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• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: BvB22_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: BvB22_C

  Dataset EGAD00001001706

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: BvB27_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: BvB27_F

  Dataset EGAD00001001719

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: BvB33_M

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: BvB33_M

  Dataset EGAD00001001732

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: BvB42_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: BvB42_C

  Dataset EGAD00001001745

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: BvB4_M

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: BvB4_M

  Dataset EGAD00001001756

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW50_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW50_C

  Dataset EGAD00001001835

• germline omni2.5

  Over 2.5 million SNP and CNV loci are screened by Illumina Infinium Omni2.5Exome-8 Kit

  Dataset EGAD00010001636

• leukemia omni2.5

  Over 2.5 million SNP and CNV loci are screened by Illumina Infinium Omni2.5Exome-8 Kit

  Dataset EGAD00010001638

• bam files Targeted BS

  Data from the paper Context-specific Effects of TGFβ/SMAD3 in Cancer Are Modulated by the Epigenome. Tufegdzic et al, Cell Reports 2015

  Dataset EGAD00001001667

• shallow whole genome sequencing dataset

  shallow whole genome sequencing dataset contains 44 samples. all the samples are early stage high ovarian high grade serous carcinoma.

  Dataset EGAD00001008588

• BAM Files MBD-SEQ

  Data from the paper Context-specific Effects of TGFβ/SMAD3 in Cancer Are Modulated by the Epigenome. Tufegdzic et al, Cell Reports 2015

  Dataset EGAD00001001668

• Exome sequencing reads

  Exome sequencing reads of two UFM individuals and their family members (totally 11 individuals) belonging to two different Fragile X families. Alignment files in BAM format are provided.

  Dataset EGAD00001002276

• UK10K NEURO ABERDEEN

  In the UK10K project we propose a series of complementary genetic approaches to find new low frequency/rare variants contributing to disease phenotypes. These will be based on obtaining the genome wide sequence of 4000 samples from the TwinsUK and ALSPAC cohorts (at 6x sequence coverage), and the exome sequence (protein coding regions and related conserved sequence) of 6000 samples selected for extreme phenotypes. Our studies will focus primarily on cardiovascular-related quantitative traits, obesity and related metabolic traits, neurodevelopmental disorders and a limited number of extreme clinical phenotypes that will provide proof-of-concept for future familial trait sequencing. We will analyse directly quantitative traits in the cohorts and the selected traits in the extreme samples, and also use imputation down to 0.1% allele frequency to extend the analyses to further sample sets with genome wide genotype data. In each case we will investigate indels and larger structural variants as well as SNPs, and use statistical methods that combine rare variants in a locus or pathway as well as single-variant approaches. This sample set comprises cases of schizophrenia with additional cognitive measurements, collected in Aberdeen, Scotland.For further information on the Aberdeen cohort please contact David St Clair (d.stclair@abdn.ac.uk).

  Study EGAS00001000109

• UK10K RARE CHD

  In the UK10K project we propose a series of complementary genetic approaches to find new low frequency/rare variants contributing to disease phenotypes. These will be based on obtaining the genome wide sequence of 4000 samples from the TwinsUK and ALSPAC cohorts (at 6x sequence coverage), and the exome sequence (protein coding regions and related conserved sequence) of 6000 samples selected for extreme phenotypes. Our studies will focus primarily on cardiovascular-related quantitative traits, obesity and related metabolic traits, neurodevelopmental disorders and a limited number of extreme clinical phenotypes that will provide proof-of-concept for future familial trait sequencing. We will analyse directly quantitative traits in the cohorts and the selected traits in the extreme samples, and also use imputation down to 0.1% allele frequency to extend the analyses to further sample sets with genome wide genotype data. In each case we will investigate indels and larger structural variants as well as SNPs, and use statistical methods that combine rare variants in a locus or pathway as well as single-variant approaches. The CHD (congenital heart disease) samples will be part of the “rare disease” group, and will undergo exome sequencing.For further information with regard to this cohort please contact Shoumo Bhattacharya (shoumo@me.com).

  Study EGAS00001000125

• Comprehensive genomic and transcriptomic analysis of three synchronous primary tumours and a recurrence from a head and neck cancer patient

  Synchronous primary malignancies occur in a small proportion of head and neck squamous cell carcinoma patients. Here, we analysed three synchronous primaries and a recurrence from one patient, by comparing the genomic and transcriptomic profiles among the tumour samples and determining the recurrence origin. We found remarkable levels of heterogeneity among the primary tumours, and through the patterns of shared mutations, we traced the origin of the recurrence. Interestingly, the patient carried germline variants which might have predisposed him to carcinogenesis, together with a history of alcohol and tobacco consumption. Mutational signature analysis confirmed the impact of alcohol exposure, with Signature 16 present in all tumour samples. Characterisation of immune cell infiltration highlighted an immunosuppressive environment in all samples, which exceeded the potential activity of T cells. Studies such as the one described here have important clinical value and contribute to personalised treatment decisions for patients with synchronous primaries and matched recurrences.

  Study EGAS00001004857

• High-resolution, patient-level dissection of IL-23 blockade in cutaneous psoriasis

  Psoriasis vulgaris and other chronic inflammatory diseases improve markedly with therapeutic blockade of IL-23 signaling in T cells, but the genetic mechanisms of response remain poorly understood. We single-cell transcriptomically profiled CD45+ immune cells isolated from lesional psoriatic skin before and after IL-23 blockade. In clinically responsive patients, a psoriatic transcriptional signature in skin-resident memory T cells was sharply attenuated. In contrast, poorly responsive patients were distinguished by enduring T17 cell activation, a mechanism distinct from alternative cytokine signaling or downstream resistance. Spatial transcriptomic analysis suggests that successful IL-23 blockade requires dampening of > 90% of IL-17-induced signaling in lymphocyte-adjacent keratinocytes, an unexpectedly high threshold. We also detected a subset of persistent, disease-specific T17 abnormalities in responsive patients, revealing an irreversible cell identity that may necessitate ongoing IL-23 inhibition. Collectively, our data establishes a patient-level paradigm for dissecting response to immunomodulatory treatments.

  Study EGAS00001007373

• Gene-Specific RNA Sequencing in PLCG2-Associated Immune Dysregulation with Cold Urticaria

  This study utilized gene-specific RNA-sequencing of PLCG2 to screen for disease causing in-frame exon-skipping transcripts of PLCG2 in a collection of 9 subjects with cold urticaria, 2 subjects with known PLCG2-associated antibody deficiency and immune dysregulation (PLAID)-causing deletions of PLCG2 (positive controls) and 3 healthy subjects (negative controls). Full length cDNA of PLCG2 was generated using gene specific reverse transcription of peripheral blood mononuclear cell RNA. The full length PLCG2 cDNA was used as the template to create Illumina sequencing libraries. To identify the underlying genetic basis for the exon-skipping transcripts, trio-based whole genome sequencing was performed for probands in whom in-frame exon-skipping transcripts of PLCG2 were identified.

  Study phs003807

• CALGB/SWOG 80405: Genome-Wide Association Study of Patients with Advanced or Metastatic Colorectal Cancer Treated with First-Line Chemotherapy Combined with Cetuximab and/or Bevacizumab

  CALGB/SWOG 80405 (NCT00265850) was a randomized phase III study of bevacizumab, cetuximab, or the combination of these two monoclonal antibodies, in addition to systemic chemotherapy for patients with untreated metastatic adenocarcinoma of the colon or rectum. We prospectively collected germline DNA and conducted genome-wide association studies using clinical outcomes and molecular features.

  Study phs003428

• Targeted DNA sequencing and mRNA sequencing data from patients with peritoneal metastasis from colorectal cancer

  Patients with peritoneal metastasis from colorectal cancer (PM-CRC) have inferior prognosis and respond particularly poorly to chemotherapy. This study aims to identify the molecular explanation for the observed clinical behavior and suggest novel treatment strategies in PM-CRC. Tumor samples (230) from a Norwegian national cohort undergoing surgery and hyperthermic intraperitoneal chemotherapy (HIPEC) with mitomycin C (MMC) for PM-CRC were subjected to targeted DNA sequencing, and associations with clinical data were analyzed. mRNA sequencing was conducted on a subset of 30 samples to compare gene expression in tumors harboring BRAF or KRAS mutations and wild-type tumors.

  Dataset EGAD50000000593

• Indigenous American Diversity and Evolution

  The Indigenous American Genomic Diversity Project (IAGDP) investigates the genomic diversity and evolutionary history of Native American populations, which remain underrepresented in global genomic research. As part of this effort, we generated high-coverage whole-genome sequences individuals sampled across eight Latin American countries. This study provides a resource for investigating population structure, demographic history, and adaptive evolution in Indigenous American populations.

  Study EGAS50000001664

• CMML Collection of WES, WGS, RNA-Seq and ERRBS data

  We first performed a comprehensive analysis of the genome of 66 chronic myelomonocytic leukemia cases using whole exome (N=49) or whole genome (N=17) sequencing for paired leukemic-control DNA. Then, we realized serial analysis of whole exome sequence in 17 cases, completed with serial RNA sequencing and DNA methylation analysis in 9 cases, including patients treated or not with hypomethylating agents.

  Study EGAS00001001264

• Expression-Based Subtypes Define Pathologic Response to Neoadjuvant Immune-Checkpoint Inhibitors in Muscle-Invasive Bladder Cancer

  Checkpoint immunotherapy (CPI) has increased survival for some patients with advanced stage bladder cancer (BCa). However, most patients do not respond. Here, we characterized the tumor and immune microenvironment in pre- and post-treatment tumors from the PURE01 neoadjuvant pembrolizumab immunotherapy trial, using a consolidative approach that combined transcriptional and genetic profiling with digital spatial profiling.

  Study EGAS00001005549

• Gremlin 1 + fibroblastic niche maintains dendritic cell homeostasis in lymphoid tissues

  Although cross-species transcriptional analysis has been generated for DCs37, transcriptomic conservation between mouse and human FRCs at single-cell resolution has been unclear. To test whether GREM1+ FRCs might also play a role in DC homeostasis in humans, we performed scRNA-seq of CD45–PDPN+ stromal cells, as well as CD45+CD11c+ immune cells from healthy human LNs of three donors.

  Study EGAS00001006211

• WES

  Exome Sequencing. 3 ug of genomic DNA from each lymph node sample were sheared and used for the construction of a paired-end sequencing library as described in the paired-end sequencing sample preparation protocol provided by Illumina. Enrichment of exonic sequences was then performed for each library using either the Sure Select Human All Exon 50 Mb or All Exon+UTRs v4 kits following the manufacturer’s instructions (Agilent Technologies). Exon-enriched DNA was pulled down by magnetic beads coated with streptavidin (Invitrogen), followed by washing, elution and 18 additional cycles of amplification of the captured library. Enriched libraries were sequenced in one lane of an Illumina GAIIx sequencer or in two lanes of a HiSeq2000 when using pools of eight samples.

  Dataset EGAD00001005424

• The Influence of Gut Microbiota on the Speciation and Toxicity of Mercury During Pregnancy

  There are few studies that have characterized maternal gut microbiota and fetal methylmercury exposure, yet microbes likely modulate this relationship. The primary objective of our pilot study was to determine associations between gut microbial taxa and mercury concentrations in multiple biomarkers (stool, hair, and cord blood). Our secondary objective was to determine the contribution of gut microbial mercury methylation to stool methylmercury.

  Study phs000970