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• Res1_HT29_exp1_MC_02.03.22

  1 sample is pure plasmid DNA and 10 samples are cell pellets for genomic DNA extraction. CRISPR PCR1 and PCR2 indexing - Please use standard Kozuke primers.

  Dataset EGAD00001012230

• Res1_HT29_exp2_MC_03.03.22

  1 sample is pure plasmid DNA and 10 samples are cell pellets for genomic DNA extraction. CRISPR PCR1 and PCR2 indexing - Please use standard Kozuke primers.

  Dataset EGAD00001012231

• High Density SNP Association Analysis of Melanoma: Case-Control and Outcomes Investigation

  This research builds upon an extensive resource of melanoma cases and hospital based controls collected over several years at the U.T. M.D. Anderson Cancer Center. The goal of this research is to identify novel susceptibility and outcome-related genes for melanoma using a systematic genome-wide association-based approach. Our goal is to conduct high-density SNP association and outcome studies. This dbGaP study contains samples from 2000 European ancestry cases and 1000 European ancestry controls using the Illumina OMNI1-Quad SNP chip. As a part of an ongoing R01 project, we have epidemiological data together with candidate gene results for 1000 of the melanoma cases and the controls. With regard to the outcome aspect of our design, as part of our melanoma Specialized Program of Research Excellence (SPORE) grant, our MelCore database contains comprehensive, prospectively maintained clinical information from all melanoma patients included in the study cohort, including primary tumor histopathology and staging information, standard and investigational blood tumor markers, details of surgical and systemic therapies, and extensive follow-up information, including time to relapse or recurrence, pattern of recurrence and survival duration. Finally, we intend to collaborate with the GenoMEL collaboration so we can jointly evaluate each other's findings. The goal of our analysis will be to identify novel genetic factors predisposing the development of melanoma, as well as genetic factors controlling melanoma stage at presentation, recurrence and progression. This study is part of the Gene Environment Association Studies initiative (GENEVA, http://www.genevastudy.org) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to melanoma through large-scale genome-wide association studies of 2000 European ancestry cases and 1000 European ancestry controls. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.

  Study phs000187

• The National Myelodysplastic Syndromes (MDS) Study

  Myelodysplastic syndromes (MDS) are the most common cause of adult bone marrow failure in the US and occur predominantly in people over the age of 60. Much of the morbidity and mortality for MDS is due to complications from low blood counts (e.g., infections and bleeding). MDS is caused by acquired DNA mutations that occur in a patient's blood cells as they grow older. Accumulating evidence suggests that MDS patients may traverse through a series of antecedent hematopoietic conditions defined by, i) clonal hematopoiesis (i.e., detectable somatic mutations in a person's blood cells) without low blood counts, a condition that affects up to 10% of individuals 70 years old and is termed Clonal Hematopoiesis of Indeterminate Potential (CHIP), or ii) clonal hematopoiesis with low blood counts (i.e., cytopenias) but no evidence of bone marrow dysplasia, termed Clonal Cytopenia of Undetermined Significance (CCUS). Nearly all CCUS patients will develop MDS over a ten year period, highlighting the prognostic importance of this disease. A better understanding of the genetic mutations, including non-coding and structural variants (SVs), occurring in CCUS and MDS could provide valuable insight into the natural history of MDS development. The NHLBI is conducting a longitudinal, observational study to create a standardized clinical dataset linked to a prospectively collected, consistently processed, and well-characterized biospecimen repository derived from approximately 1750 participants with suspected or newly diagnosed MDS or MDS/myeloproliferative neoplasm (MPN) overlap. These volunteers will donate biological specimens (like bone marrow and blood) and medical information, including details of their symptoms, how they perceive their quality of life, the treatments they receive, and what their doctor says about the severity of their illness over time. This information will be collected at pre-determined time points for the duration of the study. Study participants may be followed for life.

  Study phs002714

• Germline and Somatic Genetic Landscape of Pediatric Rhabdomyosarcoma

  Dynamic approaches that integrate population-based research and molecular biology are needed to explain the mechanisms underlying pediatric rhabdomyosarcoma (RMS) and to determine novel prevention strategies. RMS, the most common soft-tissue sarcoma in children and adolescents, has one of the poorest 5-year survival rates among all pediatric cancers (less than 65%). One of the strongest risk factors for RMS is having a cancer predisposition syndrome. The syndromes that are most commonly seen among those with RMS are Li-Fraumeni, neurofibromatosis type 1, Costello, Noonan, and DICER1. Based on smaller clinic-based studies, only about 7% of RMS cases are thought to be associated with the genes responsible for these syndromes. However, there have been no population-based assessments to support this estimate. Even in the most recent large-scale evaluations of germline mutations in predisposition genes among children with cancer, very few RMS cases were included (43 cases). Furthermore, no distinctions were made between the major histologic subtypes of RMS: embryonal (eRMS) and alveolar (aRMS), which display differences in terms of age distribution, incidence, and cytogenetics. For instance, nearly 80% of alveolar cases are driven by a chromosomal translocation between either PAX3 or PAX7 and FOXO1, whereas these fusions are not seen in embryonal cases. In fact, RMS research is shifting from categorization based on histology to fusion status (eRMS is overwhelmingly fusion-negative). Another limitation in previous studies has been the inability to evaluate the frequency of de novo germline mutations (DNMs) in cancer predisposition genes due to the absence of any well-characterized cohorts of RMS case-parent trios. Therefore, a major gap in our understanding of the role of cancer predisposition in pediatric RMS that limit translational impact is there have been no population-based assessments to determine the true impact of these mutations on pediatric RMS, which limits clinical sequencing guidelines and surveillance protocols in these children.Overall Project Strategy: The objective of this project is to advance our understanding of the relationship between cancer predisposition genes and pediatric RMS. Our central hypotheses are: 1) mutations in cancer predisposition genes are more common than expected in children with RMS; and 2) children with fusion-negative tumors have a higher burden of germline mutations than those with fusion-positive tumors. The framework for this study relies on >600 well annotated samples collected from newly diagnosed RMS patients and stored in the Children’s Oncology Group (COG) Biopathology Center.

  Study phs002304

• De Novo Mutation Rates at the Single-Mutation Resolution in the Human Genome

  We developed a method to measure the origination rates of target mutations of choice and applied it to the HbS and nearby mutations in the human beta-globin (HBB) gene, as well as to the equivalent mutations in the nearly identical delta-globin (HBD) gene in sperm cells from African and European donors. Specifically, after extracting DNA from the sperm of the donors, each sample is enriched for the HbS mutation and nearby mutations by the restriction enzyme Bsu36I, which cleaves the wild-type (WT) sequence CCTGAGG at positions 16–22 of HBB and the homologous positions of HBD while leaving the HbS mutant and other mutants in these positions intact. Next, unique barcodes are attached to the DNA fragments from these Bsu36I-treated samples in order to reduce error by consensus sequencing of copies originating from the same original fragment. To determine how many target WT sequences have been removed (scanned) by Bsu36I digestion and hence to be able to calculate the de novo mutation rate, we run a second reaction in parallel for each donor. This reaction involves the same steps as the former reaction except for digestion by Bsu36I (Bsu36I-untreated). Spiking into the Bsu36I-treated and untreated samples known amounts of mock HBB-like DNA molecules that are fully resistant to Bsu36I digestion allows to calculate in the sequence analysis stage the Bsu36I-enrichment score based on the change in their frequency between the two treatments, which in turn is used to calculate the number of scanned WT sequences. Our results show significant correspondence between de novo mutation rates and past observations of alleles in carriers, showing that mutation rates vary substantially in a mutation-specific manner that contributes to the site frequency spectrum. We also found that the overall point mutation rate is significantly higher in Africans than Europeans in the HBB region studied. Finally, the rate of the 20A>T mutation, called the “HbS mutation” when it appears in HBB, is significantly higher than expected from the genome-wide average for this mutation type. Nine instances were observed in the African HBB ROI, where it is of adaptive significance, representing at least three independent originations, and no instances were observed in the European HBB ROI or in the European or African HBD ROI.12 consented subjects; samples from two subjects were pooled

  Study phs002391

• Microbiome-Host Interactions in Oral Squamous Cell Carcinoma: a Metatranscriptomic Exploratory Study

  Oral cancer (predominantly squamous cell carcinoma; OSCC) is the 14th most prevalent malignancy worldwide, accounting for more than 300,000 new cases and 145,000 deaths annually. Despite advances in cancer treatment modalities, OSCC continues to have poor prognosis with 5-year survival rates less than 50%. Although use of tobacco and alcohol consumption constitute the major risk factors, there is emerging evidence for the role of the microbiome in OSCC. However, studies on the association between the microbiome and OSCC has so far focused on compositional analysis and has been largely limited to the bacterial component of the microbiome. The aim of this study is to characterize the transcriptional activity (function) as well as composition of the multi-kingdom microbiome associated with OSCC and correlate it with the gene expression of the host using ultra-deep metatranscriptome sequencing, which will provide new insight into the role of the microbiome in OSCC and the possible mechanisms by which the tumor’s microbial community may influence on its behavior. This project comprises RNA-Seq data from twenty OSCC tumor/normal tissue pairs and twenty tongue scraping samples from healthy controls. However, due to consent constraints, the human sequences from the control data are filtered out.

  Study phs002678

• InTEAM Consortium - Alcoholic Hepatitis

  Alcoholic hepatitis (AH) is a life-threatening condition characterized by profound hepatocellular dysfunction for which targeted treatments are urgently needed. Identification of molecular drivers is hampered by the lack of suitable animal models. By performing RNA sequencing in livers from patients with different phenotypes of alcohol-related liver disease (ALD), we describe the transcriptional programs involved in disease progression. We uncovered that development of AH is characterized by the defective activity of liver-enriched transcription factors (LETFs). The PPARG predicted activation state was found increased in early forms of ALD, while AH was associated by a marked decrease in HNF4A-dependent gene expression along with a marked expression of the fetal HNF4A isoform (P2). TGFB1, a key upstream transcriptome regulator in AH, induced the use of HNF4a P2 promoter in hepatocytes, which resulted in abnormal bile acid synthesis and defective metabolic and synthetic functions. PPARG agonists partially prevented this effect. We conclude that targeting TGFB1 and epigenetic drivers that modulate HNF4A-dependent gene expression could be beneficial to improve hepatocellular function in patients with AH. The study was conducted thanks to a multicenter collaboration under the National Institute of Alcohol Abuse and Alcoholism (NIAAA)-funded consortium: Integrated Approaches for Identifying Molecular Targets in Alcoholic Hepatitis (InTEAM).

  Study phs001807

• Examination of Engineered LINE-1 Integration Events in HeLa Cells

  Long Interspsesed Element-1 (LINE1 or L1) encodes two proteins (ORF1p and ORF2p) required for its mobilization (i.e. retrotransposition) in the human genome. Human ORF2p, a 150kDa protein, has endonuclease (EN) and reverse transcriptase (RT) activities. L1 EN is classified as apurinic/apyrimidin-like endonuclease (APE) and is responsible for initiating target-site primer reverse transcription (TPRT) during the L1 retrotransposition cycle. During canonical TPRT, the L1 EN activity makes a single-strand endonucleolytic nick at a double-strand DNA target sequence in genomic DNA. The endonucleolytic nick is typically made at an L1 EN degnerate consensus cleavage sequence (5'-TTTT/A-3') exposing a free 3' hydroxy group that can be used as a primer by the ORF2p L1 RT activity to reverse transcribe the associated L1 RNA. Here, we characterized over 21,000 de novo engineered L1 retrotransposition events in HeLa cells to determine if L1 exhibits overt integration preferences in the human genome. Bru-seq of HeLa cells to determine actively transcribed regions of the genome was also performed. This Bru-seq data was used to determine if engineered L1 integration events preferentially integrate into transcribed regions of the genome, and to determine which strand during transcription may present itself as preferential during L1 retrotransposition.

  Study phs001669

• Diverse_outcomes_of_controlled_human_malaria_infection_originate_from_host_intrinsic_immune_variation_and_not_var_gene_switching

  Falciparum malaria is clinically heterogeneous and the relative contribution of parasite and host factors in shaping disease severity remains unclear. We set out to explore the interaction between host inflammation and parasite variant surface antigen (VSA) expression, asking whether this relationship underpins the variation observed in controlled human malaria infection. We uncovered marked heterogeneity in the response of naive hosts to blood challenge with some volunteers maintaining a state of immune quiescence, others triggering interferon-stimulated inflammation and a small group showing transcriptional evidence of myeloid cell suppression. Significantly, only inflammatory volunteers experienced hallmark symptoms of clinical malaria. When we then tracked temporal changes in parasite VSA expression to ask whether variants associated with severe disease preferentially expand in naive hosts (as predicted by current theory) we found that var gene profiles were essentially unchanged after 10-days of blood-stage infection. These data therefore show that the diverse clinical outcomes of CHMI largely originate from host-intrinsic variation and there is no evidence for switching or selection of var genes in naïve hosts. 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 EGAS00001003766