantify the effect of paternal age on pathogenic and neutral alleles in sperm and investigate whether some DNMs confer a germline selective advantage. The findings of this study will provide fundamental insights into the genetic basis of autism risk and the genetic mechanism of the observed parental age effects in ASD. We will identify genes that confer significant risk for autism, and we will determine how intrinsic properties of the genome interact with extrinsic forces to determining risk for disease in offspring.

  Study phs001164

• A Missense SNP in the Tumor Suppressor SETD2 Reduces H3K36me3 and Mitotic Spindle Integrity in Drosophila

  While examining DNA from renal cell carcinoma (RCC) patients we observed a single nucleotide polymorphism (SNP; rs58906143,chr3:47163422 C→G (hg19); E902Q*) within SETD2 that was overrepresented in kidney cancer patients compared to control patients. This original study utilized directed sequencing of 14 genes. In an expanded study using a Taqman assay to study the specific SNP, a G allele was found in 72/493 cases (14.6%) and 24/356 (6.7%) controls. Analysis by ancestry revealed that there was there was a G allele in 50/119 (42.0%) cases and 21/71 (29.6%) controls in patients with African Ancestry while there was a G allele in 19/335 cases (5.7%) and 3/269 (1.1%) controls in patients with European Ancestry. These differences did not reach statistical significance. Concurrently, we studied the functional effect of this SNP in a Drosophila model. The homologous amino acid substitution at E741Q reduces H3K36me3 levels which could be rescued by wild type Set2. Additionally, the mutation resulted in significant defects in spindle morphogenesis, consistent with a role for SETD2 in alpha-tubulin methylation during mitosis. Data available through dbGAP include the 14 gene sequence files of 52 control and 128 RCC patients, the results of Taqman SNP (rs58906143) analysis in text files for 221 controls and 357 RCC patients, and compiled phenotype data including age and assigned race. Due to data use limitations, genotyping data for 8 RCC patients and 83 controls as well as GWAS data for ancestry determination will not be available on dbGaP, but will be made available on request.

  Study phs003474

• Clinical and Molecular Features of Acquired Resistance to Immunotherapy in Non-Small Cell Lung Cancer

  PD-(L)1 blockade has been shown to promote durable responses in non-small cell lung cancer (NSCLC) patients and has been rapidly incorporated into the treatment regimens for many with advanced disease. Despite this, mechanisms of acquired resistance (AR) to PD-(L)1 have not been well understood. To address the clinical and molecular landscape of AR to PD-(L)1 blockade in NSCLC patients, a large clinical cohort of AR to PD-(L)1 blockade in lung cancer was examined. In conjunction, a systematic genomic and transcriptomic analysis in a subset of patients (n = 29) with available tissue samples was conducted. To investigate the molecular mechanisms of AR to PD-1 blockade from pre- and/or post-treatment tumors, microarray-based whole transcriptome expression data for 29 tumor samples, and whole exome sequencing (WES) data from 34 tumor samples was generated from this subset. Microarray data was uploaded to the Gene Expression Omnibus (GEO) database. Most AR tumors showed retained or increased inflammatory characteristics with significant upregulation of IFNγ which was suggestive of persistent albeit insufficient anti-tumor immune response. This finding expounds upon the prior pre-clinical and translational data supporting the intricate role of IFNγ in sensitivity and resistance to immunotherapy. Whereas initial IFNγ exposure may be fundamental to T cell activation (a hallmark of immune response), persistent IFNγ related effects and upregulation may potentially signal immune dysfunction and IFNγ insensitivity in contrast. The inflammatory phenotypes identified have implications for future rational development of new immunotherapy strategies for patients with AR.

  Study phs002834

• Puerto Rico Heart Health Program (PRHHP-BioLINCC)

  Data Access NOTE: Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: To investigate morbidity and mortality from Coronary Heart Disease (CHD) in Puerto Rican rural and urban men. The objectives of the study were: (1) to identify factors related to the development of CHD, (2) compare the etiology of disease in rural versus urban men, and (3) determine the prevalence and incidence of CHD and other cardiovascular diseases in Puerto Rican males.Background: As Puerto Rico became more industrialized in the 1940s and 1950s, mortality rates for CHD increased. Since many factors related to CHD can be relatively homogenous within a population, two contrasting subgroups were selected for study in Puerto Rico: a rural population of men from a mountainous community and an urban population selected from San Juan. The NHLBI initiated the Puerto Rico Heart Health Program in May, 1965 as a prospective study of lifestyle, environmental and biological factors in the progression of cardiovascular disease in Puerto Rican men.Participants: A total of 9,824 (2,976 rural, 6,848 urban) men, age 45 to 64 were examined at the baseline exam.Design: The examination consisted of standardized questionnaires to determine education, occupation, smoking habits, and physical activity. Trained interviewers conducted a nutritional survey through a 24 hour diet recall. Subjects were also examined to determine prevalent cardiovascular, cerebrovascular and peripheral vascular abnormalities. The examination included vital capacity, a 12-lead ECG, and laboratory tests for hematocrit, glucose, serum cholesterol, serum glycercides and lipoprotein electrophoresis. A medical history was also obtained. Three additional exams, approximately three years apart, were conducted and morbidity and mortality follow-up concluded in 1980.

  Study phs003930

• High Frequency Ventilation in Premature Infants (HIFI-BioLINCC)

  Data Access NOTE: Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: To evaluate the hypothesis that high frequency oscillatory ventilation in preterm infants would reduce the incidence of mortality and pulmonary complications compared to conventional mechanical ventilation.Background: With the introduction of mechanical ventilation in preterm infants, mortality and morbidity significantly improved but remained high. The improvement in survival that accompanied the use of mechanical ventilation also brought about an increase in the incidence of pulmonary complications. The principal complication occurs in the form of bronchopulmonary dysplasia. Barotrauma and oxygen toxicity are considered to be in the pathogenesis for this disorder. Considerable interest in high frequency ventilation for preterm infants was generated when animal studies indicated high frequency ventilation to be effective in promoting gas exchange without apparent adverse effects. High Frequency Ventilation (HFV) delivers small tidal volumes at high frequencies of 4 to 15 Hz, and animal studies had indicated that HFV was associated with effective gas exchange, less barotrauma, and lower mean airway pressure. However, the efficacy and safety of HFV in preterm infants had not been studied. The HIFI Planning Phase was initiated in August 1984, and recruitment and intervention began in February, 1986. Follow-up studies continued thru September, 1988.Participants: A total of 673 infants were enrolled.Conclusions: Bronchopulmonary dysplasia incidence was similar in the two groups as was mortality and the need for ventilatory support during the first 28 days. There was a significantly greater rate of pneumoperitoneum of pulmonary origin in the high frequency group as was a greater incidence rate of intracranial hemorrhage. (HIFI Study Group, 1989, PMID: 2643039)

  Study phs004032

• Response to Hepatitis B vaccine

  Approximately 5-10% of individuals, who are vaccinated with a hepatitis B (HB) vaccine designed based on the HBV genotype C, fail to acquire protective levels of antibodies. Host genetic factors behind low immune response to the HB vaccine were investigated by GWAS and HLA association tests. GWAS and HLA association tests were carried out using a total of 1,193 Japanese individuals including 107 low responders (HBsAb ?10 mIU/mL), 351 intermediate responders (10 mIU/mL< HBsAb <100 mIU/mL), and 735 high responders (HBsAb ?100 mIU/mL). Classical HLA class II alleles were statistically imputed using the genome-wide SNP typing data. GWAS identified independent associations of HLA-DRB1-DQB1 haplotypes, HLA-DPB1 alleles and BTNL2 gene with immune response to the HB vaccine designed based on the HBV genotype C. Five HLA-DRB1-DQB1 haplotypes and two DPB1 alleles showed significant associations with response to the HB vaccine in a comparison of three groups of 1,193 HB vaccinated individuals. When frequencies of DRB1-DQB1 haplotypes and DPB1 alleles were compared between low immune responders and HBV patients, significant associations were identified for three DRB1-DQB1 haplotypes, and no association was identified for any of DPB1 alleles. In contrast, no association for DRB1-DQB1 haplotypes and DPB1 alleles was identified in a comparison between high immune responders and healthy individuals. The findings in this study clearly show the importance of HLA-DR-DQ (i.e. recognition of a HB vaccine related HBsAg by specific DR-DQ haplotypes) and BTNL2 molecules (i.e. high immune response to the HB vaccine) for response to a HB vaccine designed based on the HBV genotype C.

  Study JGAS000341

• Spatial transcriptomic data of breast cancer

  Fastq files from spatial transcriptomic of breast cancer coming from 8 Breast cancer sections. Sample preparation: frozen BC samples were chosen based on tissue structure and RNA quality (RIN > 8). The “Visium Spatial Tissue Optimization Slide and Reagent Kit” (10X Genomics; #PN-1000193) was then used to optimize permeabilization conditions for BC tissues. Briefly, sections were fixed, stained and then permeabilized at different time points to capture mRNA, and the reverse transcription was performed to generate fluorescently labeled cDNA. The permeabilization time that resulted in the highest fluorescence signal with the lowest background diffusion was chosen. The best permeabilization time for BC tissue was 18 min. Cryostat sections of 10 μm of thickness were cut and placed on Visium Spatial Gene Expression slides (10X Genomics, PN-1000184). The slide was incubated for 1 min at 37°C, then fixed with methanol for 30 min at -20°C followed by Hematoxylin and Eosin (H&E) staining and images were taken under a high-resolution microscope. After imaging, the coverslip was detached by holding the slide in water and the slide was mounted in a plastic slide cassette. The spatial gene expression process, including tissue permeabilization, second strand synthesis and cDNA amplification, was performed according to the manufacturer’s instructions (10X Genomics; #CG000239). cDNA quality was next assessed using Agilent High sensitivity DNA Kit (Agilent, #5067-4626). The spatial gene libraries were constructed using Visium Spatial Library Construction Kit (10X Genomics, PN-1000184).

  Dataset EGAD50000000322

• Genetic Basis of Pulmonary Non-tuberculous Mycobacterial Infections

  This project aims at characterizing the human host susceptibility to pulmonary non-tuberculous mycobacterial (PNTM) infections. PNTM infections occur in patients with chronic lung disease, but also in a distinct group of elderly women without lung defects but who share a common body morphology: tall and lean with scoliosis, pectus excavatum, and mitral valve prolapse. We performed whole exome and genome sequencing in extended families of patients with active PNTM. This unique collection of familial cohorts in PNTM represents an important opportunity for a high yield search for genes that regulate mucosal immunity. We also sequenced the genome of mycobacterial isolates from PNTM patients to integrate host PNTM susceptibility with mycobacterial genotypes and gain insights into the key factors involved in this devastating disease.

  Study phs000719

• The mutational characterization of adenoid cystic carcinoma

  Adenoid cystic carcinoma (ACC) typically emanate from the major and minor salivary glands of the head and neck. ACCs have high rates of perineural invasion, locoregional recurrence, and distant metastasis. Here we report sequencing of 60 tumor/normal pairs and find substantial mutational diversity. On pathway analysis, a significant percentage of mutations involved chromatin remodeling, DNA damage, protein kinase A signaling, and FGF/IGF/PI3K signaling. Whole genome sequencing and FISH confirmed the MYB-NFIB translocation as the main structural variant in ACC. Evaluation of potential driver mutations KDM6A and PIK3CA reveal that specific, observed alterations impart functional consequences. Collectively, our data delineate the ACC mutational landscape and establish a molecular foundation for investigating new therapies for this disease.

  Study phs000612

• 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

• Natural Genetic Variation in the Human Genome

  In this study, we used existing whole genome sequencing data from the TOPMed Amish and Jackson Heart Study, as well as the GTEx study, to identify mobile element insertions in the genomes of these individuals.&#160; A total of 1112 TOPMed Amish, 3331 TOPMed Jackson Heart Study, and 698 GTEx individuals were examined.&#160; We used the Mobile Element Locator Tool (MELT) developed previously by our lab, along with a Cloud-based version of MELT (CloudMELT), to discover non-reference mobile element insertions (MEIs) in these genomes.&#160; We discovered Alu, L1, SVA, and HERV-K MEIs and produced genotypes in individual genomes.&#160; Build hg19 bams were used for the TOPMed samples, and build GRCh37 bams were used for the GTEx samples in this study.

  Study phs002463