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• Characterization of the molecular signature of human monocytes in aging and myelodysplastic syndrome

  Deep immunophenotypic profiling of peripheral blood immune cells from young and older control subjects as well as patients with MDS was initially performed, using mass cytometry to identify monocyte subpopulations. Abundance of monocyte subpopulations separated the samples from patients with MDS from elderly control subjects was identified. Therefore, targeted immunophenotyping of monocytes was also performed with flow cytometry and RNA sequencing from isolated CD14+ peripheral blood longitudinally in 26 subjects, six young healthy individuals, nine older healthy individuals and eleven patients with MDS.

  Study EGAS00001007676

• Whole Exome Sequencing of Human Gastro-esophageal Cancer PDXs

  The current study investigates biomarkers of response to anti-EGFR therapies in gastro-esophageal cancer. Whole exome sequencing was performed on 26 tumors to explore potential factors influencing treatment outcomes. As part of the analysis, somatic mutations in EGFR, ERBB2, and key downstream signaling genes (KRAS and PIK3CA) were examined to exclude the presence of known mutations conferring sensitivity/resistance. The study aims to contribute to the identification of patients who may benefit from lower-toxicity regimens, improving treatment personalization and minimizing adverse effects.

  Study EGAS50000000966

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

  RNA-seq analyses were performed on tumor tissue samples of 115 advanced clear cell renal cell carcinoma patients who participated in the NIVOREN GETUG-AFU-26 trial. The samples were obtained prior to treatment initiation. RNA-seq was performed to evaluate previously published gene expression signatures. These included: the IMmotion T effector (CD8A, EOMES, PRF1, IFNG and CD274) and the IMmotion Myeloid (IL-6, CXCL1, CXCL2, CXCL3, CXCL8, and PTGS2) gene signatures represent gene expression patterns associated with T effector cells and myeloid cells, respectively, while JAVELIN Renal 101 Immuno (T-cell receptor signaling: CD3G, CD3E, CD8B, THEMIS, TRAT1, GRAP2, CD247; T-cell activation, proliferation, and differentiation: CD2, CD96, PRF1, CD6, IL7R, ITK, GPR18, EOMES, SIT1, NLRC3; Natural killer cell mediated cytotoxicity: D2, CD96, PRF1, CD244, KLRD1, SH2D1A; Chemokine: CCL5, XCL2; and Other immune response genes: CST7, GFI1, KCNA3, PSTPIP1) represents gene expression patterns associated with both innate and adaptive immune response.

  Dataset EGAD50000001541

• Sequencing data for oesophageal and related samples - ICGC DCC release 26 (WGS)

  WGS sequencing for 303 cases (620 samples) from the ICGC ESAD-UK project Tumours 50x Normals 30x HiSeq X BAM files These samples are all available in ICGC release 26

  Dataset EGAD00001003580

• Wilm's tumor sequencing data

  No. of samples: 80 (28 ULP-WGS, 26 WES, 26 RNA-SEQ) File types: FASTQ (28 ULP-WGS, 19 WES, 18 RNA) and BAM (7 WES, 8 RNA) Technology used: Sequencing - Illumina Novoseq 6000; Map/Align - Illumina DRAGEN v3.7.5; Genome assembly - GrCh38p13 Filename nomenclature: - SampleName_Passage_SampleType_TissueType_SequencingType - Passage of: PX = unknown; PZ = from patient; P0 = first passage from patient on plastic; P1 = first passage from plastic/PDX/organoid - SampleType: STN = normal; STT = tumor - SampleType STN: 00 = tissue unknown; 01 = adjacent normal; 02 = fibroblast; 03 = germline blood; 21 = cell line from patient tissue; 22 = cell line from PDX; 23 = cell line from patient fibroblast - SampleType STT: 00 = tissue unknown; 01 = primary tumor; 21 = cell line from patient; 22 = cell line from PDX - TissueType: WT = Wilm's tumor; 00 = kidney unknown; 01 = kidney left; 02 = kidney right - SequencingType: 00 = unknown; 02 = ultra-low pass whole-genome sequencing; 20 = whole-exome; 61 = bulk RNA-sequencing

  Dataset EGAD00001011111

• International Multi-Center ADHD Genetics Project

  The goal of the project is to complete a 600,000 tag SNP genome-wide association scan of 958 parent-child trios from the International Multisite ADHD Genetics (IMAGE) project, in order to assess the association of SNP markers with ADHD, analyze quantitative ADHD phenotypes, complete copy number analyses, assess parent of origin effects and season of birth effects, and test for epistasis among apparently uncorrelated genes. Acquiring DNA Samples All consent forms stipulate that the samples can only be used by researchers who have been approved by the National Institute of Mental Health (NIMH), National Institutes of Health. All consent forms, except those used at the Zürich site (N=141 subjects), explicitly indicate that the samples may be used by researchers from commercial enterprises seeking to benefit financially from the analysis of the samples. The Zürich consent does not prohibit such use. The Zürich consent form also included an "opt out" that allowed the subjects to indicate that they did not want their samples stored at the NIMH repository or used by researchers external to the project. No subjects enrolled in the project opted out. Consent groups and participant set ADHD (ADHD): 2758 (924 trios)

  Study phs000016

• Trisomy21: Risk Factors for Chromosome Nondisjunction (T21NDJ)

  The overall goal of the project is to identify genetic risk factors associated with chromosome 21 nondisjunction in the oocyte. The dataset derives from multi-site collection of live birth probands with Down syndrome due to standard trisomy 21 (T21) and their biological parents. The type of nondisjunction error (NDJ)(maternal or paternal) in all cases has been determined to be maternal in origin based on the chromosome 21 variants contributed from parent to proband. The Center of Inherited Disease with support from NICHD has conducted genome-wide genotyping using the Illuminia Human OmniExpress Plus Exome array on approximately 800 women who have been identified through their offspring with DS and have been characterized as having a maternal meiois I (MI) or meiosis II (MII) nondisjunction error. Genotypes from biological fathers of the offspring with DS can be used with the data on mothers to better define the type of nondisjunction error (MI or MII) and to refine the chromosome 21 recombination profile. We provide the type of nondisjunction error, knowing that this will be updated based on the new panel. We do not provide the recombination profile, as this can be best defined using the new comprehensive set of SNPs in the OmniExpress panel.

  Study phs000718

• Precision Medicine for Dilated Cardiomyopathy in European and African Ancestry

  The DCM Precision Medicine Study is a multi-site consortium-based cross-sectional study of families with an embedded open-label randomized controlled trial. The aims of the study are to test the hypothesis that dilated cardiomyopathy (DCM) has a substantial genetic basis and to evaluate the effectiveness of a family communication intervention in improving the uptake of preventive screening and surveillance in at-risk first-degree relatives. The Study goal was to recruit 1,300 individuals (600 non-Hispanic African ancestry, 600 non-Hispanic European ancestry, and 100 Hispanic; 50% female) meeting rigorous diagnostic criteria for idiopathic DCM (probands) and 2,600 of their relatives. The probands were inpatients or outpatients identified by heart failure and cardiac transplant cardiovascular physicians and clinical research personnel in heart failure/heart transplant programs at sites in the DCM Consortium. The DCM phenotype was selected for this study because of its prevalence and its prior inclusion in the development of virtually all pharmacotherapy for non-ischemic heart failure from reduced ejection fraction. Study procedures included obtaining family history, cardiac history, medical record review, surveys, and blood sample collection. Exome data from 1219 idiopathic DCM probands and 127 idiopathic DCM relatives are included in dbGaP.

  Study phs002641

• Rapid detection of expanded short tandem repeats in personal genomics using hybrid sequencing.

  Long expansions of short tandem repeats (STRs); i.e., DNA repeats of 2-6 nucleotides, are associated with some genetic diseases. Cost-efficient high throughput sequencing can quickly produce billions of short reads that would be useful for uncovering disease-associated STRs. However, enumerating STRs in short reads remains largely unexplored because of the difficulty in elucidating STRs much longer than 100 bp, the typical length of short reads. We propose ab initio procedures for sensing and locating long STRs promptly by utilizing the frequency distribution of all STRs and paired-end read information. We validated the reproducibility of this method using biological replicates and used it to locate an STR associated with a brain disease (SCA31). Subsequently, we sequenced this STR site in eleven SCA31 samples using SMRT? sequencing (Pacific Biosciences), determined 2.3-3.1 kb sequences at nucleotide resolution, and revealed that (TGGAA)- and (TAAAATAGAA)-repeat expansions determined the instability of the repeat expansions associated with SCA31. Our method could also identify common STRs, (AAAG)- and (AAAAG)-repeat expansions, which are remarkably expanded at four positions in an SCA31 sample. This is the first proposed method for rapidly finding disease-associated long STRs in personal genomes using hybrid sequencing of short and long reads.

  Study JGAS000002

• Quantitative analysis of a novel DNA hypermethylation panel for lung cancer diagnosis using bronchial specimens

  Non-diagnostic findings in Transbronchial Lung Biopsy (TBLB) and Endobronchial Ultrasound-guided Transbronchial Lung Biopsy (EBUS-TBLB) are not uncommon. A challenge is to improve lung cancer detection by TBLB/EBUS-TBLB. In order to improve the diagnostic yield of bronchoscopy, we used 850K methylation chip to identify methylation sites that distinguish malignant from benign lung nodules.We found that the combination of HOXA7, SHOX2,and SCT methylation analysis has the best diagnostic yield in 123 bronchial washing (sensitivity: 74·1%; AUC: 0·851) and 172 brushing samples (sensitivity: 86·1%; AUC: 0·915). We developed a kit comprising these three genes and validated the kit in 329 unique bronchial washing samples, 397 unique brushing samples, and 179 unique patients with both washing and brushing samples. The diagnostic accuracy of the panel alone in lung cancer diagnosis was 86·9%, 91·2% and 95% in bronchial washing, brushing, and washing+brushing samples, respectively. The panel's sensitivity in combination with cytology, rapid on-site evaluation (ROSE), and histology in lung cancer diagnosis was 90·8% and 95.8% in bronchial washing and brushing samples, respectively, and 100% in washing+brushing samples. Quantitative analysis of the three-gene panel improves lung cancer diagnosis by bronchoscopy.

  Study EGAS00001007089