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• 3q-capture DNA sequencing of atypical 3q26 cases

  3q-capture DNA sequencing was performed as we described previously 13. In summary, genomic DNA was fragmented using the Covaris shearing device (Covaris), and sample libraries were assembled following the TruSeq DNA Sample Preparation Guide (Illumina). After ligation of adapters and an amplification step, target sequences of chromosomal regions 3q21.1-q26.2 were captured using custom in-solution oligonucleotide baits (Nimblegen SeqCap EZ Choice XL). The design of target sequences was based on the human genome assembly hg19: chr3q21.1:126036241-130672290 - chr3q26.2:157712147-175694147. Amplified captured sample libraries were paired-end sequenced (2x100 bp) on the HiSeq 2500 platform (Illumina) and aligned against the hg19 reference genome using the Burrows-Wheeler Aligner (BWA)25

  Dataset EGAD00001006123

• The Transcriptome of PLX4032 resistance

  We have collected material from a patient who had BrafV600E mutant melanoma that was treated with PLX4032. We have germline DNA from the patient and DNA and RNA from distinct lesions before and after treatment with PLX4032. We have transcriptome sequenced these samples to obtain a snap shot of the mechanisms of resistance that are operative.

  Dataset EGAD00001000599

• Delineate genomic and epigenomic changes in esophageal squamous cell carcinoma following radiotherapy

  We performed whole-exome sequencing and whole epigenome sequencing (RRBS) of samples collected from different time points during radiotherapy from thirty-four ESCC patients. We compared the genetic and epigenetic features of the different time biopsy samples to reveal the changes in ESCC received radiotherapy.

  Dataset EGAD00001003799

• Genome-wide gene expression analysis following CRISPRi of transposable elements

  human induced pluripotent stem cells constitutely expressing the CRISPRi machinery were transduced with gRNAs targeting genomic regions of transposable elements (TEs), and differentiated to neural progenitor cells. The aim of the study was to annotate the function of these TEs in the context of early neurodevelopmental processes.

  Study EGAS00001008265

• Fragmentomics profiling and quantification of plasma Epstein-Barr virus DNA enhance prediction of future nasopharyngeal carcinoma.

  This study evaluated the clinical utility of fragmentomics analysis of plasma Epstein-Barr virus (EBV) DNA in nasopharyngeal carcinoma (NPC) screening. The first-round EBV-positive blood samples from a two-round large-scale prospective NPC screening cohort were analyzed. The EBV DNA of subjects who developed NPC in the second round displayed a distinctive mononucleosomal size pattern, an NPC-associated end motif profile, and aberrations in methylation deduced by fragmentomics-based methylation analysis (FRAGMA). Subjects with these aberrant fragmentomics features and higher EBV DNA quantity showed a dramatically increased risk of NPC development, demonstrating the potential of plasma DNA fragmentomics in predicting future cancer risk.

  Study EGAS50000000395

• Comprehensive single-cell genome analysis at nucleotide resolution using the PTA Analysis Toolbox

  We developed a comprehensive bioinformatic workflow, called the PTA Analysis Toolbox (PTATO), to accurately detect single base substitutions, insertions-deletions (indels) and structural variants in PTA-based WGS data. PTATO includes a machine learning approach and filtering based on recurrency to distinguish PTA-artefacts from true mutations with high sensitivity (up to 90%), outperforming existing bioinformatic approaches. Our results show that PTATO enables studying somatic mutagenesis in the genomes of single cells with unprecedented sensitivity and accuracy.

  Study EGAS00001007288

• The Transcriptional Landscape of SHH Medulloblastoma

  To further understand the biology of Sonic hedgehog medulloblastoma and its molecular subtypes, we studied 250 human Shh-MB using strand-specific RNA sequencing. We identified novel alterations within the cAMP dependent pathway and found that 18% of tumors have genetic events that directly target the abundance and/or stability of MYCN. We also discovered an extensive network of fusions in focally amplified regions, and several loss-of-function fusions in tumor suppressor genes PTCH, SUFU and NCOR1. Molecular convergence on a core of specific genes by nucleotide variants, copy number aberrations, and gene fusions highlights key roles of specific pathways in the pathogenesis of Sonic hedgehog medulloblastoma.

  Dataset EGAD00001006305

• RNA sequencing of surgically removed lung adenocarcinoma afterwards treated with immune checkpoint inhibitors

  Patients with lung adenocarcinoma (LUAD) from The Cancer Genome Atlas (TCGA) database were enrolled in the training cohort to establish a prognostic signature based on the expression of tumor-specific amino acid metabolism related genes. The established signature was further investigated against an original cohort, KCC-ICI, of chemotherapy combined with immune checkpoint inhibitors. The signature consisting of nine genes, KYNU, PSPH, PPAT, MIF, GCLC, ACAD8, TYRP1, ALDH2, and HDC, could effectively stratify the OS in LUAD patients. The KCC-ICI cohort confirmed the predictive ability of the established signature in the clinical response to immune checkpoint blockade therapy, which correlated with the infiltration of immune cells (e.g., T lymphocytes and nature killer cells). We discovered that the high signature risk score patients showed a significantly lower concentration of plasma-free ??-aminobutyric acid (AABA).

  Study JGAS000675

• Massively Parallel Single-Cell RNA-Sequencing of Chronic Rhinosinusitis Nasal and Sinus Tissue

  Single-cell RNA sequencing (scRNA-seq) using the SeqWell V1 platform on sinus mast cells flow cytometrically sorted from the nasal polyps of patients with chronic rhinosinsusitis (CRS) with nasal polyps (CRSwNP) and aspirin-exacerbated respiratory disease (AERD).

  Study phs002333

• RNA-Sequencing data of Fusobacterium nucleatum treated CAFs and HT-29 tumor spheroid exposed to Fusobacterium nucleatum treated CAFs conditioned medium.

  RNA-Sequencing data of CAFs (patient derived CAF180 and CAF181 as well as the CT5.3 CAF cell line) and HT-29 tumor spheroid samples performed in the context of the study of the interaction of Fusobacterium nucleatum with CRC CAFs. Fusobacterium nucleatum interacts with cancer-associated fibroblasts to enhance colorectal cancer progression

  Dataset EGAD50000001614

• Whole Exome Sequencing Bipolar cases matched controls performed at Broad Inst on cohort from Germany

  This research project was a collaboration between University Hospital Frankfurt and the Stanley Center at the Broad Institute. In this project we sequenced and analyzed the whole exomes of 823 Bipolar case/control samples from collaborators in Germany. Genomic DNA from each sample was sequenced to a mean depth of 20x. The exome used Twist capture and samples were sequenced on Illumina HiSeqX machines producing cram files.

  Dataset EGAD50000000563

• Whole Exome Sequencing of Bipolar cases, matched controls at Broad Inst on cohort from Cambridge, UK

  This research project was a collaboration between Cambridge University, UK and the Stanley Center at the Broad Institute. In this project we sequenced and analyzed the whole exomes of 2,873 Bipolar case/control samples from collaborators in UK. Genomic DNA from each sample was sequenced to a mean depth of 20x. The exome used Twist capture and samples were sequenced on Illumina HiSeqX machines producing cram files

  Dataset EGAD50000000627

• RNA-Sequencing data of patient derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroid samples

  RNA-Sequencing data of patient derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroid samples performed in the context of the characterization of an IL1R1 positive CAF population in CRC tumour samples.

  Study EGAS00001007205

• PLCRC study

  Genomic libraries (500 bps) will be generated from total genomic DNA derived from Colorectal cancer patients and subjected to short paired end sequencing on the llumina platform. Paired reads will be mapped to build 37 of the human reference genome to facilitate the generation of genome wide copy number information, and the identification of novel rearranged cancer genes and gene fusions.

  Dataset EGAD00001000947

• Whole exome sequencing data of germline and two independent primary leukemias of five patients

  The contribution of genetic predisposing factors to the development of pediatric acute lymphoblastic leukemia (ALL), the most frequently diagnosed cancer in childhood, has not been fully elucidated. Children presenting with multiple de novo leukemias are more likely to suffer from genetic predisposition. Here, we selected five of these patients and analyzed the mutational spectrum of normal and malignant tissues.

  Dataset EGAD00001002266

• Transcriptome: chondrosarcoma

  Transcriptome sequencing of nine patients diagnosed with chondrosarcoma. cDNA was generated using the NuGEN Ovation RNA-Seq FFPE system. Total RNA was randomly primed and thermally sheared and the resulting cDNA fragment was amplified. The cDNA was then mechanically sheared using sonication to generate ~250 bp fragments. Sequencing libraries were generated using the NuGEN Ovation Ultralow System V2 library prep kit and sequenced on HiSeq2500 TruSeq v3.

  Dataset EGAD00001008699

• Characterisation of the genetic landscape of cutaneous leiomyoma and leiomyosarcoma - Leiomyoma WES

  Cutaneous leiomyoma (cLM) and leiomyosarcoma (cLMS) are rare benign and malignant soft tissue neoplasms showing smooth muscle differentiation, respectively, that arise from mesenchymal cells in the dermis and subcutis. Through whole exome sequencing of cLM and cLMS cases, we observed distinct differences between the somatic mutational profile of these tumour types. FH was identified as a driver gene in cLM with genetic alterations of FH occurring via somatic point mutation, somatic copy number loss, biallelic inactivation and germline point mutations. TP53 and RB1 were identified as driver genes in the cLMS cohort, with genetic alterations of TP53 occurring via somatic and germline point mutations, copy number loss and biallelic inactivation. Using RNA-sequencing, we identified recurrent gene fusions, including CRTC1/3-MAML2 in cLMS and a novel MYLK-MAP3K2 fusion. Analysis of the cell types present in the tumour microenvironment revealed a significantly increased presence of macrophages and decreased presence of myeloid dendritic cells in the cLMS cohort relative to the cLM cohort. Additionally, we identified common driver genes between cLMS and LMS from other sites. Thus, we provide the first in-depth profile of the genetic landscape of cLM and cLMS.

  Dataset EGAD00001014787

• Characterisation of the genetic landscape of cutaneous leiomyoma and leiomyosarcoma - Leiomyoma RNA

  Cutaneous leiomyoma (cLM) and leiomyosarcoma (cLMS) are rare benign and malignant soft tissue neoplasms showing smooth muscle differentiation, respectively, that arise from mesenchymal cells in the dermis and subcutis. Through whole exome sequencing of cLM and cLMS cases, we observed distinct differences between the somatic mutational profile of these tumour types. FH was identified as a driver gene in cLM with genetic alterations of FH occurring via somatic point mutation, somatic copy number loss, biallelic inactivation and germline point mutations. TP53 and RB1 were identified as driver genes in the cLMS cohort, with genetic alterations of TP53 occurring via somatic and germline point mutations, copy number loss and biallelic inactivation. Using RNA-sequencing, we identified recurrent gene fusions, including CRTC1/3-MAML2 in cLMS and a novel MYLK-MAP3K2 fusion. Analysis of the cell types present in the tumour microenvironment revealed a significantly increased presence of macrophages and decreased presence of myeloid dendritic cells in the cLMS cohort relative to the cLM cohort. Additionally, we identified common driver genes between cLMS and LMS from other sites. Thus, we provide the first in-depth profile of the genetic landscape of cLM and cLMS.

  Dataset EGAD00001014788

• Characterisation of the genetic landscape of cutaneous leiomyoma and leiomyosarcoma - Leiomyosarcoma WES

  Cutaneous leiomyoma (cLM) and leiomyosarcoma (cLMS) are rare benign and malignant soft tissue neoplasms showing smooth muscle differentiation, respectively, that arise from mesenchymal cells in the dermis and subcutis. Through whole exome sequencing of cLM and cLMS cases, we observed distinct differences between the somatic mutational profile of these tumour types. FH was identified as a driver gene in cLM with genetic alterations of FH occurring via somatic point mutation, somatic copy number loss, biallelic inactivation and germline point mutations. TP53 and RB1 were identified as driver genes in the cLMS cohort, with genetic alterations of TP53 occurring via somatic and germline point mutations, copy number loss and biallelic inactivation. Using RNA-sequencing, we identified recurrent gene fusions, including CRTC1/3-MAML2 in cLMS and a novel MYLK-MAP3K2 fusion. Analysis of the cell types present in the tumour microenvironment revealed a significantly increased presence of macrophages and decreased presence of myeloid dendritic cells in the cLMS cohort relative to the cLM cohort. Additionally, we identified common driver genes between cLMS and LMS from other sites. Thus, we provide the first in-depth profile of the genetic landscape of cLM and cLMS.

  Dataset EGAD00001014789

• Characterisation of the genetic landscape of cutaneous leiomyoma and leiomyosarcoma - Leiomyosarcoma RNA

  Cutaneous leiomyoma (cLM) and leiomyosarcoma (cLMS) are rare benign and malignant soft tissue neoplasms showing smooth muscle differentiation, respectively, that arise from mesenchymal cells in the dermis and subcutis. Through whole exome sequencing of cLM and cLMS cases, we observed distinct differences between the somatic mutational profile of these tumour types. FH was identified as a driver gene in cLM with genetic alterations of FH occurring via somatic point mutation, somatic copy number loss, biallelic inactivation and germline point mutations. TP53 and RB1 were identified as driver genes in the cLMS cohort, with genetic alterations of TP53 occurring via somatic and germline point mutations, copy number loss and biallelic inactivation. Using RNA-sequencing, we identified recurrent gene fusions, including CRTC1/3-MAML2 in cLMS and a novel MYLK-MAP3K2 fusion. Analysis of the cell types present in the tumour microenvironment revealed a significantly increased presence of macrophages and decreased presence of myeloid dendritic cells in the cLMS cohort relative to the cLM cohort. Additionally, we identified common driver genes between cLMS and LMS from other sites. Thus, we provide the first in-depth profile of the genetic landscape of cLM and cLMS.

  Dataset EGAD00001014790

• ABCB1 expression in HCC biopsies

  We analyzed the ABCB1 expression in RNA-seq data of 134 HCCs (120 of these were previously published), including the biopsies from which the 3 doxorubicin-sensitive and 3 doxorubicin-resistant HCCOs were derived.

  Study EGAS50000000041

• Multi-region exome sequencing of lung adenocarcinoma precursors -1

  To characterize the genomic landscape of invasive lung adenocarcinoma and its precursors; to depict the genomic evolution from preneoplasia of lung to invasive lung adenocarcinoma; to decipher mechanism to drive the tumor progression.

  Study EGAS00001003439

• Rare germline variants of acute myeloid leukemia patients

  The dataset (vcf files) consists of rare germline variants of 68 Finnish acute myeloid leukemia patients. We performed exome sequencing and filtered the germline variants against ExAC total MAF<0.01 in two gene panels. The 35 genes in the panels studied here have previously been associated with hematological malignancies and/or solid tumors. The dataset contains only variants of the two gene panels.

  Dataset EGAD00001003894

• The effect of blood tube and time delay on the genome-wide methylation pattern of cfDNA

  In this study, we evaluated the effect of preservation agens on the effect of the methylation pattern of cell-free DNA. The methylation pattern was assessed with cell-free reduced representation sequencing (cf-RRBS). All 45 samples were sequenced on a NovaSeq6000, and samples are provided as raw fastq files.

  Dataset EGAD00001006007

• Massively parallel nanowell-based single-cell gene expression profiling

  Technological advances have enabled transcriptome characterization of cell types at the single-cell level providing new biological insights. New methods that enable simple yet high-throughput single-cell expression profiling are highly desirable. Here we report a novel nanowell-based single-cell RNA sequencing system, ICELL8, which enables processing of thousands of cells per sample. The system employs a 5184-nanowell-containing microchip to capture ~1300 single cells and process them. Each nanowell contains preprinted oligonucleotides encoding poly-d(T), a unique well barcode, and a unique molecular identifier. The ICELL8 system uses imaging software to identify nanowells containing viable single cells and only wells with single cells are processed into sequencing libraries. Here, we report the performance and utility of ICELL8 using samples of increasing complexity from cultured cells to mouse solid tissue samples. Our assessment of the system to discriminate between mixed human and mouse cells showed that ICELL8 has a low cell multiplet rate (< 3%) and low cross-cell contamination. We characterized single-cell transcriptomes of more than a thousand cultured human and mouse cells as well as 468 mouse pancreatic islets cells. We were able to identify distinct cell types in pancreatic islets, including alpha, beta, delta and gamma cells. Overall, ICELL8 provides efficient and cost-effective single-cell expression profiling of thousands of cells, allowing researchers to decipher single-cell transcriptomes within complex biological samples.

  Study EGAS00001002320