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• Identification_of_synthetic_lethal_genes_by_CRISPR_Cas9_library

  Sequencing is performed on PCR products from the amplification of gRNA segments introduced into cell lines (some are commercial, some are derived by collaborators, as described in HMDMC 13/076). Cellular DNA or RNA are not sequenced. This data is defined as "Other Biological/Biochemical Assay Data" under the WTSI datasharing guidelines and consequently will be released at the time of publication and/or through faculty websites. SEQUENCING DETAILS: in October 2016 3 DNA samples will be submitted for PCR amplification and purification through CGP pipeline using Thompson's custom primer set and PCR settings and sequencing with Hiseq using a custom protocol (with 3 forward reads to read sgRNA1, sgRNA2 and the index, optimized with Illumina Bespoke Sanger team); read length 50bp. The following set of samples will be submitted in later 2016 and ealry 2017 as cell pellet to be processed through CGP Cas9 pipeline (Thompson's oligos and protocols) and sequences on Hiseq (same custom sequencing protocol described above) We are utilizing a custom CRISPR/Cas9 library to identify synthetic lethal gene pairs. Cells will be transduced with LV expressing Cas9, then infected with LV expressign the library of 42'000 sgRNA pairs. Cell pellet will be collected from the cell population at different timepoints. The samples will be processed by CGP pipeline customized for the specific protocol and then sequenced to identify the 19bp of the sgRNA and quantify their representation.

  Study EGAS00001002117

• Chracterising_cellur_pathways_underlying_CD3_CD28_activation_of_human_CD4__cells

  We devised an approach to disentangle the TCR and CD28 pathways upon stimulation in naive and memory primary human CD4+ T cells (Tcons) in response to defined stimulatory signals. Isolated memory and naïve T cells were activated using anti-CD3, anti-CD28 or both in combination. As a control we cultured cells in the same conditions but without the stimuli. We carried Chipmentation using the H3K27ac antibody on 200,000 cross-linked cells. 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/

  Study EGAS00001002599

• Pediatric UBA1-mutated MDS Single-Cell Sequencing DAC

  This DAC oversees controlled access to single-cell DNA and protein sequencing data generated from a pediatric MDS patient with somatic UBA1 mutation. Access is restricted to researchers who have appropriate ethical approvals and intend to use the data for studies related to pediatric blood disorders, immunology, or VEXAS pathogenesis. The DAC evaluates requests for compliance with these conditions.

  Dac EGAC50000000947

• Cerebral organoid model reveals excessive proliferation of human caudal late interneuron progenitors in Tuberous Sclerosis Complex

  Although the intricate and prolonged development of the human brain critically distinguishes it from other mammals, our current understanding of neurodevelopmental diseases is largely based on work using animal models. Recent studies revealed that neural progenitors in the human brain are profoundly different from those found in rodent animal models. Moreover, post-mortem studies revealed extensive migration of interneurons into the late-gestational and post-natal human prefrontal cortex that does not occur in rodents. Here, we use cerebral organoids to show that overproduction of mid-gestational human interneurons causes Tuberous Sclerosis Complex (TSC), a severe neuro-developmental disorder associated with mutations in TSC1 and TSC2. We identify a previously uncharacterized population of caudal late interneuron progenitors, the CLIP-cells. In organoids derived from patients carrying heterozygous TSC2 mutations, dysregulation of mTOR signaling leads to CLIP-cell over-proliferation and formation of cortical tubers and subependymal tumors. Surprisingly, second-hit events resulting from copy-neutral loss-of-heterozygosity (cnLOH) are not causative for but occur during the progression of tumor lesions. Instead, EGFR signaling is required for tumor proliferation, opening up a promising approach to treat TSC lesions. Our study demonstrates that the analysis of developmental disorders in organoid models can lead to fundamental insights into human brain development and neuropsychiatric disorders.

  Study EGAS00001004586

• Introducing Federated EGA Affiliates: a newly defined tier in the Federated EGA Network

  We're happy to announce that we are now accepting Affiliates in the Federated EGA Network! Federated EGA is a global network of repositories enabling secure discovery and access to sensitive human data. Currently, Federated EGA consists of Central EGA (CEGA), which serves the global community, and nine national Nodes that serve respective jurisdictions. Did you know that the Federated EGA (FEGA) has always envisioned a third tier within the network? This brings us to FEGA Affiliates, recently defined in the newly approved "Federated EGA Structure and Organisation" document. This new tier broadens the range of institutions or organisations that can become part of FEGA. Thus begins a new era for the network. What is a FEGA Affiliate? A FEGA Affiliate archives and serves controlled-access data within its own governance scope, while still participating in federated discovery through the EGA catalogue. Affiliates can be individual organisations or institutions, healthcare genomics initiatives, consortia of institutions, as well as project-specific consortia (national or international). In practical terms, a FEGA Affiliate: Hosts and safeguards the data it archives. Submits non-personal metadata to CEGA so studies are discoverable and can receive EGA accessions. Manages permissions and data access workflows for its datasets. Provides data access and/or distribution, along with support, to authorised users. Key takeaways about FEGA Affiliates FEGA is now organised into three tiers: CEGA, FEGA Nodes, and FEGA Affiliates. Affiliates archive data from their own organisation and/or selected partner institutions (for example, an international consortium). Affiliates make studies discoverable through the EGA catalogue by submitting non-personal metadata for accessioning. Access decisions and conditions are managed locally by the Affiliate (e.g. distribution or access in a trusted research environment). Are you considering whether your institution or project might be a good fit as a FEGA Affiliate? Would you like to learn more about this tier? We have published a blog post that addresses potential common questions, providing answers on this topic. You can read it here.

  Blog fega-affiliates

• Autosomal Recessive CD55 Deficiency is Associated with Protein Losing Enteropathy, Thrombosis, and Complement Dysregulation

  We describe 11 patients from 8 families with homozygous LOF mutations in the complement regulatory protein CD55. Loss of CD55 is associated with increased complement activation, severe protein losing enteropathy accompanying a primary intestinal lymphangiectasia, and deep vein thrombotic events. We have named this disease CHAPLE after the principle components of the disease.

  Study phs001376

• Single_Cell_RNAseq_at_various_stages_of_HiPSCs_differentiating_toward_definitive_endoderm_and_endoderm_derived_lineages

  When comparing the differentiation capacities of pluripotent stem cell lines that have different genetic backgrounds, batch to batch experimental variablility poses a significant challenge, especially when trying to identify smaller effects. One way to address this issue is to differentiate several different lines in the same culture dish, thereby elimating experimental variation. In addition, it allows researchers to analyze many more lines with less experiments. Parallel single cell RNA-Seq exploits that individual cells are tagged and hence each cell can be reliably assigned to the donor of origin based on the genetic variants it contains. In addition, analyzing the genetic signature of single cells within a differentiating population can reveal differentation stages that are not easily detected in bulk RNAseq data. 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/

  Study EGAS00001002278

• A Polygenic Score for Acute Vaso-Occlusive Pain in Pediatric Sickle Cell Disease

  Recurrent acute pain, or vaso-occlusive pain crisis (VOP), is the most common complication of sickle cell disease and correlates strongly with increased hospital visits and early mortality (PMID: 1710777). While the genetics of VOP in sickle cell patients has been studied (PMID: 29205277, 27883292, 25102390, 30079801, 22925497, 29531649, 29620434, 19468207, 20172753, 22576309, 30031848, 24136375, 27603703, 29559808), it is not fully understood.Using whole genome sequencing, we interrogated the α-thalassemia deletion -α3.7 and 133 candidate single-nucleotide polymorphisms (SNPs) across 66 genes for associations with VOP in 327 SCCRIP participants followed longitudinally over 6 years. Twenty-one SNPs in 9 loci were associated with VOP, including 3 (BCL11A, MYB, and the β-like globin gene cluster) that regulate erythrocyte fetal hemoglobin (HbF) levels and 6 (COMT, TBC1D1, KCNJ6, FAAH, NR3C1, and IL1A) that were associated previously with various pain syndromes. An unweighted PGS integrating all 21 SNPs was associated with the VOP event rate (estimate, 0.35; standard error, 0.04; P = 5.9 × 10−14) and VOP event occurrence (estimate, 0.42; standard error, 0.06; P = 4.1 × 10−13). These associations were stronger than those of any single locus. Our findings provide insights into the genetic modulation of VOP in children with SCD. More generally, we demonstrate the utility of WGS for investigating genetic contributions to the variable expression of SCD-associated morbidities.For publications, written, and/or oral presentations resulting from use of this data, please cite the following information: "The original data description for A Polygenic Score for Acute Vaso-Occlusive Pain in Pediatric Sickle Cell Disease can be found here: (Journal Citation Blood Adv. 2021 Jul 27;5(14):2839-2851) (PMID: 34283174)."

  Study phs002470

• Selenium Chemoprevention: Benefits and Harms

  Selenium is a trace element that may have anti-carcinogenetic effect, but heterogenous treatment effects have been observed. This genome-wide association study investigates if genetic variation modifies the effect of selenium chemoprevention in the Selenium and Celecoxib Trial, a randomized, double-blind, placebo-controlled trial conducted at the University of Arizona Cancer Center. The objective of the clinical trial was to determine whether daily intake of 200 µg/d of selenium as a supplement could reduce the risk for developing metachronous colorectal adenomas. The study participants were recruited between 2001 and 2011. Genome-wide association study was performed for 1,323 study participants who provided blood sample at the time of study entry.

  Study phs002283

• eIMPACT Trial: Modernized Collaborative Care to Reduce the Excess CVD Risk of Older Depressed Patients

  Cardiovascular disease (CVD) is the #1 killer of American men and women, and its economic burden is substantial and on the rise. Adults with depression are at elevated risk of CVD events and poor CVD prognosis. Unfortunately, past clinical trials of depression treatments have not observed the anticipated cardiovascular benefits. A novel explanation for these null results is that the depression interventions in these trials, which all involved patients with preexisting CVD, were delivered too late in the natural history of CVD. Accordingly, the objective of this single-center, parallel-group, assessor-blinded randomized controlled trial was to determine whether successful depression treatment before, versus after, the onset of clinical CVD reduces CVD risk in depression. Primary care patients with depression and elevated CVD risk from a safety net healthcare system (N = 216, Mage = 59 years, 78% female, 50% Black, 46% with income <$10,000/year) were randomized 1:1 to 12 months of the eIMPACT intervention (a modernized collaborative stepped care program involving internet cognitive-behavioral therapy [CBT], telephonic CBT, and/or select antidepressants) or usual primary care for depression (primary care providers supported by embedded behavioral health clinicians and psychiatrists). The primary outcome was endothelial dysfunction (brachial flow-mediated dilation) at 12 months, and the secondary outcomes were self-reported depressive symptoms (Hopkins Symptom Checklist-20), autonomic dysfunction (high-frequency heart rate variability), systemic inflammation (interleukin-6 and high-sensitivity C-reactive protein), and platelet activation (β-thromboglobulin and platelet factor 4) at 12 months. The central hypothesis was that the eIMPACT intervention would improve endothelial dysfunction in depressed adults by decreasing depressive symptoms, autonomic dysfunction, systemic inflammation, and platelet activation. Primary results are posted to ClinicalTrials.gov at NCT02458690. The de-identified limited dataset available on BDC consists of only the individual phenotypic data needed to confirm this trial’s primary results – i.e., randomization status, primary and secondary outcome variables, and participant characteristics utilized in the hypothesis-testing models (age, sex, race, education, income, and systolic blood pressure). We also provide the SAS code to replicate the results of the hypothesis-testing models reported in Table 4 and Supplemental Tables 1-3 in the main outcomes paper (#2 in Selected Publications). Of note, the user will need to specify the file path for the dataset to run the SAS code. Instructions for requesting individual-level data are available on BDC at https://biodatacatalyst.nhlbi.nih.gov/resources/data/. Apply for data access in dbGaP. Upon approval, users may begin accessing requested data in BDC. For questions about availability, you may contact the BDC team at https://biodatacatalyst.nhlbi.nih.gov/contact.

  Study phs003283