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• Prevention and Early Treatment of Acute Lung Injury (PETAL) - Low Tidal Volume Universal Support Feasibility of Recruitment for Interventional Trial (LOTUS FRUIT) (PETAL-LOTUS FRUIT-BioLINCC)

  Data Access NOTE: Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: The two main goals of PETAL-LOTUS FRUIT were to conduct a prospective, observational study within all PETAL Network sites to determine the frequency of and outcomes from acute respiratory failure and the current usual care for tidal volume ventilation in patients with and without acute respiratory distress syndrome (ARDS), and to simulate the design and power of the proposed LOTUS trial. Background: A previous study demonstrated improved survival among patients with ARDS receiving tidal volume (Vt) targeted to 6 ml/kg of predicted body weight (PBW). As a result, low–tidal volume ventilation (LTVV) is now recommended for all patients with ARDS, although penetration of this evidence-based practice has been limited, especially early in mechanical ventilation. LTVV may also benefit patients without ARDS. Consequently, there has been increasing call to apply LTVV for all patients with acute respiratory failure upon initiation of mechanical ventilation. The PETAL Network considered performing a pragmatic stepped-wedge, cluster-randomized, controlled, hybrid implementation trial to examine systematic implementation of a default 6 ml/kg PBW LTVV strategy in patients with acute respiratory failure requiring intubation to improve adherence to LTVV and decrease mortality in acute respiratory failure. Trial planning may be better estimated by simulation than routine, simplistic calculations, but such simulations require detailed data of initial parameters. Participants: 2848 patients from 49 hospitals were enrolled. Enrollment varied by hospital, ranging from 4 to 100 patients, the maximum enrollment allowed per site. Design: PETAL-LOTUS FRUIT was a multicenter, prospective, observational cohort study of patients with acute respiratory failure on mechanical ventilation in the PETAL Network hospitals. For all patients, baseline demographic data, the hospital location, indication for intubation (hypoxemic or hypercapnic respiratory failure or both, altered level of consciousness, or surgery), type of intensive care unit (ICU), and Sequential Organ Failure Assessment score in the first 24 hours after intubation were collected. Baseline ventilator data immediately after intubation, arterial blood gas results and oxygen saturation as measured by pulse oximetry, and presence of ARDS was also collected for all patients. ARDS was defined as a ratio of arterial oxygen tension to fraction of inspired oxygen (FiO2) less than or equal to 300 with a chest radiograph within 24 hours of the qualifying ratio of arterial oxygen tension to FiO2 that had bilateral infiltrates unexplained by mass, collapse, or effusion. For the first 50 patients enrolled at each hospital, daily data on ventilator mode, Vt, and presence of ARDS for the first 3 days after intubation was collected. Vt indexed to PBW was calculated from the set Vt for patients on ventilator mode with volume settings. For patients on pressure ventilation modes, Vt was calculated from the ratio of minute ventilation (in ml/min) to the respiratory rate. Enrolled patients were followed until hospital discharge or 28 days for clinical outcomes including mortality, ventilator-free days, and length of stay. To determine the possible improvement in mortality that could be observed with a reduction in Vt from current usual care in the PETAL-LOTUS FRUIT cohort to 6 ml/kg PBW, mortality was estimated as a function of initial Vt. Five models based on data from three distinct patient populations were used. 500 simulations of a stepped-wedge, cluster-randomized clinical trial using the model with greatest predicted benefit for lowering the Vt to 6 ml/kg PBW in PETAL-LOTUS FRUIT sites were performed. Conclusions: Use of initial tidal volumes less than 8 ml/kg predicted body weight was common at hospitals participating in the PETAL Network. After considering the size and budgetary requirement for a cluster-randomized trial of LTVV versus usual care in acute respiratory failure, the PETAL Network deemed the proposed trial infeasible (PMID: 30407869).

  Study phs003791

• Metabolic and molecular consequences of the TBC1D4 p.Arg684Ter variant in human skeletal muscle

  Skeletal muscle of Inuit homozygous carriers of the common Greenlandic TBC1D4 p.Arg684Ter variant is severely insulin resistant but have normal metabolic responses during exercise

  Dataset EGAD50000000059

• PacBio data: Rapid brain tumor classification from sparse epigenomic data

  This dataset contains 16 samples sequenced in pools on SMRT Cells 25M on a PacBio Revio instrument. One unaligned BAM file per sample is provided.

  Dataset EGAD50000000798

• mFAST-SeqS

  mFAST‑SeqS, or modified Fast Aneuploidy Screening Test‑Sequencing System, is a streamlined and cost-effective approach to estimate the fraction of ctDNA in blood samples by detecting genome-wide aneuploidy in cfDNA

  Dataset EGAD50000001670

• RNA sequencing of AML with 3q26 rearrangements

  RNA sequencing of 44 AML cases with diverse 3q26 rearrangements. This dataset is complementary to EGAD00001000726 (which only contains t(3;3)/inv(3)) and to EGAD00001006123.

  Dataset EGAD00001015629

• Single-cell colony targeted DNAseq

  Targeted DNA sequencing was applied to colonies grown from single-cells of patient A.6. The protocol followed is described in https://doi.org/10.1038/s41467-021-21650-1 and the methods of the manuscript

  Dataset EGAD00001010193

• Strand-specific RNA Sequencing of initial and recurrent gliomas

  Four RNA-sequencing datasets from two patients with initial low-grade glioma and copy number alteration at IDH1 upon recurrence. Data is provided as bam files.

  Dataset EGAD00001003764

• Poikiloderma syndrome RNAseq

  We will sequence the RNA of lymphoblast samples, transformed with EBV, which have poikiloderma syndrome with mutations in c16orf57. The aim of the experiment is to characterise RNA structural effects in this disease.

  Dataset EGAD00001000324

• Chondromyxoid fibroma

  Chondromxoid fibroma is a benign tumour of bone with unknown underlying pathogenesis. To determine pathognomic genomic event in chondromyxoid fibroma whole genome sequencing will be undertaken to reconstruct rearrangements and find underlying mutations.

  Dataset EGAD00001001063

• Exome sequencing of Congenital Heart Disease families Toronto

  The exome sequencing is performed using Agilent SureSelect 50Mb exome v3 and Hiseq 75bp paired reads with an mean sequencing coverage target of 50X.

  Dataset EGAD00001000799

• 300BCG study ATAC-seq data: human population variation of trained immunity

  ATAC-seq dataset for the paper: Title Multi-omics analysis of human population variation in immune function and in vivo response to BCG vaccination Abstract Immune responses are tightly regulated, yet highly variable between individuals. To investigate human population variation of trained immunity, we immunized healthy individuals with Bacillus Calmette-Guérin (BCG). This live attenuated vaccine induces not only an adaptive immune response against tu-berculosis, but also triggers innate immune activation and memory. We established personal immune profiles and chromatin accessibility maps over a time course of BCG vaccination in 323 individuals. This large resource uncovered genetic and epigenetic predictors of baseline immunity and BCG vaccine response. We found that BCG vaccination enhances the innate immune response only in individuals with dormant immune states at baseline, suggesting that exogeneous induction of trained immunity is not a universal booster of innate immunity, but specifically elevates weak innate immune responses. This study advances our understanding of BCG’s heterologous immune-stimulatory effects and trained immunity in humans. Moreover, our results highlight the value of epigenetic cell states as an “endo-phenotype” that connects immune function with genotype and the environment.

  Dataset EGAD50000000123

• Neuroblastoma patient Total RNA Seq data

  Tumor Total RNA Seq data of primary neuroblastomas. This is an update of the „Berlin Neuroblastoma Dataset” (EGAS00001004022). This data was used for the analysis of circular RNA expression and regulation in neuroblastoma.

  Dataset EGAD00001008124

• Somatic mutation and clonal evolution normal breast tissue WGS

  Cancer is a genetic disease caused by an accumulation of mutations, however many of these mutations have been identified in pathologically normal tissue. We aim to use laser-capture microscopy (LCM) to sample individual clones from breast tissue to identify whether cancer-associated mutations appear in this normal tissue, assess the mutational burden present, and identify the mutational processes causing these mutations. We will sample from a wide age range of individuals (<20 to >70 years old) to determine whether these processes differ in pre- and post-menopausal women. We will also be comparing the tissue from healthy individuals (samples from breast reduction surgery) to those at elevated risk of breast cancer (mastectomy from BRCA1/2 patients) and those who have breast cancer (adjacent normal, distal normal, and tumour tissue from mastectomy). This will allow us to determine how these processes are different between these groups of individuals, and gain insight into the earliest stages of tumour development. . This dataset contains all the data available for this study on 2023-03-09.

  Dataset EGAD00001010123

• Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - wgs

  Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

  Dataset EGAD00001011181

• Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - 2mm targeted

  Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

  Dataset EGAD00001011184

• Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - nanoseq

  Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

  Dataset EGAD00001011183

• The mutational landscape of human somatic and germline cells

  During the course of a lifetime normal human cells accumulate mutations. Here, using multiple samples from the same individuals we compared the mutational landscape in 29 anatomical structures from soma and the germline. Two ubiquitous mutational signatures, SBS1 and SBS5/40, accounted for the majority of acquired mutations in most cell types but their absolute and relative contributions varied substantially. SBS18, potentially reflecting oxidative damage, and several additional signatures attributed to exogenous and endogenous exposures contributed mutations to subsets of cell types. The mutation rate was lowest in spermatogonia, the stem cell from which sperm are generated and from which most genetic variation in the human population is thought to originate. This was due to low rates of ubiquitous mutation processes and may be partially attributable to a low cell division rate of basal spermatogonia. The results provide important insights into how mutational processes affect the soma and germline.

  Dataset EGAD00001006641

• Genetic landscape of SMM

  Identifying high risk smoldering myeloma patients and progression mechanism is a prerequisite to implement effective inception strategies and curve myeloma related morbidity and mortality. We hypothesize that genomics may help identify determinants of progression that may help predict outcome and offer effective chemo preventive targets. Eighty-two patients underwent a custom targeted panel sequencing with an additional capture for the translocation loci. These results were compared to 223 newly diagnosed patients (EGAS00001003223 and EGAD00001004117) and 17 MGUS and 10 early myeloma patients. DNA was obtained from either CD138+ cells from the bone marrow of multiple myeloma patients (tumor) or from stem cell harvests or peripheral blood cells from the same patient (control). 100 ng of DNA was fragmented, end-repaired, and adapters ligated using the HyperPlus kit (KAPA Biosystems). After PCR amplification the libraries were hybridized with probes against either a targeted panel consisting of 140 genes and chromosomal regions (Nimblegen) using SeqCap reagents (Nimblegen). Hybridized libraries underwent further amplification before being sequenced on a NextSeq500 (Illumina) using 75 bp paired end reads. Overall, these data highlight the importance of dysregulation of the MAPK pathway in the progression to MM.

  Dataset EGAD00001005285

• Somatic mutation and clonal evolution normal breast tissue TGS (2020-01-15)

  Cancer is a genetic disease caused by an accumulation of mutations, however many of these mutations have been identified in pathologically normal tissue. We aim to use laser-capture microscopy (LCM) to sample individual clones from breast tissue to identify whether cancer-associated mutations appear in this normal tissue, assess the mutational burden present, and identify the mutational processes causing these mutations. We will sample from a wide age range of individuals (<20 to >70 years old) to determine whether these processes differ in pre- and post-menopausal women. We will also be comparing the tissue from healthy individuals (samples from breast reduction surgery) to those at elevated risk of breast cancer (mastectomy from BRCA1/2 patients) and those who have breast cancer (adjacent normal, distal normal, and tumour tissue from mastectomy). This will allow us to determine how these processes are different between these groups of individuals, and gain insight into the earliest stages of tumour development. . This dataset contains all the data available for this study on 2020-01-15.

  Dataset EGAD00001005787

• Rapid Acceleration of Diagnostics - Underserved Populations (RADx-UP): COVID-19 Testing and Prevention in Correctional Settings

  This study will work with diverse correctional facilities across MN, RI, WA, and FL to characterize the incidence of COVID-19 disease progression and related outcomes. The goal is to identify barriers and facilitators to develop strategies to improve testing in these under-served populations by: Increasing the reach, access, uptake, and impact of COVID-19 testing among incarcerated people and staff in prison and jails. Individuals in congregate settings have been disproportionately affected by COVID-19, with correctional settings accounting for 39 of the 50 largest cluster outbreaks in the country to date. Schema of Correctional Facilities: Correctional facilities are amplifiers of infectious diseases for structural reasons: 1) Dormitory-style living and overcrowded conditions make social distancing nearly impossible 2) They have a focus primarily on security not health 3) Their medical departments are under-resourced and often disconnected from local public health agencies. Correctional facilities must be the focus of urgent intervention to understand the incidence of COVID-19, how it spreads in correctional facilities, and durable long-term strategies to reduce transmission, including testing and vaccines. However, our work from the COVID Prison Project shows that correctional systems have implemented a range of testing strategies, without coordination, such that synthesizing the information on COVID-19 incidence, outcomes and optimal testing strategies (including repeat testing and contact tracing) has been challenging. Incarcerated people decline testing due to concerns about confidentiality, implications for release, and fear of placement in solitary confinement. Through interviews we will identify ethical concerns and potential solutions for COVID-19 testing and vaccine strategies in correctional facilities using a community-engaged strategy. The project's work from the COVID Prison Project shows that correctional systems have implemented a range of testing strategies, without coordination, such that synthesizing the information on COVID-19 incidence, outcomes and optimal testing strategies (including repeat testing and contact tracing) has been challenging. Incarcerated people decline testing due to concerns about confidentiality, implications for release, and fear of placement in solitary confinement. Through interviews we will Identify ethical concerns and potential solutions for COVID-19 testing and vaccine strategies in correctional facilities using a community-engaged strategy. Goals: 1. Identify ethical concerns and potential solutions for COVID-19 testing and vaccine strategies in correctional facilities using a community-engaged strategy. 2. Characterize incidence of COVID-19, disease progression, and related-outcomes and effectiveness of testing and contact tracing in correctional facilities. Participant Selection: a. Potential subjects must be currently incarcerated at key facilities in Washington, Rhode Island, Minnesota, and Florida. These facilities are Everglades Correctional Institution and Homestead Correctional Institution in Florida, Shakopee and Stillwater correctional facilities in Minnesota, the Rhode Island Department of Corrections, and Yakima County Jail in Washington. b. Participating correctional facilities in Florida, Minnesota, Rhode Island, and Washington will provide de-identified data on approximately 16,859 incarcerated adults and correctional staff. Data sources include deidentified data from medical records, administrative data, and policy documents pertaining to COVID-19. c. 3 series of focus groups (6, 12, 18 months) x 3 distinct groups (incarcerated people, medical providers, and correctional leaders) x 4 sites=36 total focus groups over the study period. d. Will utilize 74,812 COVID-19 tests to test and re-test a total of 16,859 incarcerated people and correctional staff for active infection over a six-month period in the FL, MN, and RI state prison systems and the Yakima County Jail in WA.

  Study phs003361

• Starr County Health Studies' Genetics of Diabetes Study

  An initial observation in the 1970s that Starr County, Texas, had the highest diabetes-specific mortality of any of the 254 Texas counties led to the establishment of a field office in Rio Grande City, Texas (the county seat of Starr County) and the initiation of a series of studies to understand the epidemiology and genetics of type 2 diabetes, its complications and related conditions in this predominantly (97%) Mexican American population. The field office opened in February 1981 and has operated continuously since then. During this time, three systematic surveys of the population have been conducted as well as family and longitudinal studies. Culturally sensitive diabetes education programs have been developed and implemented and also a weight loss intervention. In total, more than 23,000 Mexican American individuals have been examined with more than 200,000 aliquots of biological specimens stored. Collectively, these studies are known as the Starr County Health Studies. The present Genetics of Diabetes Study has the goal of identifying loci/alleles that underlie susceptibility to type 2 diabetes in this high risk population using genome wide markers and association testing. The study makes use of two primary resources that have been developed in order to identify 1,000 type 2 diabetes cases and 1,000 disease free controls. In the first instance we have identified a subset of unrelated cases from the total cases that we have identified. Where multiply affected sibships were available, the youngest onset case with detailed phenotyping (including assessment of diabetic retinopathy) was selected. Controls came from a recent survey to establish a representative sample of the Starr County population. Blocks were randomly selected, households on selected blocks enumerated and one individual randomly selected from each household for a detailed examination. The examination included an oral glucose tolerance test. Those included as controls are those with no prior diagnosis of diabetes and a negative oral glucose tolerance test. This collection of cases and controls provides the opportunity to identify susceptibility loci for type 2 diabetes and its complications, specifically diabetic retinopathy and albuminuria. The data set also allows the examination of impaired fasting glucose and impaired glucose tolerance. The samples are split between those born in the United States and those born in Mexico and this gives a natural contrast for examining genotype and environmental interactions. It is anticipated that the understanding that will come will lead to strategies for delaying and preventing the onset of diabetes and its complications.

  Study phs000143

• Framingham Heart Study-Cohort (FHS-Cohort) - Imaging

  The Framingham Heart Study (FHS) is a population-based, observational cohort study initiated in 1948 to prospectively investigate the determinants of cardiovascular disease to guide public health prevention. The FHS began by recruiting an Original Cohort of 5,209 men and women between the ages of 30 and 62 from the town of Framingham, Massachusetts, who had not yet developed overt symptoms of cardiovascular disease or suffered a heart attack or stroke. The Original cohort Exam 1 took place between 1948 and 1953. Since that time the cohort has had a total of 32 biennial exams (ending in 2014) and event follow-up through 2022. In 1971, the FHS added the Offspring cohort, comprising 5124 children whose parents were enrolled in the Original cohort and the spouses of the children. This cohort on average has been examined every three to four years. However, there was an eight year gap between Exam 1 and Exam 2 and a seven year gap between Exam 7 and Exam 8. The latest exam (10) was completed in 2022. In 2002, the transgenerational FHS design was facilitated with the recruitment of 4095 children of the Offspring cohort (Third Generation), and 103 spouses of the Offspring who were not previously enrolled in the study (New Offspring Spouses, NOS). These cohorts have completed 3 exams through 2019. To reflect the changing demographic characteristics of the greater Framingham community, the FHS additionally recruited and enrolled 2 cohorts comprising racial and ethnic minority groups, termed Omni-1 and Omni-2, (n = 506 and 410, respectively) in 1995 and 2002, respectively. These cohorts included individuals of African American, Hispanic, Asian, Indian, Native American, and Pacific Islander descent. The OMNI-1 cohort have completed 5 exams through 2022. The OMNI-2 cohort have completed 3 exams through 2019. Data available for request include Echocardiogram images, available from the following exams in each cohort. Original Cohort: exams 18-32; Offspring cohort: exams 3-10; Third Generation, NOS and OMNI-2 cohorts: exams 1-3; OMNI-1 cohort: exams 1-5.CT image data at one or two timepoints were added for 4427 participants in the offspring, third generation, and OMNI1 and OMNI2 cohorts.Summary level phenotypes for the Framingham Cohort study participants can be viewed at the top-level study page phs000007 Framingham Cohort. Individual level phenotype data and molecular data for all Framingham top-level study and substudies are available by requesting Authorized Access to the Framingham Cohort study phs000007.

  Study phs003593

• Homozygous inactivation of CHEK2 is linked to a familial case of multiple primary lung cancer with accompanying cancers in other organs

  In clinical practice, there are a number of cancer patients with clear family histories, but not belonging to existing familial malignancies. Recent advances in genomic technologies have enhanced the possibility of identifying causative genes in such cases. Two siblings, an elder sister and a younger brother, were found to have multiple primary lung cancers at the age of 60. The former subsequently developed breast cancer, and had a history of myoma uteri. The latter had initially developed prostate cancer at the age of 59, and had a history of colon cancer. SNP genotyping revealed that approximately 10% of the genomes were homozygous in both patients. Exome sequencing revealed non-synonymous mutations in four genes in the runs of homozygosity: CHEK2, FCGRT, INPP5J, and SFI1. Evolutionary conservation of primary protein structures suggested the functional importance of the CHEK2 mutation, R474C. This mutation altered the tertiary structure of CHK2 by disrupting the salt bridge between R474 and E394. No such structural changes were observed with the other three mutated genes. Subsequent cell-based transfection analysis revealed that CHK2 R474C was unstable and scarcely activated. We concluded that CHEK2 is a causative gene in this case of familial cancer. Although homozygous inactivation of CHEK2 in mice led to cancers in multiple organs, accumulation of additional human cases is needed to establish its pathogenic role in humans.

  Study JGAS000057

• Exome sequencing in HIV+ Viremic Non-Progressors (VNPs) and HIV+ Progressors

  This dataset contains 184 paired fastq files sequences with Illumina NovaSeq600 from 38 participants. Relevant clinical and demographical data is also included.

  Dataset EGAD50000000111

• WGS of Biobank iPSC lines

  WGS data from healthy reference iPSC lines. The median coverage is 41-50x. >85% have a coverage of >30x. 97% of the variants are known.

  Dataset EGAD00001008769