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• HSC_colony_many_years_post_allogeneic_bone_marrow_transplant___Bait_set_2

  This study looks at human donors and recipients of allogeneic blood & marrow marrow transplantation. Each transplant "pair" (donor & recipient) underwent the transplant procedure 10 -30 years prior to sampling - the majority for an underlying diagnosis of leukemia. We will perform whole-genome sequencing on tens to hundreds of single HSPC (haematopoietic stem and progenitor cell)-derived colonies per individual. We will infer the phylogeny of these cells (those from both donor & recipient within a pair) by analysing the somatically acquired mutations within each cell. The structure of the phylogeny will allow estimates of hitherto unknown parameters such as the number of HSCs that engraft long-term, the dynamics of the engraftment process on the HSC level, and the additional mutation burden acquired through the arduous transplant procedure. This TGS part of the study is used for assessing the contribution of clones to mature blood subsets, and better timing mutations relative to transplantation.

  Study EGAS00001005534

• HSC_colony_many_years_post_allogeneic_bone_marrow_transplant___Bait_set_3

  This study looks at human donors and recipients of allogeneic blood & marrow marrow transplantation. Each transplant "pair" (donor & recipient) underwent the transplant procedure 10 -30 years prior to sampling - the majority for an underlying diagnosis of leukemia. We will perform whole-genome sequencing on tens to hundreds of single HSPC (haematopoietic stem and progenitor cell)-derived colonies per individual. We will infer the phylogeny of these cells (those from both donor & recipient within a pair) by analysing the somatically acquired mutations within each cell. The structure of the phylogeny will allow estimates of hitherto unknown parameters such as the number of HSCs that engraft long-term, the dynamics of the engraftment process on the HSC level, and the additional mutation burden acquired through the arduous transplant procedure. This TGS part of the study is used for assessing the contribution of clones to mature blood subsets, and better timing mutations relative to transplantation.

  Study EGAS00001006572

• Protracted Neuronal Recruitment in the Temporal Lobe of Young Children

  This study describes a stream of migrating neurons directed to the human entorhinal cortex. This migration is among the most protracted in the developing human brain, with young neurons still arriving at 2-3 years of age. We did not observe a similar migratory process in the early postnatal macaque brain, which suggests that this migration may be uniquely delayed or extended into early postnatal human life. Using immunohistochemistry and single‐cell RNA sequencing (scRNA‐seq), we identified these late-arriving neurons as being mainly CGE-derived LAMP5+/RELN+ interneurons.

  Study phs003509

• NIDDK International IBD Genetics Consortium Repository Global Screening Array

  The purpose of this GWAS meta-analysis is to assess IBD risk alleles using data collected by members of the International IBD Genetics Consortium and their collaborators around the world. Data from over 30 cohorts have been identified and are being combined for analysis. Genotyping has been conducted using a variety of chips with most samples genotyped using GSAMD-24v1-0 or GSA-CHO-Custom. Individual level genotype data will be made available whenever possible (some groups are only able to provide summary statistics due to institutional and/or governmental restrictions on data sharing), together with information on sex, self-reported ancestry, IBD affection status and diagnosis. This first batch includes data from North American sites who are members of the NIDDK-funded IBD Genetics Consortium. Additional data will be provided in an update as soon as they have gone through the QC process.

  Study phs002336

• SUDC Registry and Research Collaborative

  The Sudden Unexplained Death in Childhood Registry and Research Collaborative (SUDCRRC), created at NYU Langone Health in 2014, connects academic investigators, forensic pathologists, and medical examiner and coroner partner offices to study sudden unexpected pediatric deaths, aged 1 month to 18 years, whose death is unexplained or unclear at the end of the public mandated investigation, including autopsy. Each case includes collection and analysis of all records (medical history from prenatal records throughout life, death scene investigation, autopsy/toxicology/ancillary death investigation reports including photographs and histology slides), biospecimens, and in-depth family interviews. Whole exome sequencing is performed on each deceased child and both biological parents. Additional studies are pursued when indicated by pathology review. Each case receives a multidisciplinary masked review process and parental written consent is obtained. The NYU institutional review board approved this study.

  Study phs003383

• Exploiting immune cell receptor information to quantify index switching in single cell transcriptome sequencing experiment

  By offering high sequencing speed and ultra-high-throughput at a low price, Illumina next-generation sequencing platforms has been widely adopted in recent years. However, an experiment with multiplexed library could be at risk of molecular recombination, known as “index switching”, which causes certain amount of reads to be assigned to an incorrect library. It is reported that a new advance, exclusion amplification (ExAmp) in conjunction with the patterned flow cell technology introduced on HiSeq 3000/HiSeq 4000/HiSeq X sequencing systems, potentially suffers from a higher rate of index switching than conventional bridge amplification. We took advantage of the diverse but highly cell-unique expression of immune cell receptors to quantify index switching on single cell RNA-seq data that were sequenced on HiSeq 3500 and HiSeq 4000. By utilizing the unique T-cell receptor (TCR) expression, we could quantify the spread-of-signal from many different wells (n=51 from total three batches) due to index switching. We used TraCer to reconstruct full-length TCR from all samples, and then used Kallisto to quantify TCR gene expression. We found index switching in all three batches of experiments investigated. The median percentage of incorrectly detected markers was estimated to be 4.2% (interquartile range (IQR): 2.0%-8.7%). We did not detect any consistent pattern of certain indices to be more prone for switching than others, suggesting that index switching is a stochastic process. We confirm that index switching is a problem that affects all samples run in multiplexed libraries on Illumina HiSeq 3500 and HiSeq 4000 platforms.

  Study EGAS00001002911

• A Genome Wide Scan of Lung Cancer and Smoking

  The majority of cases of lung cancer are the culmination of a dynamic process that begins with smoking initiation, proceeds through dependency and smoking persistence, continues with lung cancer development and ends with progression to disseminated disease or response to therapy and survival. We are conducting a whole genome study of lung cancer and smoking to examine critical steps in lung cancer progression. This study is a genome-wide association study (GWAS) to investigate the genetic determinants of lung cancer risk. The study design efficiently allows identification of genes that also contribute to smoking persistence and outcome from lung cancer using a single GWAS of 5,900 subjects using the primary GENEVA dataset, derived from two studies. The first is the Environment and Genetics in Lung Cancer Etiology Study (EAGLE), a population-based, biologically intensive, case-control study from the Lombardy region of Italy including ~2000 newly diagnosed lung cancer cases and ~2000 age-, gender- and region- matched controls. The second is the Prostate, Lung, Colon and Ovary Study (PLCO) Cancer Screening Trial from which we have selected ~850 lung cancer cases and ~850 controls, also matched on age and gender. Understanding the basis for the well-established hereditary component of lung cancer and smoking persistence could provide new insights into etiology, prevention, and treatment, and have an enormous impact on public health. The same GWAS genotyping data in the two studies will be used to investigate the genetic determinants of smoking persistence. Specifically, we will analyze current smokers and former smokers from EAGLE and PLCO for diverse smoking phenotypes, including persistence of smoking as well as ever/never smoking comparisons, quitting attempts, and the Fagerström index of tobacco addiction. PLCO participants are all European-Americans and EAGLE involves subjects from Italy. EAGLE is a case-control study and contains 3937 phenotyped subjects. PLCO is a screening trial with a cohort design and contains 1651 phenotyped subjects. 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 lung cancer and smoking through large-scale genome-wide association studies of population-based samples of lung cancer cases and 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 phs000093

• Successful Clinical Response in Pneumonia Therapy (SCRIPT)

  The goal of this study is to iteratively identify, validate and refine biomarkers to predict clinical failure, and identify novel targets for therapy, beyond traditional antibiotics, for patients with severe pneumonia requiring intubation, including severe community-acquired pneumonia (CAP), hospital-acquired pneumonia, and ventilator-associated pneumonia (HAP/VAP). We hypothesize that factors within the alveolar microenvironment in many patients with pneumonia prevent the active process of pneumonia resolution.The major emphasis will be on HAP. Mechanically ventilated CAP patients are a very high-risk group for subsequent VAP, and therefore CAP samples will be included to determine baseline bacteria, microbiome, and host defense patterns for those that do or do not develop HAP/VAP. Hospital-acquired pneumonia is the leading cause of death from nosocomial infections. Even in patients receiving pathogen-appropriate therapy, reported clinical failure rates are increasing, approaching 50% in recent clinical trials. Current approaches to improve outcomes in patients with pneumonia almost exclusively focus on the development of antibiotics to address the problem of resistance. However, the prevalence of antibiotic-resistant pathogens is insufficient to explain the high rates of clinical failure. Instead, we hypothesize that factors within the alveolar microenvironment in many patients with pneumonia prevent the active process of pneumonia resolution. These factors include pathogen-specific adaptations to the injured lung that modulate the innate and adaptive immune response, as well as changes to the alveolar microbiome, driven by selective pressure within our modern intensive care units. Understanding this complex adaptive system requires the integration of clinical information with unbiased measures of the host, pathogen, and microbiome changes within the alveolar microenvironment. These measures must be repeated over time to identify factors that distinguish successful from failed therapy for pneumonia sufficiently early during the clinical course to allow for effective interventions. To address this challenge, we have assembled a talented group of investigators in the Successful Clinical Response In Pneumonia Therapy (SCRIPT) Systems Biology Center. We will leverage our routine clinical practice of safe alveolar sampling in mechanically ventilated patients with pneumonia with repeated non-bronchoscopic bronchoalveolar lavage (NBBAL) sampling over the course of pneumonia. From this fluid, we will combine flow cytometry with multi-omic technologies (cell population-specific transcriptomics, epigenomics, shotgun microbiome sequencing, and pathogen-specific sequencing). Our systems scientists will integrate these genomic data with robust clinical -omics with the goal of identifying biomarkers that can be prospectively tested in patients and causally evaluated in humanized mouse models.The addition of a pooled sample artificially increases the number of automatically computed subjects by one.

  Study phs002300

• Nanopore_and_Illumina_sequencing_of_human_glioblastomas

  Liquid biopsy analysis refers to methods designed to detect tumour-specific material (e.g., circulating tumour cells or tumour DNA) in body fluids, such as urine or blood samples. A widely-used liquid biopsy approach consists of genotyping the circulating tumour DNA (ctDNA) through sequencing of plasma/serum DNA. Although useful in the context of metastatic disease (where the concentration of ctDNA is high), current liquid biopsy technologies show limited sensitivity of detection for the early detection of cancer, and low specificity, as cancer-related mutations accumulate in healthy tissues as part of the ageing process, thus making it difficult to distinguish these from tumour mutations, and because sequencing errors and true mutations show overlapping profiles. Therefore, developing liquid biopsy protocols with increased sensitivity and specificity represents an urgent clinical need. Here we harness extrachromosomal circular DNA (eccDNA) elements, which are circular DNA structures physically separated from the chromosomes of up to several Mbp long pervasive in human cancers, for liquid biopsy analysis. In this pilot study we will focus on the analysis of glioblastomas, because there is strong evidence for the presence of eccDNA in these tumour types, and because developing liquid biopsy approaches for brain tumours to reduce the invasiveness of brain tumour biopsies remains an unmet clinical need.

  Study EGAS00001005812

• Genomes of Relapsing Neuroblastoma

  Neuroblastoma is a malignancy of the developing sympathetic nervous system that is often lethal when relapse occurs, but the molecular mechanisms behind this process are poorly defined. We here used whole-exome sequencing, mRNA expression, array CGH and DNA methylation analysis to holistically characterize 16 paired samples from neuroblastoma patients at diagnosis and relapse. The mutational burden significantly increased in relapsing tumors accompanied by altered mutational signatures and reduced subclonal heterogeneity. Global allele frequencies at relapse indicated clonal mutation selection during disease progression. Promoter methylation patterns were consistent over disease course and patient-specific. Recurrent alterations at relapse included mutations in the putative CHD5 neuroblastoma tumor suppressor, chromosome 9p losses, DOCK8 mutations, inactivating mutations in PTPN14 and a relapse-specific activity pattern for the PTPN14 target gene, YAP. Recurrent new mutations in HRAS, KRAS, DOCK8 and genes mediating cell-cell interaction in 13/16 relapse tumors also indicate disturbances in signaling pathways mediating mesenchymal transition. Our data shed first light on genetic alteration frequency, identity and evolution in neuroblastoma.

  Study EGAS00001001387