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• Profiling the Microbiome of Pediatric Gut with Metagenomic Short-Read Sequencing

  This dataset contains short-read metagenomic sequencing of stool, as well as intestinal tissue and tissue washes, from preterm infants. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Dataset EGAD00001016052

• RRBS data from TRACERx non-small cell lung cancer (NSCLC) tumours and matched normal adjacent tissue.

  TRACERx (TRAcking Cancer Evolution through therapy (Rx)) is a prospective cohort study designed to investigate intratumor heterogeneity (ITH) in relation to clinical outcome, and to determine the clonal nature of driver events and evolutionary processes in early stage non-small cell lung cancer (NSCLC).

  Dataset EGAD00001015534

• Helleday_HRAS Project

  This experiment is looking at the mutational signatures generated by engineered HRAS mutations by using whole genome sequence generated on massively parallel next generation sequencers.

  Dataset EGAD00001000302

• Isotype-resolved sequencing of B cell receptor in measles virus infection (2017-09-13)

  Isotype-resolved sequencing of B cell receptor in measles virus infection 1) This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute please see http://www.sanger.ac.uk/datasharing/ This dataset contains all the data available for this study on 2017-09-13.

  Dataset EGAD00001003749

• RRBS sequencing data of ovarian cancer, breast cancer, control tissues, and white blood cell DNA.

  The dataset comprises 8 breast cancer, 11 ovarian cancer, 1 benign tumour, 18 normal tissue, 2 endometrium, and 23 white blood cell samples. Genome wide methylation analysis was performed by Reduced Representation Bisulfite Sequencing (RRBS) on Illumina HiSeq 2500. Data is provided as FASTQ files

  Dataset EGAD00001003822

• Whole exome profiling of spatial biopsies of high grade serous epithelial ovarian cancer patients

  This data set is comprised of data from seven distinct high grade serous epithelial ovarian cancer (HGS-EOC) partients, from whom multiple biopsies were taken at the time of surgery, from the ovary and from different locations in the peritoneal cavity. This data set contains 28 samples, sequenced with a whole exome sequencing approach.

  Dataset EGAD00001004154

• RNA-seq data from hypothalamic tissue from individuals with Prader-Willi syndrome and age-matched controls.

  RNA-seq data (bam files) from the hypothalamus of 4 individuals with Prader-Willi syndrome and 4 age-matched control individuals. Detailed information about the study design, case-control matching and RNA-seq data processing is provided in the accompanying publication [Bochukova et al (2018) Cell Reports].

  Dataset EGAD00001004034

• ENGAGE - Amendment "500 genes exon sequencing"

  The ENGAGE project is a FP7 funded EU project aiming to combine genetic and phenotype information from European population based cohorts. In this sub-project we aim to do whole exome sequencing of individuals selected from Health 2000 and FINRISK cohorts. Individuals have been selected based on their metabolic trait phenotypes

  Dataset EGAD00001000403

• 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

• Whole Genome Sequencing of hiPS cells

  Human induced pluripotent stem (hiPS) cells hold great promise for regenerative medicine. Safety issues of use of hiPS cells however remain to be addressed. One of such issues is mutations derived from somatic donor cells and introduced during genome manipulation. We sequence whole genomes of hiPS cells and analyzed mutations. Our study brings hiPS cell technology one step closer to application to regenerative medicine.

  Dataset EGAD00001000362

• Whole genome sequencing

  The diversity and heterogeneity within high-grade serous ovarian cancer (HGSC) is not well understood. We performed whole genome sequencing on primary and metastatic sites from highly clinically annotated HGSC samples. Samples were obtained pre-treatment based on a laparoscopic triage algorithm from patients who underwent R0 tumor debulking, or received neoadjuvant chemotherapy (NACT) with excellent or poor response.

  Dataset EGAD00001005240

• IBD Whole Genome Sequencing (2019-08-14)

  Whole genome sequences at 15X depth of patients with Inflammatory Bowel Disease. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ . This dataset contains all the data available for this study on 2019-08-14.

  Dataset EGAD00001005254

• Predictor_ChemoNEAR_TNBC (2019-08-14)

  In this study a collection of core biopsies from breast cancer patients receiving neoadjuvant chemotherapy as part of the ChemoNEAR trial will be investigated. The study is intended to detect early acquired resistance in women with diagnosed breast carcinoma. Samples will undergo whole genome sequencing and analysis, including use of HR Predict. . This dataset contains all the data available for this study on 2019-08-14.

  Dataset EGAD00001005255

• Sequencing data for personalized therapy design and endotype identification

  Whole exome sequencing of 15 DNA samples, and whole genome sequencing of 2 matched DNA samples. Whole exome sequencing is of RMS samples (both alveolar and embryonal) and from cell lines as well as patient samples. Patient samples are of pediatric RMS patients.

  Dataset EGAD00001005458

• Whole genome sequencing of glioblastoma reveals enrichment of non-coding constraint mutations in known and novel genes

  The dataset comprises of an aggregate level VCF (version 4.1), containing the somatic point and indel mutations found across the glioblastoma cohort (SweGBM-1, n=38 samples). The VCF file is in accordance with the HTS format specifications (https://samtools.github.io/hts-specs/).

  Dataset EGAD00001006084

• Human tumour ChIP-seq.

  We profiled 16 patient tumour samples by ChIP-seq. H3K27ac and Input are provided for 16 samples and H3K27me3 is provided for 14 samples. Among the 16 samples, 9 are G34WT and 7 are G34R/V. The raw fastq or bam files are provided.

  Dataset EGAD00001006100

• Whole exome sequencing of patient derived cell lines

  Whole exome sequencing of 3 patients derived cell lines and patient blood (N = 6 samples), performed using Agillent SureSelect All Exon V5 and Illumina HiSeq 4000. Data is in raw fastq format (N = 10 fastq pairs, 20 files total), as some samples were split between two lanes.

  Dataset EGAD00001007738

• Mucosal RNAseq data

  This is the RNAseq data from mucosal biopsies.

  Dataset EGAD00001008214

• Multiple Myeloma ChipSeq data on six histone modifications

  The data contained in this dataset is ChipSeq BAM files aligned to reference genome hg38. The ChipSeq was based on a combination of six histone modifications as follows: H3K4me1, H3K4me3, H3K9me3, H3K27me3, H3K27Ac and H3K36me3. The samples are patient-derived xenografts generated by passaging primary patient CD138+ selected cells through the SCID-rab myeloma mouse model.

  Dataset EGAD00001008353

• Mixture of 2 (closer mtDNA)

  Mixture of 2 unrelated individuals (of close mtDNA haplogroup) sequenced by 10x as a scRNA-seq. The dataset was then processed by Cell Ranger and deconvoluted to yield each individuals genetic profile. The clustering of SNPs is submitted as the processed file. The Sequencing fastqs are submitted as unprocessed files.

  Dataset EGAD00001008727

• Single-cell RNA sequencing of chronic-phase chronic myeloid leukemia patients

  Single-cell RNA sequencing of viably frozen cells from 12 samples from four chronic-phase chronic myeloid leukemia patients. The raw data is available as fastq files.

  Dataset EGAD00001009086

• Phase II Therapeutic Trial of Mexiletine in Non-Dystrophic Myotonia (IND #77,021)

  Non-dystrophic myotonias are a group of rare muscle disorders caused by abnormalities in different muscle cell membrane proteins. Patients experience delayed muscle relaxation that causes impaired physical activity, stiffness, and pain. Mexiletine has been shown to be beneficial for symptoms of myotonia in case reports of patients with non-dystrophic myotonia, however, current management of these patients primarily depends on individual practitioners' preference. This study is a placebo-controlled, double-blind, cross-over treatment trial using mexiletine in non-dystrophic myotonias. The results, if positive, will permit the identification of mexiletine as an effective therapy for myotonia, making it a first-line therapy for patients with non-dystrophic myotonia. The specific aim of this proposal is to perform a randomized, double-blind, placebo-controlled cross-over study to assess whether mexiletine improves both quantitative and qualitative measures of myotonia in patients with non-dystrophic myotonia. Given the rarity of non-dystrophic myotonia, large randomized controlled treatment trials in these disorders have not been feasible in the past. Primary Outcome Measure: Patient-assessed symptom: stiffness as measured by an Interactive Voice Response Diary (IVR). Secondary Outcome Measures: a) patient-assessed pain, weakness, and fatigue as measured by IVR; b) clinical myotonia assessment; c) quality of life as measured by INQoL, SF36; d) a quantitative measure of grip myotonia; e) measurement of CMAP after short and long exercise; f) grading of myotonia on needle EMG.

  Study phs001311

• Genetics of Disorders Affecting Tooth Structure, Number, Morphology and Eruption

  The long-term objective of this research project is to discover the complete spectrum of genes that contribute to the etiologies of genetic disorders of dentition. Inherited tooth defects can be isolated (the only symptom) or syndromic (having additional symptoms), and can be caused by mutations in many different genes. Clinically, it can be difficult to distinguish among the diverse forms. Making an accurate diagnosis would be greatly improved if reliable tests could identify the specific genetic defect that causes the disease in each case. Current technology can identify the numerous sequence variations throughout a patient's exome, but the disease-causing variation among them cannot be identified unless it is already on the list of genes that potentially cause the disease. A diagnosis based upon the genetic defect that causes the disorder distinguishes between isolated and syndromic tooth defects. A precise diagnosis permits formulation of a more accurate prognosis, which informs treatment decisions. The benefits of accomplishing our aims are to 1) enable genetic testing to achieve a precise and accurate diagnosis, and thereby optimize treatment, and 2) improve our understanding of normal and pathological tooth formation, leading to future improvements in treatment and eventually cures. Our short-term objectives are to 1) recruit kindreds with inherited disorders affecting their dentition, characterize their dental phenotype (and non-dental phenotypes when applicable) and the distribution of the disorder throughout the family, and 2) determine the genetic etiology of their disorders.

  Study phs001491

• National Institute on Alcohol Abuse and Alcoholism (NIAAA) Postmortem Prefrontal Cortex eQTL and mQTL Study

  Mapping expression and methylation quantitative trait loci (eQTLs and mQTLs) using genome-wide genotype, transcriptome, and DNA methylome data can provide an unbiased approach to identify novel functional variants. One critical issue of the eQTL/mQTL analysis is that the role of genetic variants in regulating gene expression (or DNA methylation) can be tissue- or cell-specific. To unravel causal variants from disease-associated loci, it would be necessary to map eQTLs and mQTLs in both patients and controls. Those eQTLs and mQTLs in patients are more likely to be causal variants for the disease. Identification of disease- and tissue-specific eQTLs and mQTLs will help disentangle the role of the specific tissue in disease development as well. In the present study, we mapped eQTLs and mQTLs in postmortem prefrontal cortex of patients with alcoholism or alcohol use disorder (AUD) and matched control subjects by integrative analyses of genome-wide SNP genotype, mRNA transcriptome, and DNA methylome data. As AUD is comorbid with schizophrenia (SCZ), bipolar disorder (BIP), major depressive disorder (MDD), and attention deficit/hyperactivity disorder (ADHD), we further examined the co-localization of PFC eQTLs/mQTLs and GWAS-identified SNPs (mainly noncoding SNPs) that were associated with AUD as well as comorbid SCZ, BIP, MDD, and ADHD. Our study demonstrated the enrichment of PFC eQTLs/mQTLs in the above psychiatric disorder-associated genetic variants identified by genome-wide association studies (GWAS).

  Study phs001981

• A Phase I/II Study of Revlimid (lenalidomide) in Combination with Vidaza (azacitidine) in Patients with Advanced Myelodysplastic Syndrome (MDS)

  This single-arm study design has been selected to investigate the safety of combination therapy with Vidaza® (azacitidine) and Revlimid® (lenalidomide) in a population of 18 participants with advanced MDS for the Phase I portion, and 18 participants for the Phase II portion. The multi-center nature of the study should enhance the general applicability of the results. Participants with advanced MDS were chosen because it is expected that the combination of the two drugs will by myelosuppressive, which can be considered a necessary toxicity to effect improvements in PR and CR rates in this advanced population, akin to participants with AML. Finally, the combination was chosen to be studied because currently available therapies in this population, and their effectiveness, are limited, and single-agent Vidaza® (azacitidine), while effective at delaying transformation to AML or death, is not curative. The doses of Revlimid® (lenalidomide) in this study are similar to those that were demonstrated to have an effect and to be well-tolerated in participants with MDS. Doses for Vidaza® (azacitidine) are similar to those used in the pivotal trial, though for a 5-day treatment period instead of 7 to minimize toxicity for the first 3 blocks of participants, and then at a lower dose over a protracted period of time to explore the safety of a 10-day treatment course.

  Study phs001318