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• Nanopore whole-genome sequencing of human sarcomas

  We performed single and multi-region nanopore whole-genome sequencing on human sarcoma samples from adult and paediatric patients.

  Study EGAS50000000651

• scRNA-seq of monocultures and co-cultures of PDAC-PDOs and CAFs

  scRNA-seq of monocultures and co-cultures of patient-derived PDAC organoids and matched CAFs. 3 sample sets per patient.

  Dataset EGAD00001009655

• To determine the transcriptional profiles of Ovarian carcinomas (UW cohort)

  Specific BRCA and immune configurations determine optimal response to platinum-based chemotherapy in triple negative breast and ovarian carcinomas (UW_OvCa_RNAseq)

  Study EGAS00001006012

• Multimodal Immune Profiling to Determine Mechanisms of COVID-19 Clinical Trajectory in Uganda

  We conducted a prospective cohort study of adults (RESERVE-U-C19) admitted to Entebbe Regional Referral Hospital (ERRH), a national COVID-19 referral center, across three viral variant-driven phases of the pandemic in Uganda. In this cohort, which reflects the entire spectrum of SARS-CoV-2 infection, we integrated clinical data with serum proteomics (N=306) and whole-blood transcriptomics (N=100) to determine a range of host responses associated with COVID-19 severity, SARS-CoV-2/HIV co-infection, and circulating viral variants. Beyond the prognostic importance of myeloid cell-driven immune activation and lymphopenia, we show that multifaceted impairment of host protein synthesis and extensive redox imbalance define core metabolic signatures of severe COVID-19, with central roles for IL-7, IL-15, and lymphotoxin-α in COVID-19 respiratory failure. While prognostic signatures were generally consistent in SARS-CoV-2/HIV-coinfection, type I interferon responses uniquely scaled with COVID-19 severity in persons living with HIV. Throughout the pandemic, COVID-19 severity peaked during phases dominated by A.23/A.23.1 and Delta B.1.617.2/AY variants, with Delta phase COVID-19 distinguished by exaggerated pro-inflammatory myeloid cell and inflammasome activation, NK and CD8+ T-cell depletion, impaired host protein synthesis, and upregulation of viral cell entry and trafficking pathways. Data from this study available through dbGaP include raw RNA-Seq data from whole-blood of adult participants (N=100).

  Study phs003246

• NIMH (National Institute of Mental Health) De Novo Mutation Identification in Taiwanese Schizophrenia Trios

  The substantial reproductive impact of schizophrenia, for which affected individuals have fewer than half as many offspring as unaffected individuals do, implies that mutations of largest effect will frequently be de novo mutations. Ascertaining exome sequence variation in father-mother-offspring trios allows such mutations to be identified and distinguished from the far-larger amount of rare variation that is inherited by each individual. The pursuit of this approach in a large, well-powered cohort of trios can also provide lessons that inform the development of such gene discovery strategies more generally in human genetics. Schizophrenia trios from the Taiwanese population are being collected by Dr. Ming Tsuang (PI, UC San Diego, California) and investigators in Taiwan (PI, Dr. Hai Gwo Hwu; both funded by NIMH grant 1R01MH085560; Expanding Rapid Ascertainment Networks of Schizophrenia Families in Taiwan). A total of 3800 trios are anticipated to be collected by May 2013. This represents a highly homogenous national sample from the same ancestral population. DNA samples will be obtained from the NIMH Repository, Rutgers University Cell and DNA Repository (described below) and stored at the Broad Institute. Genetic and data analyses will be performed at the Broad Institute. We propose to sequence the whole exome of trios by hybrid capture and Illumina next generation sequencing and perform targeted genotyping and validation of variants (SNPs, indels and CNVs) using several molecular methods, to include emulsion-based PCR and Sanger sequencing.

  Study phs001196

• Enrichment of Lung Microbiome with Supraglottic Taxa which is Associated with Increased Pulmonary Inflammation

  Background: The lung microbiome of healthy individuals frequently harbors oral organisms. Despite evidence that micro-aspiration is commonly associated with smoking-related lung diseases, the effects of lung microbiome enrichment with upper airway taxa on inflammation has not been studied. We hypothesize that the presence of oral microorganisms in the lung microbiome is associated with enhanced pulmonary inflammation. Methods: We sampled bronchoalveolar lavage (BAL) from the lower airways of 29 asymptomatic subjects (9 never-smokers, 14 former-smokers and 6 current-smokers). We quantified, amplified, and sequenced 16S rRNA genes from BAL samples by qPCR and 454 sequencing. Pulmonary inflammation was assessed by exhaled nitric oxide (eNO), BAL lymphocytes and neutrophils. Results: BAL had lower total 16S than supraglottic samples and higher than saline background. Bacterial communities in the lower airway clustered in two distinct groups that we designated as pneumotypes. The rRNA gene concentration and microbial community of the first pneumotype was similar to that of the saline background. The second pneumotype had higher rRNA gene concentration and higher relative abundance of supraglottic-characteristic taxa (SCT), such as Veillonella and Prevotella, and we called it pneumotypeSCT. Smoking had no effect on pneumotype allocation, alpha or beta diversity. PneumotypeSCT was associated with higher BAL lymphocyte-count (p = 0.007), BAL neutrophil-count (p = 0.034) and eNO (p = 0.022). Conclusion: A pneumotype with high relative abundance of supraglottic-characteristic taxa is associated with enhanced subclinical lung inflammation.

  Study phs000633

• Rapid Whole Genome Sequencing for Genetic Disease Diagnosis in Neonatal Intensive Care Units

  Monogenic diseases are frequent causes of neonatal morbidity and mortality, and disease presentations are often undifferentiated at birth. More than 3,500 monogenic diseases have been characterized, but clinical testing is available for only some of them and many feature clinical and genetic heterogeneity. As such, an immense unmet need exists for improved molecular diagnosis in infants. Because disease progression is extremely rapid, albeit heterogeneous, in newborns, molecular diagnoses must occur quickly to be relevant for clinical decision-making. We describe 50-hour differential diagnosis of genetic disorders by whole-genome sequencing (WGS) that features automated bioinformatic analysis and is intended to be a prototype for use in neonatal intensive care units. Retrospective 50-hour WGS identified known molecular diagnoses in two children. Prospective WGS disclosed potential molecular diagnosis of a severe GJB2-related skin disease in one neonate; BRAT1-related lethal neonatal rigidity and multifocal seizure syndrome in another infant, identified BCL9L as a novel, recessive visceral heterotaxy gene (HTX6) in a pedigree, and ruled out known candidate genes in one infants. Sequencing of parents or affected siblings expedited the identification of disease gene in prospective cases. Thus, rapid WGS can potentially broaden and foreshorten differential diagnosis, resulting in fewer empirical treatments and faster progression to genetic and prognostic counseling. Reprinted from Saunders et. al, Rapid Whole-Genome Sequencing for Genetic Disease Diagnosis in Neonatal Intensive Care Units. Sci. Transl. Med. 4, 154ra135 (2012; PMID: 23035047) with permission from AAAS.

  Study phs000564

• LCLF1.0 Data

  In this study, we investigated ad libitum food intake of 20 healthy adult volunteers who each completed a 4-week stay at the National Institutes of Health (NIH). During their stay, they consumed a low-carbohydrate, high-fat (LCHF) diet and a low-fat, high-carbohydrate (LFHC) diet for 2 weeks each, in random order. We collected information about energy intake and metabolic changes in response to the two test diets. The test diets were presented to subjects in amounts exceeding their daily energy requirements, and subjects were instructed to eat as much or as little of each diet as desired. This study implemented 7-day rotating menus for each test diet. The diets were matched for presented calories and protein, but the LCHF diet was low in carbohydrate (~10% of calories) and high in fat (~75% of calories) whereas the LFHC diet was high in carbohydrates (~75% of calories) and low in fat (~10% of calories). The two test diets had a common foundation of vegetables with low amounts of digestible carbohydrates such as lettuce, spinach, kale, cabbage, cauliflower, zucchini, tomato, asparagus, broccoli, peppers, brussels sprouts, and green beans. The LCHF diet included meat, poultry, fish, eggs, dairy, and nuts. The LFHC diet included legumes, rice, root vegetables, soy products, corn, lentils, peas, whole grains, bread, and fruit. The test diets were designed using a standard computerized nutrition database, and blood samples were collected from the subjects.

  Study phs003187

• Identification of RNA biomarkers in Parkinson's disease patients

  Parkinson?s disease (PD) is an age-related, chronic and progressive neurodegenerative disorder characterized by a loss of dopaminergic neurons and subsequent motor symptoms. These overt motor symptoms are often preceded by prodromal non-motor symptoms. Though a number of genetic and environmental factors have been identified to play a role in PD, more exact methods for both diagnosing and assessing prognosis are yet to be discovered. By analyzing the transcriptome of early-stage PD patients, this study aims to identify genes (including important non-coding RNAs) and pathways altered at disease onset that may be used as novel biomarkers for PD diagnosis as well as potential new drug targets. The study consists of three main sources of data: first year blood transcriptomes, second year blood transcriptome and matched neural stem cell (NSC)/neuron transcriptomes. All transcriptome libraries were synthesized and sequenced using no-amplification non-tagging cap analysis of gene expression (nAnT-iCAGE) on the Illumina HiSeq 2500 platform. Resulting data was mapped to the human genome annotation (hg38), processed CAGE tags were clustered ready for differential expression analyses. First year blood sequencing consisted of 22 PD patients and 10 healthy controls across four lanes. In the second year, a further four lanes were sequenced containing 17 PD patients (12 patients from the first year and 5 new patients) along with 10 healthy controls and 5 first year blood samples matching the new second year patients.

  Study JGAS000119

• Relapse CHL study

  Classical Hodgkin Lymphoma (CHL) is characterized by a complex tumor microenvironment (TME) that supports disease progression. While immune cell recruitment by Hodgkin and Reed–Sternberg (HRS) cells is well-documented, the role of non-malignant B cells in relapse remains unclear. Using single-cell RNA sequencing (scRNA-seq) on paired diagnostic and relapsed CHL samples, we identified distinct shifts in B cell populations, particularly an enrichment of naïve B cells and a reduction of memory B cells in early-relapse compared to late-relapse and newly diagnosed CHL. The enrichment of naïve B cells in early relapse biopsies was confirmed in independent validation cohorts using scRNA-seq and immunohistochemistry. Notably, naïve B cells in early-relapse samples exhibited high expression of LGALS9, an immunosuppressive molecule known to interact with T cell immunoglobulin and mucin domain 3 (TIM-3) on regulatory T cells (Tregs). Cell-cell interaction analysis revealed the importance of interactions between LGALS9+ naïve B cells and TIM-3+ Tregs in the early-relapse setting. Spatial analysis by imaging mass cytometry confirmed close proximity of LGALS9+ naïve B cells with TIM-3⁺ CD4⁺ T cells and HRS cells, pointing to their role in shaping an immunosuppressive niche. Our findings highlight a previously unrecognized population of LGALS9⁺ naïve B cells with immunoregulatory potential in early-relapse CHL and provide new insights into the spatial and transcriptional architecture of the relapsed TME in CHL.

  Study EGAS00001008222