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• PETAL trial Whole Exome Sequencing (WES) from Tumor Samples

  Associated with Molecular profiling of DLBCL patients treated in the PETAL trial. Whole Exome Sequencing (WES) of 224 Tumor Samples. WES was used for Molecular Profiling by simultaneous screening of mutations. Data is Complementary to sWGS.

  Dataset EGAD50000001172

• Epigenomic dataset of Human Hepatocellular Carcinoma for EpiHK

  This dataset is generated for EpiHK. It contains Histone PTM ChIP-seq, WGBS, RNA-seq of Human Hepatocellular Carcinoma and tumor adjacent normal tissue sample.

  Study EGAS50000000039

• Whole Exome Sequencing and RNA-Seq to Characterize the Somatic Breast Cancer Landscape Among Latinas in California

  Somatic mutational profiles are increasingly being used to guide treatment. However, there is a dearth of data from non-European populations. To address this gap, we conducted paired tumor/normal whole exome paired-end sequencing and tumor RNA-Seq on 146 breast tumors from 140 Hispanic/Latina (H/L) women with breast cancer. We characterized somatic mutations, copy number alterations, tumor subtypes [Prediction Analysis of Microarray 50 (PAM50)], Catalogue Of Somatic Mutations In Cancer (COSMIC) mutation signatures and expression profiles, and compared them to breast tumors from non-Hispanic White (White) women in The Cancer Genome Atlas (TCGA). Using MutSigCV, we found that the most commonly mutated genes, including TP53, RUNX1, PTEN, PIK3CA, MAP3K1, GATA3, CDH1 and CBFB, were similar to those in breast tumors from non-Hispanic white women. Novel findings were that outliers of BLTP2 (aka KIAA0100) over-expression and COSMIC mutational signature 16 were more common in tumors from H/L women than White women. We also identified that the known germline APOBEC3A/B deletion variant was significantly more common in H/L women and was associated with indigenous American ancestry. Data available through dbGaP will be whole-exome sequencing (WES) and RNA sequencing (RNA-Seq) data, as well as phenotypic data, including estrogen receptor, progesterone receptor, and HER2 receptor status, tumor histology, stage, and grade, and age at diagnosis.

  Study phs003218

• Whole transcriptome sequencing data of 3 histiocytic tumors with CLTC::SYK fusions

  The 3 tumor samples are PMLBM000JFR, PMLBM000JFT, and PMLBM000JFF. All samples are from different patients: Case 9 (PMLBM000JFR), Case 10 (PMLBM000JFT), and Case 12 (PMLBM000JFF) from the article by Kemps et al (Blood 2024 - In production). Methods: Total RNA was isolated and the generated libraries were sequenced on a NovaSeq 6000 (as described in Hehir-Kwa, et al. JCO Precis Oncol 2022). Data files: Provided are .cram and .crai files.

  Dataset EGAD50000000834

• RA-Map, A multi-omic survey of whole blood and subsets in early rheumatoid arthritis and vaccine study controls

  Rheumatoid arthritis (RA) is a chronic inflammatory disorder of unknown aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the molecular heterogeneity and pathogenesis of RA, we performed a comprehensive clinical and molecular profile of 267 RA patients for up to 18 months to establish a high quality biobank of barcoded samples that included plasma, serum, peripheral blood cells, whole blood RNA, RNA from lymphocyte and monocyte subsets, genomic DNA and urine. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and auto-antibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource for the development and application of targeted therapies for RA and reveal further insights into disease pathogenesis and therapeutic response.

  Study EGAS00001004424

• BPH Tissues for Cell Culture and Analysis - Spatial Transcriptomics Identifies Candidate Stromal Drivers of Benign Prostatic Hyperplasia

  The study goal was to apply spatial transcriptomics to identify candidate stromal drivers of benign prostatic hyperplasia (BPH). Laser microdissection (LCM) with RNA-seq of the stroma adjacent to hyperplastic and budding BPH ducts identified secreted factors including IGF1 and CXCL13. Single‐cell RNA sequencing (scRNA‐seq) revealed their co-expression from BPH fibroblasts. Additional studies sought to define similarities to embryonic prostate development, as well as therapeutic applications. Subjects were those who underwent prostatectomy for prostate or bladder cancer, with concurrent BPH, and who consented to use of surplus tissue for research studies. LCM/RNA-seq studies included 5 patients, and scRNA-seq studies included 1 patient. Phenotypic data submitted to this study include patient age, sex, prostate size, and international prostate symptom score (IPSS). Sequencing was done on an Illumina NovaSeq 6000 (LCM/RNAseq) and Illumina HiSeq X-Ten (scRNA-seq). The data processing pipeline utilized Kallisto (LCM/RNA-seq) and Cell Ranger (scRNA-seq). Data submitted are raw sequencing (Fastq) files.

  Study phs003477

• Dynamics of genome architecture and chromatin function during human B cell differentiation and neoplastic transformation

  Despite recent advances, the dynamics of genome architecture and chromatin function during human cell differentiation and its potential reorganization upon neoplastic transformation remains poorly characterized. Here, we integrate in situ Hi-C and nine additional omic layers to define and biologically characterize the dynamic changes in three-dimensional (3D) genome architecture across normal B cell differentiation and in neoplastic cells from different subtypes of chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) patients. Beyond conventional active (A) and inactive (B) compartments, an integrative analysis of Hi-C data uncovers a highly-dynamic intermediate compartment enriched in poised and polycomb-repressed chromatin. During B cell development, we detect that 28% of the compartments change at defined maturation stages and mostly involve the intermediate compartment. The transition from naive to germinal center B cells is associated with widespread chromatin activation, which mostly reverts into the naive state upon further maturation of germinal center cells into memory B cells. The analysis of CLL and MCL neoplastic cells points both to entity and subtype-specific alterations in chromosome organization. Remarkably, we observe that large chromatin blocks containing key disease-specific genes alter their 3D genome organization. These include the inactivation of a 2Mb region containing the EBF1 gene in CLL and the activation of a 6.1Mb region containing the SOX11 gene in clinically aggressive MCL. This study indicates that 3D genome interactions are extensively modulated during normal B cell differentiation and that the genome of B cell neoplasias acquires a tumor-specific 3D genome architecture.

  Study EGAS00001004763

• Integrative genomic analysis identifies key pathogenic mechanisms in primary mediastinal large B-cell lymphoma

  Primary mediastinal large B-cell lymphoma (PMBL) represents a clinically and pathologically distinct subtype of large B-cell lymphomas. Furthermore, molecular studies, including global gene expression profiling, have provided evidence that PMBL is more closely related to classical Hodgkin lymphoma (cHL). Although targeted sequencing studies have revealed a number of mutations involved in PMBL pathogenesis, a comprehensive description of disease-associated genetic alterations and perturbed pathways is still lacking. Here, we performed whole-exome sequencing of 95 PMBL tumors to inform on oncogenic driver genes and recurrent copy number alterations. The integration of somatic gene mutations with gene expression signatures provides further insights into genotype-phenotype interrelation in PMBL. We identified highly recurrent oncogenic mutations in the JAK-STAT and NF-kB pathways, and provide additional evidence of the importance of immune evasion in PMBL (CIITA, CD58, B2M, CD274, PDCD1LG2). Our analyses highlight the IRF-pathway as a putative novel hallmark with frequent alterations in multiple pathway members (IRF2BP2, IRF4, IRF8). In addition, our integrative analysis illustrates the importance of JAK1, RELB and EP300 mutations driving oncogenic signaling. The identified driver genes were significantly more frequently mutated in PMBL as compared to diffuse large B-cell lymphoma, whereas only a limited number of genes were significantly different between PMBL and cHL, emphasizing the close relationship between these entities. Our study, performed on a large cohort of PMBL, highlights the importance of distinctive genetic alterations for disease taxonomy with relevance for diagnostic work-up and therapeutic decision-making.

  Study EGAS00001003746

• Subset of EGAS00001005112 (The INFORM Precision Medicine Study for High-Risk Pediatric Malignancies, 17 exomes) which is used in EGAS00001005243 (Radiation-induced gliomas represent H3-/IDH-wild type pediatric gliomas with recurrent PDGFRA amplification and loss of CDKN2A/B)

  Part of the project: The INFORM Precision Medicine Study for High-Risk Pediatric Malignancies resulted in the publication of this study: Radiation-induced gliomas represent H3-/IDH-wild type pediatric gliomas with recurrent PDGFRA amplification and loss of CDKN2A/B. This dataset contains the subset of 17 patient exome sequencing data.

  Dataset EGAD00001007864

• Circulating Tumor DNA Analysis Profiles of Repotrectinib in NTRK fusion–positive advanced solid tumors: a phase 1/2 trial

  The dataset contains circulating tumor DNA (ctDNA) profiles from frozen plasma samples of 593 patients from the TRIDENT-1 clinical trial. Plasma was processed with centrifugation and automated liquid handling systems, and cell-free DNA was extracted using the Qiagen QIAsymphony platform. ctDNA libraries were constructed with the Guardant360 2.11 assay, which used targeted, hybridization-based capture and barcoding of cfDNA fragments for digital analysis, followed by high-throughput sequencing on the Illumina NextSeq 550 instrument. Sequencing data were processed and interpreted using the Bioinformatics Pipeline (BIP v3.5.2 or later) for variant calling and quantification and managed within LabVantage LIMS (v3.7 or later) to support sample tracking and workflow integration. Aligned read files are provided in bam and bai formats.

  Dataset EGAD50000002249