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• HiChIP bulk

  This dataset gather HiChIP data for H3K27ac mar in MM.1S cell line in control and Dex condition, both in two biological replicates

  Dataset EGAD00001011138

• Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - RNA-Seq

  This study aims to investigate the dysregulation of RNA translation and identify functional non-canonical open reading frames (ORFs) as potential targets for medulloblastoma treatment. The study involves ribosome profiling and RNAseq of medulloblastoma tissues and cell lines to observe the translation of non-canonical ORFs. Multiple CRISPR-Cas9 screens will be used to identify functional non-canonical ORFs implicated in medulloblastoma cell survival.

  Dataset EGAD00001011192

• Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - Ribo-Seq

  This study aims to investigate the dysregulation of RNA translation and identify functional non-canonical open reading frames (ORFs) as potential targets for medulloblastoma treatment. The study involves ribosome profiling and RNAseq of medulloblastoma tissues and cell lines to observe the translation of non-canonical ORFs. Multiple CRISPR-Cas9 screens will be used to identify functional non-canonical ORFs implicated in medulloblastoma cell survival.

  Dataset EGAD00001011193

• ATAC-Seq/Hi-C/4C-Seq dataset for Malignant rhabdoid study

  Study describing the dynamics of chromatin organization within malignant rhabdoid tumors. This study describes how this chromatin organization changes upon SMARCB1 rescue within patient-derived organoid models from malignant rhabdoid tumors. Identification of a novel super-enhancer of MYC and identification of patient-specific enhancer utilization to activate MYC expression in these tumors.

  Dataset EGAD00001011820

• V(D)J and 5' Gene Expression data of bone marrow cells from patients with aplastic anemia

  Viably frozen blood MNCs from 9 cGVHD patients were sorted with BD Influx Cell sorter, to enrich for CD45+ cells. Gene and V(D)J transcript profiles were studied with 10x Genomics Chromium Single Cell Immune Profiling platform. The Chromium Single Cell 5’RNAseq run and library preparation were done using the Chromium Next GEM Single Cell Immune Profiling version 1.1 chemistry. The raw data was processed using Cell Ranger v3.1 pipelines.

  Dataset EGAD00001012117

• Comprehensive Deep Sequencing Atlas in HCC tumors

  The atlas aims to unravel the intricate genetic landscape of HCC, providing a detailed characterization of genomic alterations, transcriptomic profiles, and key mutations associated with liver tumors. The integration of WGS, RNAseq, and WES data offers a holistic perspective, facilitating a deeper understanding of the molecular mechanisms driving HCC pathogenesis. The resulting atlas serves as a valuable resource for researchers, clinicians, and the broader scientific community, contributing to advancements in HCC diagnostics, prognostics, and therapeutic interventions.

  Dataset EGAD00001015343

• ICU transcriptomics: Assessing the role of the host immune response in patients with ventilator-associated pneumonia

  This is a study of 100 patients with the aim to provide transcriptomic sequencing data analysis of cells isolated from bronchioalveolar lavage and blood samples from critically ill patients with pneumonia on an intensive care unit in order to investigate the host contribution to disease. 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/

  Dataset EGAD00001015407

• Whole-genome sequencing of rhabdomyosarcoma tumouroids (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the whole-genome sequencing of RMS tumoroids data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015707

• Single-cell RNA-sequencing of rhabdomyosarcoma tumouroids (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the single-cell RNA sequencing of RMS tumouroids data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015708

• Whole Genome-sequencing of rhabdomyosarcoma tumour tissue (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the whole-genome sequencing of RMS tumours data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015709

• Bulk RNA-sequencing of rhabdomyosarcoma tumour tissue (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the bulk RNA sequencing of RMS tumours data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015714

• Whole Genome-sequencing of rhabdomyosarcoma tumour tissue (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the whole-genome sequencing of RMS tumours data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015716

• Bulk RNA-sequencing of rhabdomyosarcoma tumour tissue (2025-09-30)

  This study investigates high-risk rhabdomyosarcoma (RMS) using multiple single-cell and spatial genomic technologies. We generated and analysed single-cell and single-nucleus RNA-sequencing, chromatin accessibility, and spatial transcriptomics data from primary tumours and validation samples. These datasets characterise cellular diversity within rhabdomyosarcoma and identify cell states associated with aggressive disease. The data support research into tumour biology, risk stratification, and therapeutic target discovery. This repository houses the bulk RNA sequencing of RMS tumours data. . This dataset contains all the data available for this study on 2025-09-30.

  Dataset EGAD00001015718

• BLUEPRINT September 2016, ChIPmentation Activated B-Cell-Like Diffuse Large B-Cell Lymphoma from lymph node, on Genome GRCh38

  ChIPmentation data for 2 sample(s) Activated B-Cell-Like Diffuse Large B-Cell Lymphoma from lymph node, on Genome GRCh38. 3 run(s), 3 experiment(s), 3 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002944

• BLUEPRINT September 2016, ChIPmentation Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma from lymph node, on Genome GRCh38

  ChIPmentation data for 2 sample(s) Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma from lymph node, on Genome GRCh38. 6 run(s), 6 experiment(s), 6 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002946

• BLUEPRINT September 2016, ChIP-Seq T-cell Acute Lymphocytic Leukemia from capillary blood, on Genome GRCh38

  ChIP-Seq data for 4 sample(s) T-cell Acute Lymphocytic Leukemia from capillary blood, on Genome GRCh38. 7 run(s), 7 experiment(s), 7 alignment(s). Part of BLUEPRINT (September 2016).Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_chipseq_analysis_ebi_20140811

  Dataset EGAD00001002952

• Whole-genome and transcriptome sequencing of NUT midline carcinoma

  In this study, we sequenced three NUT midline carcinoma genomes and their transcriptomes (NMC1, NMC2 and Ty-82), and two paired normal blood samples (for NMC1 and NMC2). Whole-genome sequencing libraries were generated by PCR-free methods, and sequencing run was made in HiSeq X machines. Transcriptome (mRNA) sequencing was performed in HiSeq 2500 machines. PCR duplicates-marked, indel-realigned, and base-recalibrarted BAM files are provided in our dataset.

  Dataset EGAD00001003117

• Smith-Lemli-Opitz Syndrome: A Longitudinal Clinical Study of Patients Receiving Cholesterol Supplementation

  Smith-Lemli-Opitz syndrome (SLOS) is a disorder of cholesterol production by the body. It is caused by changes in the DHCR7 gene, which is the blueprint for an enzyme called 7-dehydrocholesterol- delta7-reductase. This enzyme is necessary for the production of cholesterol by all cells in the body. People with SLOS often have malformations of major organs, slow growth, feeding difficulties and intellectual disability or learning problems. Because patients with SLOS cannot make enough cholesterol, it has been proposed that cholesterol supplementation (either with egg yolk or liquid suspensions of cholesterol) could help improve the symptoms of the disease. However, despite the widespread use of cholesterol supplementation, it is still not known whether it works or not. The study will try to provide an answer to this question by studying the disease and its progression while patients are receiving cholesterol. The clinical features of SLOS are thought to be related to low cholesterol and buildup of toxic cholesterol precursors (substances from which cholesterol is formed). But how exactly low cholesterol and toxic precursors contribute to the disease is poorly understood. This knowledge is critically important because it should help discover new therapeutic targets and develop treatments of the disease in the long run. The study will try to fill this gap with a comprehensive clinical and biochemical testing of the study participants over the course of several years. Last, a limitation of previous SLOS research studies has been their low number of participants. This is understandable because SLOS is a rare diseases and few research groups are working on it. However, in order to fully understand the disease, researchers need to study as many patients as possible. This study is unique in that it is run by a network of several highly specialized clinical research sites across the country. Having several sites involved increases the researcher's ability to recruit and study large number of patients, and centralize patients' information in a comprehensive SLOS clinical registry. This registry will be key to identify markers for diagnostic testing, screening and measuring outcomes in future studies of treatment. The purpose of this study is to learn as much as possible about Smith-Lemli-Opitz Syndrome (SLOS) by following a large group of affected children and adults over time. In this study, we will measure cholesterol and other similar chemicals in blood and urine, evaluate development and behavior, do limited medical evaluation, and carry out brain imaging studies.This study will help researchers: learn more about what causes SLOS and how SLOS changes with age, note differences in features of SLOS among those affected, evaluate the effect of giving extra cholesterol in this condition, and develop ways to evaluate whether treatments developed in the future will be helpful.

  Study phs001430

• The Human Virome in Children and its Relationship to Febrile Illness

  Definition of the human microbiome is an important scientific priority. This study will expand the scope of the investigation to include viruses, which account for a substantial proportion of infectious disease morbidity and mortality, especially in children. The long-term goal of this project is to describe the human virome in children and to investigate its relevance to febrile illnesses in children. The project will also seek to understand the relationship of the immune system to the composition of the virome. Thus, the project's specific aims are 1) To elucidate the spectrum of viruses that can be detected using non-biased, high throughput sequencing on samples of blood, respiratory, and gastrointestinal secretions from healthy children and to use this information as a basis for understanding the role of viruses in acute febrile illnesses without an obvious source, and 2) to investigate the effect of various forms of immunosuppression on the spectrum of viruses detected in children, and to use this information as a basis for understanding the role of viruses in acute febrile illnesses occurring in these children. Our preliminary studies show that diverse viruses can be detected in children having undiagnosed fever. To carry out the specific aims, well children will be enrolled prior to having elective surgery, and febrile otherwise well children will be enrolled from the Emergency Department at St. Louis Children's Hospital. Immunocompromised children will be recruited from hematopoietic stem cell and solid organ transplant clinics, the HIV/AIDS clinic, and the rheumatology/immunology clinic from the same hospital. Children with fever will have samples obtained at the time of the febrile illness and at 1 and 6-month follow-up visits. Selected samples from each study group will be analyzed at the Genome Center at Washington University (GCWU) using next generation 454 high throughput sequencing to detect and sequence all viral sequences present. We anticipate detecting and sequencing a broad range of viruses, including previously unrecognized agents. A variety of techniques will be used to investigate the significance of viruses detected. Virus-specific PCR assays will be used to determine the frequency and extent of viruses detected by sequencing, using the full range of samples collected. Host response to the detected viruses will be investigated using serologic analysis, cytokine profiling, and microarrays to characterize host gene expression. These studies will take advantage of follow-up samples to compare the acute response with the response in the convalescent period. This study will draw upon the expertise and technological assets of one of the world's most powerful sequencing centers to provide the research community with a comprehensive sequence data base of the viruses that are present in children, which can be used to improve our understanding of the causes of febrile illnesses in young children, many of which are currently undiagnosed.

  Study phs000264

• Coagulation and Fibrinolysis in a Pediatric Insulin Titration Trial

  Summary of the Design and Aims: The Coagulation and Fibrinolysis in a Pediatric Insulin Titration Trial (CAF-PINT) is an ancillary study to the HALF PINT (NCT01565941) randomized, controlled trial that was originally designed to study changes in inflammatory and thrombosis pathways in the setting of an interventional trial. The parent HALF PINT study was designed to study the impact of tight glycemic control (TGC) using an explicit insulin titration algorithm to safely achieve a normal glucose in target range of 80-110 mg/dL versus 150-180mg/dL on clinical outcomes among critically ill hyperglycemic children with Heart and Lung Failure. The CAF PINT study collected blood samples pre randomization and at 2 and 4 days after randomization. Blood samples collected in EDTA tubes were centrifuged at local sites to separate the plasma from cell pellets and frozen prior to shipment. In addition, 0.5 mL of whole blood collected in PAXgene tubes modified for use in pediatrics frozen 24 hours after collection prior to shipment.Population Information: Setting: Twenty-one academic children's hospitals (HALF-PINT) and 1 academic children's hospital (IIT-SBPP). Participants: Critically ill hyperglycemic children requiring mechanical ventilation/vasoactive support (n=293).Interventions and Exposures: Patients in HALF PINT were randomized to achieve a low target glucose (80-110 mg/dL) vs. a higher target (150-180 mg/dL). The primary trial was stopped early due to low likelihood of achieving a statistically significant difference in the primary outcomes. Molecular Technologies Employed: Plasma biomarkers were assayed on thawed plasma using a Luminex panel. RNA was extracted from PAXgene Blood RNA Kits modified for pediatric use. Extracted RNA was sequenced with the Novaseq S4 system (Illumina) to generate 2 x 150 base paired end reads to a target depth of 50 million read-pairs per sample.Principal Findings of the Study: We tested for heterogeneity of treatment effects according to baseline blood inflammatory proteins using logistic regression with individual biomarkers as interaction terms and Cox regression analysis using biomarker-derived latent classes. Children with higher inflammatory proteins including TNFR-1, IL-6, IL-8, and IL-10 had lower mortality when treated with insulin to a target glucose of 80-110 mg/dL as compared to 150-180 mg/dL (interaction p<0.05). Causal forest estimates ranged from a 40% mortality reduction to a 15% mortality increase with TGC, depending on each patient’s individual biomarker profile. Latent class categorization strongly interacted with TGC with respect to mortality (Cox regression interaction p=0.005). Specifically, patients with higher inflammation benefited from TGC (6% mortality with TGC vs. 48% mortality, p=0.004) whereas hypoinflamed patients showed a trend towards harm (14% mortality with TGC vs. 7% mortality, p=0.055).Data available through dbGaP: Transcriptomic (Gene Counts) and phenotype data

  Study phs003016

• Acute Respiratory Distress Network (ARDSNet) Study 04 Assessment of Low Tidal Volume and Elevated End-Expiratory Volume to Obviate Lung Injury (ALVEOLI-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. BiospecimensAccess to Biospecimens is through the NHLBI Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC). Biospecimens from ARDSNet-ALVEOLI include Plasma and DNA. Please note that use of biospecimens in genetic research is subject to a tiered consent. Available Data Outcome data regarding organ failure free days are not available. Objectives The ARDS Network is a consortium of clinical centers and a coordinating center to design and test novel therapies for the treatment of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS). The ARDS Network 01/03 trials included an investigation of the efficacy and safety of Ketoconazole and Respiratory Management in the treatment of ALI and ARDS (KARMA). The Ketoconazole arm of the KARMA study was later stopped due to an inability to show efficacy. Participants continued to be randomized to the respiratory management arms of the study (ARMA), which compared two ventilator strategies: a tidal volume of 6 mL/kg versus 12 mL/kg. The LARMA phase of the study investigated the efficacy of Lisofylline and Respiratory Management. The objective of the ALVEOLI study was to compare clinical outcomes of participants with ALI and ARDS treated with a higher end-expiratory lung volume/lower FiO2 versus a lower end-expiratory lung volume/higher FiO2 ventilation strategy. The ALVEOLI study tested the hypothesis that mortality from ALI and ARDS would be reduced with a mechanical ventilation strategy designed to prevent lung injury from repeated collapse of bronchioles and alveoli at end-expiration. Background Most participants requiring mechanical ventilation for ALI and ARDS receive positive end-expiratory pressure (PEEP) of 5 to 12 cm of water. Higher PEEP levels may improve oxygenation and reduce ventilator-induced lung injury but may also cause circulatory depression and lung injury from overdistention. PEEP levels higher than traditional levels may reduce ventilator-induced lung injury by decreasing the proportion of nonaerated lung and higher PEEP levels may allow arterial-oxygenation goals to be met at a lower level of inspired oxygen (FiO2). Participants A total of 550 participants were randomized to receive mechanical ventilation with either lower or higher PEEP levels, which were set according to different tables of predetermined combinations of PEEP and fraction of inspired oxygen. Conclusions Participants with acute lung injury and ARDS who receive mechanical ventilation with a tidal-volume goal of 6 ml per kilogram of predicted body weight and an end-inspiratory plateau-pressure limit of 30 cm of water, clinical outcomes were statistically similar whether lower or higher PEEP levels are used. (Brower, et al., 1004; PMID: 15269312).

  Study phs003714

• Combined Tumor and Immune Signals From Genomes or Transcriptomes Predict Outcomes of Checkpoint Inhibition in Melanoma

  Cancer immunotherapy with checkpoint blockade (CPB) leads to improved outcomes in melanoma and other tumor types, but a majority of patients do not respond. High tumor mutation burden (TMB) and high levels of tumor-infiltrating T cells have been associated with response to immunotherapy, and integrative models using DNA and RNA have improved predictions of clinical benefit. However, identification of immune and tumor-intrinsic features in models using DNA or RNA alone have not been comprehensively explored in melanoma. In this study, we sequenced DNA and RNA of tumors from 67 melanoma patients receiving CPB, and aggregated this cohort with previously published data, yielding whole exome sequencing (WES) data for 189 patients and bulk RNA sequencing data for 178 patients. Using these datasets, we derived genomic and transcriptomic factors that predict overall survival (OS) and response to immunotherapy. Using whole exome DNA data alone, we calculated T cell burden (TCB) and B cell burden (BCB) based on rearranged TCR/Ig DNA sequences, and found that melanoma patients with high TMB and either high TCB or high BCB survived longer and had higher response rates, as compared to patients with low TMB and either low TCB or low BCB. Next, using bulk RNA-Seq data, differential expression analysis identified 83 genes which are associated with high or low OS. By combining pairs of immune-expressed genes with tumor-expressed genes, we identified three gene pairs which are associated with response and survival (Bonferroni P<0.05). All three gene pair models were validated in an independent cohort (n=180) (Bonferroni P<0.05). The best performing gene pair model included the lymphocyte-expressed MAP4K1 (Gene ID: 11184) and the transcription factor TBX3 (Gene ID: 6926) which is overexpressed in poorly differentiated melanomas. We concluded that RNA-based (MAP4K1 and TBX3) or DNA-based (TCB and TMB) models combining with immune and tumor measures improve predictions of outcome after checkpoint blockade in melanoma.

  Study phs002683

• Genetic Analysis of the Chiari I Malformation

  This study used whole exome sequencing (WES) on families affected with Chiari I Malformation (CM1). Individuals were recruited from the Republic of Tartarstan in the Russian Federation, where CM1 has a high prevalence (approximately 413 out of 100,000). At least one-third of these affected individuals have an affected relative. In collaboration with Dr. Enver Bogdanov of Kazan State Medical University, seven extended families affected with CM1 were identified. Eligible participants for this study were required to 1) have CM1 and a family member with syringomyelia or CM1, or 2) be a family member of a patient with CM1 and have at least two immediate family members diagnosed with CM1. Adults and minors were eligible for this study and recruitment was through self and physician referral. Patients were excluded if they had a contraindication to MRI scanning, were unable to understand the risks of testing, were under one year of age, or could not undergo MRI scanning without sedation. Study participants underwent SPGR (Spoiled Gradient Recalled) and T1-weighted MR-imaging of the brain and cervical spinal cord to assess the volume of the posterior fossa, as well as the presence of CM1. Individuals were defined as having CM1 if the inferior aspect of the cerebellar tonsils were lying ≥=2 mm caudal to the foramen magnum. Individuals were defined as having a small posterior fossa volume if the ratio of the posterior fossa volume to the supratentorial volume was < 0.15. Sixty-two patients (both cases and controls) from the seven extended families had DNA extracted from blood lymphocytes contained in 10 milliliters of stored blood. Whole exome sequencing (WES) was performed by the National Intramural Sequencing Center (NISC). These genotype data, as well as the case-control phenotype data on CM1 diagnosis and small posterior fossa diagnosis, were made available to dbGaP.

  Study phs001795

• Effect of the Placental Transcriptome on Stunting in a Longitudinal African Cohort

  Mammals with placentas and flowering plants evolved genomic imprinting in nutritive tissues, the placenta and endosperm, respectively. In these tissues, the genomes inherited from the mother and father are in conflict over resource allocation to offspring. In imprinted genes, transcription is repressed on the paternal or the maternal allele, resulting in allele specific expression (ASE). We investigated the variation in ASE of imprinted genes in term human placentas in order to detect loss of imprinting (LOI), which leads to partial expression of the repressed allele. We collected the placental tissue from birth to women in our multigenerational, prospective cohort study in Mali, West Africa. We followed the women from their own infancies, early childhood to adulthood (age 18+ years). Contingent on prior informed consent, we collected placental tissue and umbilical cord tissue. We conducted RNA-Seq of the fetal compartment of the placentas and targeted DNA-Seq of the umbilical cord tissue, which is fetal, and of saliva samples from parents. Our sequencing effort produced two datasets. The first dataset is the whole transcriptome RNA-Seq dataset of 111 biopsies (59 placentas) and genotyping of 96 genes. Birth length, weight, and placental weight for the children associated with this dataset are listed in the phenotype file (DOI: 10.1093/molbev/msz226). The second dataset includes targeted RNA-Seq of 262 samples (251 placentas) and targeted DNA-Seq for 766 genes. The genes were selected because they met any one of the following criteria: (1) imprinted and reported in some studies, (2) highly expressed in placenta, or (3) relevant to diseases of interest in this cohort (https://doi.org/10.1093/g3journal/jkab176). This study provides the first systematic analysis of variation in LOI across genes and individuals in a human population, and should shed light on the hypothesis that the modulation of imprinting is an epigenetic mechanism and plays a role in the regulation of offspring growth.

  Study phs001782

• Global Microbiome Conservancy Sequence Data

  The human body is a complex ecosystem, hosting tens of billions of bacteria, primarily in the gut. This community, known as the 'gut microbiome', is vital to human health, affecting functions ranging from metabolism, immunity, and development, to behavior. Conversely, reduced microbiome diversity and other imbalances of the gut community (dysbiosis) are associated with many diseases of the industrialized world, such as metabolic syndrome, asthma, and inflammatory bowel diseases among others. Microbiome-based interventions thus hold the potential to revolutionize our understanding of, and therapeutic approaches to, many aspects of human health and disease. Despite many advances, current understanding of the human microbiome is largely limited to majority ethnic groups in industrialized nations, and does not reflect the full diversity of human commensal microbiota. In addition to the scientific ramifications of minority underrepresentation, there are significant translational and ethical implications as well: first, failing to capture the full diversity of healthy human microbiota may limit our ability to understand and generate effective therapeutics for many microbiome-associated diseases. Second, underrepresented groups are less likely to benefit from microbiome-based medical advances tailored to well-studied populations, propagating healthcare inequities.  Human gut microbial diversity is diminishing around the globe, due to the spread of industrialized diets and lifestyles, which are associated with reduced microbiome biodiversity. The Global Microbiome Conservancy (GMbC) is a non-profit collaboration between scientists and communities around the world that aims to 1) preserve the full biodiversity of the human gut microbiome, 2) characterize its evolution across populations and host lifestyles and 3) investigate its interactions with the human host. We are collecting gut microbiome and human DNA samples from diverse populations around the world, from isolated groups to urbanized populations, to culture and study this essential biodiversity and to preserve it in a living "seed bank" of bacterial isolates as a long-term safeguard against future extinctions. Human genetic data for the samples sequenced in this study can be found in phs002205.

  Study phs002235