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• Neoplastic pancreatic cysts and associated cancers

  Data from a study of 148 samples from IPMNs, MCNs, and small associated invasive carcinomas from 18 patients using whole exome or targeted sequencing. Sequencing data from 77 samples out of the 148 samples in the complete study are available in this dataset, based on the permissions given by the participating patients and the informed consents.

  Dataset EGAD00001006229

• Shallow whole genome sequencing on stage 1 epithelial ovarian cancer

  BAM files (aligned against the hg38 genome) from a shallow whole-genome sequencing experiment (median depth 0.5X) on 218 samples from Stage 1 epithelial ovarian cancer biopises. Samples labeled "bis" or "tris" with the same ID are relapses; "left" or "right" samples indicate, in the case of bilateral tumor, from which ovary the sample was taken.

  Dataset EGAD00001006881

• Targeted sequencing of Burkitt lymphoma tumour samples from the UK's Haematological Malignancy Research Network

  Targeted sequencing was applied to an unselected population-based Burkitt lymphoma cohort (n=39) diagnosed in the UK's Haematological Malignancy Research Network catchment population of ~4 million (14 centres). DNA extracted from tumour samples was sequenced with a 293-gene panel using the Illumina HiSeq 2500. All data are provided in the CRAM format.

  Dataset EGAD00001007658

• RNA sequencing of Human Organoid Lines

  The study will use RNA sequencing to aid in benchmarking different culture conditions in a set of genetically annotated human organoid lines. The data will be used to assess whether there are any clonal differences introduced when culturing these lines in different conditions.

  Dataset EGAD00001007971

• OMRF SLEGEN GWAS Data from European-American Women with Lupus

  "Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with complex etiology but strong clustering in families (lambda(S) = approximately 30). We performed a genome-wide association scan using 317,501 SNPs in 720 women of European ancestry with SLE and in 2,337 controls, and we genotyped consistently associated SNPs in two additional independent sample sets totaling 1,846 affected women and 1,825 controls. Aside from the expected strong association between SLE and the HLA region on chromosome 6p21 and the previously confirmed non-HLA locus IRF5 on chromosome 7q32, we found evidence of association with replication (1.1 x 10-7 < P(overall) < 1.6 x 10-23; odds ratio = 0.82-1.62) in four regions: 16p11.2 (ITGAM), 11p15.5 (KIAA1542), 3p14.3 (PXK) and 1q25.1 (rs10798269). We also found evidence for association (P < 1 x 10-5) at FCGR2A, PTPN22 and STAT4, regions previously associated with SLE and other autoimmune diseases, as well as at > or =9 other loci (P < 2 x 10-7). Our results show that numerous genes, some with known immune-related functions, predispose to SLE." Reprinted from Nature Genetics, 2008 Feb; 40(2):204-10, PMID:18204446, with permission from Nature Publishing Group. Data submitted to dbGaP includes 297 samples from Oklahoma. (Please see also Study Accession: phs000216.v1.p1)

  Study phs000202

• DLK1 Distinguishes Subsets of NF1-Associated Malignant Peripheral Nerve Sheath Tumors with Divergent Molecular Signatures

  Study Design and Aims We aimed to investigate the molecular mechanisms underlying the malignant transformation of pre-existing neurofibromas (PNST) to malignant peripheral nerve sheath tumors (MPNST) in individuals with neurofibromatosis type 1 (NF1). Our primary focus was on the role of DLK1 in this transformation process and its potential as a biomarker for diagnosis, risk assessment, and therapeutic stratification. Population InformationThis study consisted of a case set of peripheral nerve sheath tumor specimens, including plexiform neurofibromas, atypical neurofibromas, and MPNSTs, acquired under IRB approval at our institution. The majority of the subjects had neurofibromatosis type 1. Principal Findings DLK1 Overexpression: The study found that DLK1 is significantly increased in MPNST compared to non-malignant neurofibromas.Early Marker: DLK1 overexpression may precede histological changes indicative of malignancy.Serum Levels: Higher serum levels of DLK1 were observed in both mice and humans with MPNST.Molecular Stratification: Divergent levels of DLK1 expression identified distinct MPNST subsets with unique molecular characteristics and potential therapeutic targets.Clinical Implications: Overexpression of DLK1 was associated with the reactivation of embryonic signatures, an immunosuppressive microenvironment, and poorer overall survival in NF1-MPNST patients. Data Availability Whole exome sequencing, bulk RNA sequencing, and single-cell RNA sequencing data from this study will be made available through the database of Genotypes and Phenotypes (dbGaP) to support further research and validation studies.

  Study phs003835

• Landscape of somatic mutations and clonal evolution in mantle cell lymphoma

  Mantle cell lymphoma (MCL) is an aggressive tumor, but a subset of patients may follow an indolent clinical course. To understand the mechanisms underlying this biological heterogeneity, we performed whole-genome and/or whole-exome sequencing on 29 MCL cases and their respective matched normal DNA, as well as 6 MCL cell lines. Recurrently mutated genes were investigated by targeted sequencing in an independent cohort of 172 MCL patients. We identified 25 significantly mutated genes, including known drivers such as ataxia-telangectasia mutated (ATM), cyclin D1 (CCND1), and the tumor suppressor TP53; mutated genes encoding the anti-apoptotic protein BIRC3 and Toll-like receptor 2 (TLR2); and the chromatin modifiers WHSC1, MLL2, and MEF2B. We also found NOTCH2 mutations as an alternative phenomenon to NOTCH1 mutations in aggressive tumors with a dismal prognosis. Analysis of two simultaneous or subsequent MCL samples by whole-genome/whole-exome (n = 8) or targeted (n = 19) sequencing revealed subclonal heterogeneity at diagnosis in samples from different topographic sites and modulation of the initial mutational profile at the progression of the disease. Some mutations were predominantly clonal or subclonal, indicating an early or late event in tumor evolution, respectively. Our study identifies molecular mechanisms contributing to MCL pathogenesis and offers potential targets for therapeutic intervention.

  Study EGAS00001000510

• 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

• Impaired HLA Class I Antigen Processing and Presentation as a Mechanism of Acquired Resistance to Immune Checkpoint Inhibitors in Lung Cancer

  Mechanisms of acquired resistance to immune checkpoint inhibitors (ICIs) are poorly understood. The purpose of this study was to investigate whether alterations in genes encoding components of the HLA Class I antigen processing and presentation machinery or interferon signaling pathways play a role in acquired resistance to PD-1 or PD-L1 antagonistic antibodies. Whole exome sequencing was performed on tumor samples collected from patients with advanced non-small cell lung cancer at the time of resistance to PD-1 axis inhibitors and on available matched pre-treatment and normal samples. Patient-derived xenografts successfully established from the ICI-resistant samples were also exome sequenced. Additionally, RNA sequencing was performed on cases with sufficient tissue.

  Study phs001464

• Whole exome sequencing in multiplex cleft families from a consortium

  Building upon our previous linkage and association studies, we will use whole exome sequencing studies of second and third degree affected relatives drawn from multiplex families. Our specific aims are: 1) To conduct whole exome sequencing on affected members (2° and 3° relatives) drawn from multiplex cleft families from a consortium to identify novel genes causing non-syndromic oral clefts; 2) To confirm and test the role of rare variants in these novel genes through confirmatory Sanger sequencing, plus linkage information using additional members available in these multiplex families. This whole exome sequencing approach will combine evidence from linkage studies and large scale sequencing to identify novel genes causing oral clefts in multiplex cleft families.

  Study phs000459