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• Idiopathic Pulmonary Fibrosis Network (IPFnet) Prednisone, Azathioprine, and N-Acetylcysteine: A Study That Evaluates Response in Idiopathic Pulmonary Fibrosis (IPFNet-Panther-IPF-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 initial objective of the PANTHER-IPF study was to evaluate the effectiveness of a drug combination of prednisone, azathioprine, and N-acetylcysteine in the treatment of mild-to-moderate idiopathic pulmonary fibrosis (IPF) compared to N-acetylcysteine alone or placebo. After interim analysis presented safety concerns regarding the three drug regimen, the protocol was modified to evaluate only N-acetylcysteine effectiveness. Background: IPF is a chronic, progressive lung disease of unknown cause that is characterized by the histopathological or radiologic patterns of usual interstitial pneumonia in a typical clinical setting. The median survival of participants with idiopathic pulmonary fibrosis after diagnosis is 2 to 5 years. To date, no pharmacologic therapies have been shown to improve survival. Acetylcysteine has been suggested as a beneficial treatment for idiopathic pulmonary fibrosis, although data from placebo-controlled studies are lacking.Design: Patients with mild-to-moderate impairment in pulmonary function were randomly assigned to receive a three-drug regimen (prednisone, azathioprine, and acetylcysteine), acetylcysteine alone (plus matched placebos for prednisone and azathioprine), or matched placebos for each of the active therapies. After the planned midpoint interim analysis, the data and safety monitoring board recommended discontinuation of the three-drug regimen because of an excess in the number of deaths, hospitalizations, and serious adverse events among patients in the combination-therapy group, as compared with the placebo group. After NHLBI accepted this recommendation on October 14, 2011, the three-drug regimen was discontinued and patients were recruited for only the acetylcysteine group and the placebo group. Patients were seen at the clinical centers for screening, at baseline, and at 4, 15, 30, 45, and 60 weeks. The primary outcome measure was change in FVC over 60 weeks.Conclusions: As compared with placebo, acetylcysteine offered no significant benefit with respect to the preservation of FVC in patients with idiopathic pulmonary fibrosis with mild-to-moderate impairment in lung function. In addition, there were no significant differences between the acetylcysteine group and the placebo group in the rates of death or acute exacerbation.

  Study phs004071

• Conjunctival fibrosis and the innate barriers to Chlamydia trachomatis intracellular infection: a genome wide association study

  This data comes from a genome-wide association study in 1090 cases of scarring trachoma and 1531 controls from a non-selected multi-ethnic sampling of The Gambia. The data constitutes hard base calls at 1457295 features from the HumanOmni2.5-8 (Omni2.5) BeadChip. Three genotype-calling algorithms were used : Illuminus (Bioinformatics 2007, 23:2741–6), GenCall (Patent US7035740, 2006) and GenoSNP (Bioinformatics 2008, 24:2209–14). Data from each calling algorithm was filtered to retain only SNPs with a call rate ≥ 0.98. To obtain a merged set of SNPs, all genotypes that matched across call-sets were retained, whilst those that mismatched between call-sets were set to missing. Genotypes that were present in one call set and missing in others were also retained. The merged SNP set contained 1467876 SNPs, which were filtered for call rate ≥ 0.99 and Hardy-Weinberg equilibrium P value < 5 x 10-8. The case and control groups were approximately equivalent with respect to gender and ethnicity. 70% of cases and 63% of controls were female. Self-described ethnic composition of the cases was 29% Jola, 27% Mandinka, 21% Wolof, 10% Fula and 13% other/no data. In controls the composition was 25% Jola, 24% Mandinka, 21% Wolof, 8% Fula and 22% other/no data. Median age was 49 (range 32-60) in cases and 37 (range 12-52) in controls (t = -3.6019, P = 0.0003). This data set has substantial levels of population structure, which reflects extensive networks of pairwise kinship between participants. First pass tests of association in EMMAX (Nat Genet 2010, 42:348–54) led to genome-wide deflation of the test statistics (λ = 0.982 SE = 1.74e-05) that could be directly attributed to the differing age and gender distributions between cases and controls. Modelling the phenotype to adjust for age and gender successfully controlled for this and no genome-wide deviation from the null was subsequently observed (λ = 1.001, SE = 8.7 x 10-7). Neither principal components analysis (PCA) nor tests of proportional identity by state (IBS) variance in PLINK identified significant levels of within or between group genetic variance. The phenotypes submitted in the phenotypes file include both uncorrected (case/control status) and corrected (age and gender corrected case/control status) phenotypes, as well as age and self-described ethnicity.

  Study EGAS00001001516

• WGS data of paediatric BCR::ABL1 acute lymphoblastic leukemia

  The dataset includes FASTQ and CRAM files from diagnostic and matched remission (control) samples of one BCR::ABL1 ALL patient (ALLT-399). Sequencing library was made using PCR free-based WGS library preparation (PCR-), using Novogene NGS DNA Library Prep Set Kit (Cat No. PT004). Both diagnostic (90x) and remission (30x) samples were sequenced using NovaSeqX Plus.

  Dataset EGAD50000002185

• Genomic Analysis of a Metastatic Fusion-negative Embryonal Rhabdomyosarcoma

  Autopsy-derived, later snap-frozen tissue fragments from a 5-year-old female with recurrent metastatic fusion-negative embryonal rhabdomyosarcoma (RMS) primary tumor of the left thigh were analyzed. No quality matched tissue was available. Prior panel analysis identified 2 prominent genetic changes: NRAS Q61K, PIK3CA H1047R, CDKN2A/B loss, and ERBB3 overexpression.

  Dataset EGAD00001009973

• Whole genome sequencing and whole exome sequencing of DIPG tumors and matched normal tissue

  Diffuse Intrinsic Pontine Glioma (DIPG) is a fatal brain cancer that arises in the brainstem of children with no effective treatment. To understand what drives DIPGs we integrated whole-genome-sequencing with methylation, expression and copy-number profiling.

  Dataset EGAD00001003305

• Dataset on keratinocytic gene expression pattern in Hidradenitis suppurativa

  Human skin samples were obtained from HS patients after informed consent (Ethical vote, University of Würzburg; No. 306/12). Lesional and perilesional were taken and epidermis and dermis separated. Isolated epidermal keratinocytes were further processed for RNA isolation. mRNA was extracted from five pairwise-matched lesional and perilesional epidermal HS pellets and RNA sequencing was performed.

  Dataset EGAD00001008005

• Patient-derived organoids cohort raw FASTQ from SGMedical

  Raw FASTQ files for a glioblastoma multiforme organoid study, including exome sequencing and RNA-seq. 29 runs (paired-end), 58 FASTQ.c4gh files (R1/R2). Short-read Illumina; library strategies include exome capture and stranded total RNA-seq (see Experiment records for kit/instrument details). No processed results are included; access is controlled under the selected Policy.

  Dataset EGAD50000001741

• MGRB dataset. Samples that were not included in the paper.

  This dataset comprises 1440 whole genome sequenced samples from the Medical Genome Reference Bank. https://sgc.garvan.org.au/initiatives/mgrb The files are provided in cram format, aligned to hs37d5 with decoys, with no further processing applied. The dataset also contains phenotype information for each sample.

  Dataset EGAD00001005095

• Tumor Mutation Burden, Expressed Neoantigen and Immune Microenvironment in Diffuse Gliomas

  A consistent correlation between tumor mutation burden (TMB) and tumor immune microenvironment has not been observed in gliomas as in other cancers. Driver germline and somatic mutations, TMB, neoantigen, and immune cell signatures were analyzed using whole exome sequencing (WES) and transcriptome sequencing of tumor and WES of matched germline DNA in a cohort of 66 glioma samples (44 IDH-mutant and 22 IDH-wildtype). Fourteen samples revealed a hypermutator phenotype (HMP). Eight pathogenic (P) or likely pathogenic (LP) germline variants were detected in 9 (19%) patients. Six of these 8 genes were DNA damage repair genes. P/LP germline variants were found in 22% of IDH-mutant gliomas and 12.5%of IDH-wildtype gliomas (p= 0.7). TMB was correlated with expressed neoantigen but showed an inverse correlation with immune score (R =−0.46, p= 0.03) in IDH-wildtype tumors and no correlation in IDH-mutant tumors. Antigen Processing and Presentation (APP) score correlates with immune score. The APP is higher in non-hypermutator phenotype (NHMP) samples versus HMP samples in the IDH-wildtype gliomas, but higher in HMP samples versus NHMP samples in the IDH-mutant gliomas. Conclusion: TMB was inversely correlated with the immune score in the IDH-wildtype gliomas, and showed no correlation in the IDH-mutant tumors. The APP was correlated with the immune score, and may be further investigated as a biomarker for response to immunotherapy in gliomas. Studies of germline variants in a large glioma cohort are warranted.

  Study phs002653

• Whole Exome Sequencing of One Nuclear Family with Non-syndromic Sensorineural Hearing Loss

  Our goal is to find genes responsible for non-syndromic sensorineural hearing loss. Blood samples were collected from the JS6 family affected with hearing loss. The family is of Caribbean Hispanic ethnicity. Family JS6 consisted of two deaf siblings, JS6.001 (Male) and JS6.002 (Female) and healthy parents, JS6.100 (mother) and JS6.200 (father). The siblings had no other medical findings. Audiometry tests and Rinne and Weber tuning fork tests identified sensorineural hearing loss in the two siblings. We performed whole exome sequencing of the four individuals and identified a recessive mutation, p.(Arg186Trp), in the CIB2 gene in the two affected siblings. Both parents were unaffected carriers.

  Study phs000969