Search Results - EGA European Genome-Phenome Archive

GIS-LUNGTCR1-2016_VAL-FASTQ

This dataset contains FASTQ files of targeted Amplicon deep-sequencing data, for validation of the mutations found in WES. There are 16 patients and 95 samples in total, including 16 controls and 79 tumors. 140 fastq in total, multiple runs for some of the samples. Please refer to the sample-ID from filename for merging.

Dataset EGAD00001001981

FASTQ file for paper titled "Discovery of immunotherapy targets for pediatric solid and brain tumors by exon-level expression"

This data set includes 27 full-length transcript sequence generated from PacBio IsoSeq that were used for verify the cancer-specific exons identified in three genes: FN1, COL6A3 and TNC. The data were generated from PDX models of osteosarcoma patients.

Dataset EGAD00001015356

SNP Array Data for EGAS00001004666

Dataset EGAD00010002257

Heart

Whole-Exome-Sequencing of 5 pooled patients for SNP-based demultiplexing

Study EGAS50000000655

Asian Genome Project(BioBank Japan genotype data)

Biobank Japan registrants sequenced for Asian Genome Project

Study JGAS000647

FFPE_Normal_Panel_V3_Cancer_Panel

FFPE normal panel generation for use with V3 cancer panel 0618521

Study EGAS00001000836

Oxford Nanopore sequencing for APL

Raw fast5 file of Oxford Nanopore sequencing for an APL patient sample

Dataset EGAD00001008151

snv calls for subclonal reconstruction

single nucleotide variant calls from somatic sniper, vcf format. input for subclonal reconstruction

Dataset EGAD00001003753

DATA FILES FOR SJLGG

Dataset EGAD00001000695

Identifying autosomal recessive mutations causing neurological disorders

The objective of this study is to resequence of targeted intervals containing autosomal recessive variants causing neurological disorders in consanguineous pedigrees. Using homozygosity mapping, three intervals of very different sizes have previously been unambiguously mapped for three different neurological diseases: 2.4Mb, 8Mb and 14.3Mb in size, for Microlissencephaly, Severe Mental Retardation and Complicated hereditary spastic paraplegia respectively. This study is a pilot to assess how well custom targeted resequencing performs across a broad size range of intervals. The study design is to use a different custom capture probe set for each interval, pulldown from a single patient from each family, and sequence 1 lane using Illumina paired-reads for each sample. Candidate variants will be followed up in the families themselves, and in patients with similar phenotypes from outbred populations.

Study EGAS00001000023

Genome-Wide Association Study of Amyotrophic Lateral Sclerosis in Finland

The genetic etiology of amyotrophic lateral sclerosis (ALS) is not well understood. Finland has one of the highest incidence of ALS in the world, making it an ideal population for study. To identify genetic risk factors for this fatal neurodegenerative disease, we undertook a genome-wide association study of 405 Finnish patients diagnosed with ALS and 497 Finnish controls. Two loci that exceeded the Bonferroni threshold for genome-wide significance were identified. One was located on chromosome 21q22, corresponding to the known autosomal recessive D90A allele of the SOD1 gene. The other was detected on the short arm of chromosome 9, which had been previously identified in linkage studies of families with ALS. Together, these two loci account for most of the increased incidence of ALS observed in this population.

Study phs000344

Evolutionary Origins of Recurrent Pancreatic Cancer

Surgery is the only curative option for patients with Stage I/II pancreatic cancer, nonetheless most patients will recur after surgery and die of their disease. To identify novel opportunities for management of recurrent pancreatic cancer we performed whole exome or targeted sequencing of 10 resected primary cancers and their matched intrapancreatic recurrences or distant metastases. We identified that recurrent disease develops from a monophyletic or polyphyletic origin, and this distinction has potential clinical relevance. In all patients, treatment induced genetic bottlenecks led to a modified genetic landscape and subclonal heterogeneity for driver gene alterations in part due to intermetastatic seeding. In one patient what was believed to be recurrent disease was an independent (second) primary tumor. These findings strongly advocate for routine post-treatment sampling in the management of recurrent pancreatic cancer.

Study EGAS00001004097

Clonally resolved single-cell multi-omics identifies routes of cellular differentiation in acute myeloid leukemia

In this study we generated single-cell whole transcriptome and surface marker expression data for 24 samples of 19 AML patients as well as one healthy donor. We followed the CITEseq protocol with the 3' 10x Genomics scRNAseq kit version 3.1 To increase the coverage of the mitochondrial genome we generated mitochondrial libraries following a protocol termed Optimized 10x. Based on TAPseq, we generated libraries to increase the coverage of selected nuclear SNVs. Exome sequencing was generated for 15 patients to identify nuclear variants. Bulk ATAC was obtained for 9 samples to facilitate the discovery of mitochondrial SNVs. MutaSeq (modified version of SmartsSeq2) was performed on cells from 3 patients. Targeted DNAseq from single-cell derived colonies was generated for 1 patient.

Study EGAS00001007078

Prediction of plasma ctDNA fraction and prognostic implications of liquid biopsy in advanced prostate cancer

No consensus strategies exist for prognosticating metastatic castration-resistant prostate cancer (mCRPC). Circulating tumor DNA fraction (ctDNA%) is increasingly reported by commercial and laboratory tests but its utility for risk stratification is unclear. Here, we intersect ctDNA%, treatment outcomes, and clinical characteristics across 738 plasma samples from 491 male mCRPC patients from two randomized multicentre phase II trials and a prospective province-wide blood biobanking program. ctDNA% correlates with serum and radiographic metrics of disease burden and is highest in patients with liver metastases. ctDNA% strongly predicts overall survival, progression-free survival, and treatment response independent of therapeutic context and outperformed established prognostic clinical factors. Recognizing that ctDNA-based biomarker genotyping is limited by low ctDNA% in some patients, we leverage the relationship between clinical prognostic factors and ctDNA% to develop a clinically-interpretable machine learning tool that predicts whether a patient has sufficient ctDNA% for informative ctDNA genotyping (available online: https://www.ctDNA.org). Our results affirm ctDNA% as an actionable tool for patient risk stratification and provide a practical framework for optimized biomarker testing.

Study EGAS50000000211

Longitudinal genome-wide analysis of progressive chronic lymphocytic leukemia under uniform front-line therapy of pentostatin, cyclophosphamide, and rituximab

Samples from two-center prospective phase 2 clinical trail conducted at Ohio State University (Columbus, OH) and Mayo Clinic (Rochester, MN) were analyzed in 12 cases. All patients had progressive CLL as defined by National Cancer Institute (NCI) Working Group criteria. Patients provided written informed consent for correlative studies according to the Declaration of Helsinki on an institutional review board approved protocol for the collection and use of samples for research purposes from both participating institutions. Eligible patients received a regimen consisting of pentostatin (2 mg/m2), cyclophosphamide (600 mg/m2), and rituximab (375 mg/m2) provided intravenously on day 1 of a 21-day cycle for a maximum of 6 cycles. Responses were assessed by NCI Working Group criteria and included a bone marrow evaluation and two-color flow cytometry 2 months after completion of therapy. Peripheral blood samples from these patients collected longitudinally before (Pre-Baseline), at (Baseline) and after therapy (Relapse) were analyzed for genomic heterogeneity and clonal complexity by high throughput Exome sequencing.

Study phs000794

POISED (Peanut Oral Immunotherapy: Safety, Efficacy, and Discovery)

Phase 2 POISED (Peanut Oral Immunotherapy: Safety, Efficacy, Discovery) Study In this randomized, double-blind, placebo-controlled (DBPC) clinical trial, blinded placebo group received oat flour, whereas in active participants, dosage was built-up for over ~ 52 weeks and subsequently maintained on 4000 mg peanut protein, daily for next 52 weeks. 80 (98.77%) per-protocol active participants passed the food challenge at week 104. Subsequently, for 12 weeks, peanut ingestion was avoided in a randomized group of 51 blinded active participants (i.e., peanut avoidance group). 21 (41.2%) participants in the peanut avoidance group passed the 4000 mg double-blind, placebo-controlled food challenge (DBPCFC) without any allergic reaction at week 117, thus demonstrating sustained unresponsiveness. These 21 participants continued oral immunotherapy (OIT) for every three months and afterwards were allowed to continue peanut OIT discontinuation if they passed. 8 participants passed the DBPCFCs, 12 months after peanut discontinuation (week 156), i.e. they achieved long-term sustained unresponsiveness with no allergic reaction in response to food challenge. For detailed description, please refer to Chinthrajah et al., PMID: 31522849.

Study phs003071

NHLBI TOPMed: Whole Genome Sequencing of Venous Thromboembolism (WGS of VTE)

This study consists of 338 VTE cases from an inception cohort of Olmsted County, MN residents (OC) with a first lifetime objectively-diagnosed idiopathic VTE during the 40-year study period, 1966-2005. All living study subjects were invited to provide a whole blood sample at the Mayo Clinical Research Unit for leukocyte genomic DNA and plasma collection. For living study subjects who did not provide a blood sample, we retrieved any leftover blood ("waste" blood) from samples collected as part of routine clinical diagnostic testing and used this to extract DNA after obtaining patient consent. For deceased cases, with IRB approval, we extracted DNA from any available stored tissue within the Mayo Tissue Archive. This "tissue" DNA has been successfully genotyped in prior studies. Three trained and experienced study nurse abstractors reviewed the complete medical records in the community of all potential cases. Note: WGS sample IDs for the previous GENEVA study cases (phs000289) are included in this dataset. The phenotypes for the GENEVA study are located under the above phs number.

Study phs001402

DCIS fresh frozen fragmentomics dataset

Ductal carcinoma in situ (DCIS) is a non-obligate precursor lesion of breast cancer (BC). Often detected by mammography, most cases are managed through surgical and/or radiotherapy approaches. Today, it is not possible to predict which patients will progress to invasive disease. Here, we evaluated high-depth whole-genome sequenced (WGS) DCIS, enriched for highgrade clinical lesions, to understand whether deep WGS could reveal biological insights and/or personalized therapeutic vulnerabilities that may be targetable. We find genomic locations that are likely susceptible to producing the initiating lesion for structural variations (SVs) prone to subsequent evolution, termed SHOREs (Susceptibility HOtspots for Rearrangements and ongoing Evolution). We additionally highlight individualized therapeutic potential that would otherwise not be appreciable without WGS. We posit that holistic WGS profiling could offer a more precise stratification approach, discerning higher-risk cases for prospective clinical studies on personalized therapies, from truly low-risk cases suitable for active monitoring. To substantiate our WGS findings, we also performed RNAseq on the same samples, this EGA study contains the RNAseq data.

Study EGAS50000001475

DNA methylation atlas of normal human cell types

DNA methylation is a fundamental epigenetic mark that governs chromatin organization, cell identity, and gene expression. Here we describe a human methylome atlas, based on deep whole-genome bisulfite sequencing allowing fragment-level analysis across thousands of unique markers for 39 cell types sorted from 205 healthy tissue samples. Replicates of the same cell-type are >99.5% identical, demonstrating robustness of cell identity programs to genetic variation and environmental perturbation. Unsupervised clustering of the atlas recapitulates key elements of tissue ontogeny, and identifies methylation patterns retained since gastrulation. Loci uniquely unmethylated in an individual cell type often reside in transcriptional enhancers and contain DNA binding sites for tissue-specific transcriptional regulators. Uniquely hyper-methylated loci are rare and are enriched for CpG islands, polycomb targets, and CTCF binding sites, suggesting a novel role in shaping cell type-specific chromatin looping. The atlas provides an essential resource for interpretation of disease-associated genetic variants, and a wealth of potential tissue-specific biomarkers for use in liquid biopsies.

Study EGAS00001006791

Inference of transcription factor binding from cell-free DNA enables tumor subtype prediction and early detection

Deregulation of transcription factors (TFs) is an important driver of tumorigenesis, but non-invasive assays for assessing transcription factor activity are lacking. We Here we developed and validated a minimally invasive method for assessing TF activity based on cell-free DNA sequencing and nucleosome footprint analysis. We analyzed whole genome sequencing data for >1,000 cell-free DNA samples from cancer patients and healthy controls using a newly developed bioinformatics pipeline developed by us that infers accessibility of TF binding sites from cell-free DNA fragmentation patterns. We observe patient-specific as well as tumor-specific patterns, including accurate prediction of tumor subtypes in prostate cancer, with important clinical implications for the management of patients. Furthermore, we show that cell-free DNA TF profiling is capable of detection of early-stage colorectal carcinomas. Our approach for mapping tumor-specific transcription factor binding in vivo based on blood samples makes a key part of the noncoding genome amenable to clinical analysis.

Study EGAS00001003206

Epigenome and transcriptome profiling of chronic lymphocytic leukemia patients

Chronic lymphocytic leukemia (CLL) is characterized by substantial clinical heterogeneity, despite relatively few genetic alterations. To provide a basis for studying epigenome deregulation in CLL, we established genome-wide chromatin accessibility maps for 88 CLL samples from 55 patients using the ATAC-seq assay, and we also performed ChIPmentation and RNA-seq profiling for ten representative samples. Based on the resulting dataset, we devised and applied a bioinformatic method that links chromatin profiles to clinical annotations. Our analysis identified sample-specific variation on top of a shared core of CLL regulatory regions. IGHV mutation status – which distinguishes the two major subtypes of CLL – was accurately predicted by the chromatin profiles, and gene regulatory networks inferred for IGHV-mutated vs. IGHV-unmutated samples identified characteristic differences between these two disease subtypes. In summary, we discovered widespread heterogeneity in the chromatin landscape of CLL, established a community resource for studying epigenome deregulation in leukemia, and demonstrated the feasibility of chromatin accessibility mapping in cancer cohorts and clinical research.

Study EGAS00001001821

International Standards for Cytogenomic Arrays

The International Standards for Cytogenomic Arrays (ISCA) Consortium is a rapidly growing group of clinical cytogenetics and molecular genetics laboratories committed to improving quality of patient care related to clinical genetic testing using new molecular cytogenetic technologies including array comparative genomic hybridization (aCGH) and quantitative SNP analysis by microarrays or bead chip technology. The ISCA Consortium is now working with the sequencing community to extend the goals of standardization, collaboration, and data sharing. To reflect this combined effort, we are becoming ICCG, or the International Collaboration for Clinical Genomics. Efforts of the Consortium include: Clinical Utility: The ISCA Consortium has made recommendations regarding the appropriate clinical indications for cytogenetic array testing (Miller et al. AJHG 2010, PMID: 20466091). Currently, discussions are focused on pediatric applications for children with unexplained developmental delay, intellectual disability, autism and other developmental disabilities. A separate committee has been developed to address appropriate cancer genetic applications (http://www.urmc.rochester.edu/ccmc/). Evidence-based standards for cytogenomic array design: The Consortium will develop recommendations for standards for the design, resolution and content of cytogenomic arrays using an evidence-based process and an international panel of experts in clinical genetics, clinical laboratory genetics (cytogenetics and molecular genetics), genomics and bioinformatics. This design is intended to be platform and vendor-neutral (common denominator is genome sequence coordinates), and is a dynamic process with input from the broader genetics community and evidence-based review by the expert panel (a Steering Committee with international representation). Public Database for clinical and research community: It is essential that a publicly available database be created and maintained for cytogenetic array data generated in clinical testing laboratories. This will be integrated into the current dbGaP database at NCBI/NIH and released through dbVar, and curated by a committee of clinical genetics laboratory experts. The very high quality of copy number data (i.e., deletions and duplications) coming from clinical laboratories combined with expert curation will produce an invaluable resource to the clinical and research communities. Standards for interpretation of cytogenetic array results: Using the ISCA Database, along with other genomic and genetics databases, the Consortium will develop recommendations for the interpretation and reporting of pathogenic vs. benign copy number changes as well as imbalances of uncertain clinical significance. Membership in the ISCA Consortium is open to all individuals and laboratories involved in cytogenetic array testing who are committed to free data sharing and to participation in a process to develop evidence-based standards and guidelines to improve patient care. ISCA is available through dbVar: http://www.ncbi.nlm.nih.gov/dbvar/studies/nstd37/ http://www.ncbi.nlm.nih.gov/dbvar/studies/nstd75/ http://www.ncbi.nlm.nih.gov/dbvar/studies/nstd45/ http://www.ncbi.nlm.nih.gov/dbvar/studies/nstd101/

Study phs000205

Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations

It is well established that autism spectrum disorders (ASD) have a strong genetic component; however, for at least 70% of cases, the underlying genetic cause is unknown. Under the hypothesis that de novo mutations underlie a substantial fraction of the risk for developing ASD in families with no previous history of ASD or related phenotypes-so-called sporadic or simplex families-we sequenced all coding regions of the genome (the exome) for parent-child trios exhibiting sporadic ASD, including 189 new trios and 20 that were previously reported. Additionally, we also sequenced the exomes of 50 unaffected siblings corresponding to these new (n = 31) and previously reported trios (n = 19), for a total of 617 individual exomes from 209 families deposited in dbGaP. Here we show that de novo point mutations are overwhelmingly paternal in origin (4:1 bias) and positively correlated with paternal age, consistent with the modest increased risk for children of older fathers to develop ASD. Moreover, 39% (49 of 126) of the most severe or disruptive de novo mutations map to a highly interconnected beta-catenin/chromatin remodelling protein network ranked significantly for autism candidate genes. In proband exomes, recurrent protein-altering mutations were observed in two genes: CHD8 and NTNG1. Mutation screening of six candidate genes in 1,703 ASD probands identified additional de novo, protein-altering mutations in GRIN2B, LAMC3 and SCN1A. Combined with copy number variant (CNV) data, these results indicate extreme locus heterogeneity but also provide a target for future discovery, diagnostics and therapeutics.

Study phs000482

NHLBI TOPMed: Genetic Epidemiology of COPD (COPDGene)

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States, and the only leading cause of death that is steadily increasing in frequency. This project established a racially diverse cohort that is sufficiently large and appropriately designed for genome-wide association analysis of COPD. A total of 10,720 subjects were recruited, including control smokers and nonsmokers, definite COPD cases (GOLD Stage 2 to 4), and subjects not included in either group (GOLD 1 and PRISm). This cohort is being used for cross-sectional analysis, and long-term longitudinal follow-up visits after five years and after ten years are also being performed. The primary focus of the study is to identify the genetic risk factors that determine susceptibility for COPD and COPD-related phenotypes. Detailed phenotyping of both cases and controls, including chest CT scan assessment of emphysema and airway disease, will allow identification of genetic determinants for the heterogeneous components of the COPD syndrome. The aims for this study are: Precise phenotypic characterization of COPD subjects using computed tomography, as well as clinical and physiological measures, that will provide data to enable the broad COPD syndrome to be decomposed into clinically significant subtype; Genome-wide association studies will identify genetic determinants for COPD susceptibility that will provide insight into clinically relevant COPD subtypes; Distinct genetic determinants influence the development of emphysema and airway disease. The TOPMed analysis will include approximately 10,500 subjects with whole genome sequencing after quality control is completed. Comprehensive phenotypic data for COPDGene subjects is available through dbGaP study phs000179.

Study phs000951

Data Access Committee for the DNA sequencing data included in the study "A generalizable machine learning framework for classifying DNA repair defects using ctDNA exomes”

Dac EGAC00001003111

"Usage of small amounts of DNA for Illumina sequencing"

Dataset EGAD00001000034

Dataset for TIX

All files for TIX individuals

Dataset EGAD50000000426

RNAseq for 4 pdx and 1 cell-line

RNAseq for #1049, #111, #1217, #206, COV362

Dataset EGAD50000000032

PBMC

Whole-Exome-Sequencing of 5 pooled patients for SNP-based demultiplexing

Study EGAS50000000654

DATA FILES FOR SJINF RNASeq

Dataset EGAD00001001098

Deep sequencing of melanoma for driver mutations

Dataset EGAD00001001445

Australian genomes

Mapped data (bam files) for high-throughput whole genome sequence data for 83 modern Aboriginal Australians

Dataset EGAD00001002001

NIDDK IBD Genetics Consortium Ulcerative Colitis Genome-Wide Association Study

This dataset contains data for 1,028 white, non-Hispanic, European ancestry individuals with ulcerative colitis who were included in a genome-wide association study published by Silverberg et al. (2009). These individuals were ascertained in North America and selected to have either left-sided or extensive disease (i.e., individuals with proctitis only were excluded). Genotyping was performed using the Illumina HumanHap300v2 (n = 540) and HumanHap550v3 (n = 488) Genotyping BeadChips at the Feinstein Institute for Medical Research. Control data (not included) were obtained from the NIDDK IBD Genetics Consortium's Crohn's Disease GWAS (available from dbGaP) and from studies 64 and 65 deposited in the Illumina iControlDB. Seven hundred eighty individuals in this dataset were taken from the NIDDK IBD Genetics Consortium cell line repository (http://www.niddkrepository.org). These individuals are identified in the file dbGaP_SubjectDS.txt. The subject IDs for these individuals may be used to request corresponding samples for follow-up research through the repository. In addition, complete phenotype data for these individuals are included, collected using the Consortium's forms and phenotyping manual (both included). The remaining 248 individuals were identified from pre-existing collections ascertained by members of the Consortium or their collaborators. For these samples, several of the items in the phenotype file are incomplete. Those who wish to replicate the results in Silverberg et al. should note that 6 individuals with missing genotype rates > 0.07 were excluded from that analysis (leaving 1,022 affected samples total). In addition, the minor allele frequencies (MAFs) reported in the publication were calculated using only those individuals who were included in the allelic association tests (n = 977 for SNPs included in the HumanHap300 and n = 476 for SNPs included only in the HumanHap550). These tests were performed using conditional logistic regression on gender-ancestry strata; individuals who were not placed in a stratum (using the procedure described in the supplementary information for Silverberg et al.) were excluded. The indicator variables hh300 and hh550 in the file dbGaP_PhenotypeDS.txt identify the samples included in the allelic association tests, and may be used to replicate the published MAFs among affected individuals.

Study phs000345

Phase II trial of targeted immune-depleting chemotherapy and reduced-intensity allogeneic hematopoietic stem cell transplantation using 8/8 and 7/8 HLA-matched unrelated donors and utilizing two graft-versus-host disease prophylaxis regimens for the treatment of leukemias, lymphomas, and pre-malignant blood disorders

Background: Major problems with stem cell transplantation (SCT) for cancer treatment are a lack of suitable donors for patients without an HLA tissue-matched sibling and graft-versus-host disease (GVHD), a serious side effects of immune-suppressing chemotherapy that is given to bring the cancer under control before SCT. In GVHD, the patient's immune system attacks the transplanted donor cells. This study will try to improve the results of SCT from unrelated HLA-matched donors using targeted immune-depleting chemotherapy to bring the cancer under control before transplantation and to lower the chance of graft rejection, followed by reduced-intensity transplant chemotherapy to make the procedure less toxic. Objectives: To evaluate the safety and effectiveness of targeted immune-depleting chemotherapy followed by reduced-intensity transplant chemotherapy in patients with advanced cancers of the blood and immune system. To evaluate the safety and effectiveness of two different drug combinations to prevent GVHD. Both regimens have been successful in preventing GVHD, but they work by different mechanisms and affect the rebuilding of the immune system after the transplant. Eligibility: People 18 to 74 years of age with advanced or high-risk cancers of the blood and immune system who do not have a suitable HLA-matched sibling. Design: All patients receive chemotherapy before transplant to treat the cancer and suppress immune function. All patients receive a conditioning regimen of cyclophosphamide for 4 days and fludarabine for 4 days before SCT to prepare for the transplant. Patients are randomly assigned to one of two combination drug treatments to prevent GHVD as follows: Group 1: Tacrolimus starting 3 days before SCT and continuing for 6 months, plus methotrexate on days 1, 3, 6, and 11 post-SCT, plus sirolimus starting 3 days before the SCT and continuing through day 14 following SCT. Group 2: Alemtuzumab for 4 days starting 8 days before SCT, plus cyclosporine starting 1 day before SCT and continuing for 6 months. Patients receive the donor's stem cells and immune cells 2 days after the conditioning regimen. Patients are followed at the clinic regularly for the first 6 months after SCT, and then less often for at least 5 years. Some visits may include bone marrow aspirates and biopsies, blood draws, and other tests to monitor disease status. A skin biopsy, oral mucosa biopsy, and saliva collection are done to study chronic GVHD.

Study phs002021

OLD DATA FILES FOR SJMB - Superseded by EGAD00001001864

Dataset EGAD00001000269

RNAseq for 8 PDX

RNAseq for #111, #1177, #206, #201, #29, #931, WO-19, WO-2

Dataset EGAD50000000116

Preeclampsia InterPregGen Consortium: GWAS meta-analysis summary statistics for European fetal preeclampsia cases versus controls and GWAS genotype data for European fetal preeclampsia cases

Study EGAS00001001048

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