4116 results for "*oma"

in 49.88 milliseconds.

• Pre-neoplastic liver colonization by 11p15.5 altered mosaic cells in young children with hepatoblastoma

  Additional datasets linked to EGAS00001006692

  Dataset EGAD00001011097

• Detection of somatic mutations of angioimmunoblastic T-cell lymphoma

  Study EGAS00001007333

• WES data for study of the microenviroment of angioimmunoblastic T-cell lymphoma

  Exome sequencing data for study of the microenviroment of angioimmunoblastic T-cell lymphoma

  Dataset EGAD00001011581

• Sequential Antigen-loss and Branching Evolution in Lymphoma after Anti-CD19 and Anti-CD20 Targeted T Cell Engaging Immunotherapy

  CD19 CAR T cells and CD20 targeting T cell engaging bispecific antibodies have been approved in B-cell Non-Hodgkin lymphoma lately, heralding a new clinical setting where patients are treated with both approaches, sequentially. The aim of our study was to investigate the selective pressure of CD19 and CD20 directed therapy on the clonal architecture in lymphoma. Using a broad analytical pipeline, we identified truncating mutations in the gene encoding CD20 conferring antigen loss in 80% of patients relapsing from CD20 bispecs. Pronounced T cell exhaustion was identified in cases with progressive disease and retained CD20 expression. We also confirmed CD19 loss after CAR T cell therapy and report the case of sequential CD19 and CD20 loss. We observed branching evolution with re-emergence of CD20 positive subclones at later time points and spatial heterogeneity for CD20 expression in response to targeted therapy. Our results highlight immunotherapy as an evolutionary bottleneck selecting for antigen-loss variants but also complex evolutionary pathways underlying disease progression from these novel therapies.

  Study EGAS00001007561

• scRNA-seq, WES, and bulk RNA-seq on longitudinal samples from 7 Lymphoma patients treated with CD20xCD3 bispecific antibodies

  We performed scRNA-seq on 15 fresh lymph node core biopsies from 7 Lymphoma patients treated with CD20xCD3 bispecific antibodies. We also performed whole-exome sequencing (WES) and bulk RNA-seq on formalin-fixed paraffin embedded (FFPE) tumor samples from these patients. WES was additionally performed on matched germline samples (blood) for each patient.

  Dataset EGAD00001011350

• Single-cell RNA-seq data of angioimmunoblastic T-cell lymphoma

  Single-cell RNA-seq data of angioimmunoblastic T-cell lymphoma

  Dataset EGAD00001011361

• WES raw data set for the study "Genomic profiling of localized (lFL) and systemic follicular lymphoma (sFL) reveals novel insights into FL pathogenesis"

  221 patient samples including 164 initial tumor (TI) samples (53/164 fresh frozen TI samples, and 111/164 formalin-fixed paraffin-embedded (FFPE) TI samples), 22 paired matched normal samples, and 35 unpaired normal samples from healthy donors; FASTQ file format, Agilent SureSelect Human All Exon V6 Kit (Agilent Technologies, Inc., Santa Clara, California, USA)

  Dataset EGAD00001011369

• OncoScan SNP data set for systemic follicular lymphoma (sFL)

  122 unpaired initial tumor samples (122 FFPE samples) of sFL patients measured with OncoScan SNP microarrays, Affymetrix CEL intensity data file types (Thermo Fisher Scientific, Waltham, Massachusetts, USA)

  Dataset EGAD00010002592

• OncoScan SNP data set for localized follicular lymphoma (lFL)

  149 unpaired initial tumor samples (133/149 FFPE and 16/149 fresh frozen samples) of lFL patients measured with OncoScan SNP microarrays, Affymetrix CEL intensity data file types (Thermo Fisher Scientific, Waltham, Massachusetts, USA)

  Dataset EGAD00010002593

• Study of the microenvironment of angioimmunoblastic T-cell lymphoma

  Dac EGAC00001002756

• Whole genome sequencing of Osteosarcoma clonal evolution

  Multiple large-scale genomic profiling efforts have been undertaken in osteosarcoma to define the genomic drivers of tumorigenesis, therapeutic response, and disease recurrence. The spatial and temporal intratumor heterogeneity could also play a role in promoting tumor growth and treatment resistance. Here, we conducted longitudinal whole-genome sequencing of 37 tumor samples from eight patients with osteosarcoma that relapsed or became refractory to initial therapy. We found that the chemoresistant population in recurrent osteosarcoma is subclonal at diagnosis, emerges at the time of primary resection due to selective pressure from neoadjuvant chemotherapy, and is characterized by unique oncogenic amplifications.

  Dataset EGAD00001011285

• HDAC inhibitor quisinostat in synovial sarcoma cell lines

  An RNA Seq study of the effects of HDAC inhibitor Quisinostat on six different synovial sarcoma cell lines

  Dataset EGAD00001003810

• VRK3 depletion in Pontine Diffuse Midline Glioma DMG-K27 altered cells

  In order to investigate possible mechanisms underlying the phenotype of cell fitness decline observed following decrease of VRK3 in pontine DMG-K27 altered cells 7, we examined differences in global gene expression. RNA-seq was performed 44h and 60h post-transduction with two distinct shRNAs targeting VRK3 to be able to evaluate the early impact of VRK3 knock-down (KD) in four independent in vitro models of DMG

  Dataset EGAD00001010097

• Low-coverage whole-genome sequencing of cancer and healthy plasma circulating DNA

  Plasma samples from patients with melanoma (stage II/III/IV) and breast cancer (stage IV) as well as healthy individuals were subjected to low-coverage whole-genome sequencing (less than 10x average depth). This dataset contains raw fastq files from 39 breast cancer, 127 melanoma and 42 healthy control plasma samples.

  Dataset EGAD00001011817

• Multiregional single cell RNA sequencing of human renal cell carcinoma

  The dataset comprises of 5' single cell RNA sequencing with TCR enrichment with 10x Genomics' Chromium technology of multiregional biopsies of human renal cell carcinomas. Biopsies from different tumour regions, the tumour-normal interface, normal kidney, normal adrenal, metastatic regions, peri-nephric fat, and peripheral blood were sequenced from 12 patients with kidney tumours.

  Dataset EGAD00001008030

• Linked-Read Medulloblastoma DAC

  Dac EGAC00001003236

• RNA-Seq Medulloblastoma data

  RNA-Seq data from 12 medulloblastoma samples, all group 4 medulloblastomas. The data consists of BAM files aligned using STAR

  Dataset EGAD00001010850

• Nanopore medulloblastoma data

  Nanopore data from 3 medulloblastoma samples of which 2 are tumor-normal pairs sequenced with the MinIon and one is tumor only data sequenced on the PromethIon. The data consists of BAM files aligned using minimap2

  Dataset EGAD00001010851

• PacBio medulloblastoma datasets

  PacBio data from 5 medulloblastoma tumor-normal pairs. The data consists of BAM files aligned using NGMLR

  Dataset EGAD00001010852

• Detection and genomic analysis of BRAF fusions in Juvenile Pilocytic Astrocytoma through the combination and integration of multi-omic data

  Juvenile Pilocytic Astrocytoma (JPAs) are highly vascular tumors and show pervasive immune infiltration, which can lead to low tumor cell purity in clinical samples. In some instances, this results in gene fusions that are difficult to detect with conventional omics approaches including RNA-Seq. To this effect, we applied RNA-Seq as well as linked-read whole-genome sequencing and in situ Hi-C as new approaches to detect and characterize low-frequency gene fusions at the genomic, transcriptomic and spatial level. Overall, we demonstrate the power of integrating multi-omic datasets to identify low frequency fusions and characterize the JPA genome at high resolution.

  Study EGAS00001006388

• Linked-Read Medulloblastoma data

  Linked-read data from 25 medulloblastomas and their matching control. Dataset consists of 25 group 4 medulloblastomas (G4) as well as 2 sonic hedgehog medulloblastomas (SHH-MB) samples and 2 group 3 medulloblastomas. The data consists of BAM files generated by the LongRanger pipeline developed by 10x Genomics

  Dataset EGAD00001010849

• Complex structural variation patterns in pediatric solid tumors WGS

  Paired tumor-normal whole genome sequencing data from primary tumors of patients diagnosed with neuroblastoma, Ewing sarcoma, Wilms tumor, hepatoblastoma and rhabdomyosarcoma

  Dataset EGAD00001011378

• Germline BAMs from patients with both uveal and cutaneous melanoma

  Germline BAMs from blood/saliva samples from patients diagnosed with both uveal and cutaneous patients. Reads have been aligned, deduplicated and recalibrated.

  Dataset EGAD00001011676

• Efficacy of two different FGFR-inhibitors in a patient with extrahepatic cholangiocarcinoma harboring an FGFR2 mutation

  Cholangiocarcinomas (CCAs) is a type of cancer with few effective systemic therapies. Elucidation of the molecular landscape of the disease from genomic studies based on next generation sequencing (NGS) has contributed to the introduction of new targeted therapies. One of these treatments consists of a class of small molecules that target members of the FGFR family of receptor tyrosine kinases. These drugs are effective and have been approved for cholangiocarcinomas with fusions or rearrangements of FGFR genes. In contrast, the role of these inhibitors in cholangiocarcinomas with mutations in FGFR genes is less well defined. We report here a patient with a cholangiocarcinoma bearing a FGFR2 p.Ser252Trp mutation. The patient was treated with two different FGFR inhibitors, as the first caused ocular toxicity. She obtained clinical benefit from both. This case illustrates the efficacy of FGFR inhibitors on cholangiocarcinoma with specific point mutations. This is the first case to report the clinical benefit of these drugs in FGFR2 p.Ser252Trp mutation. Clinical benefit can be sustained, as seen in our patient. Our case also shows that FGFR inhibitors-induced adverse effects, such as ocular toxicities, may not recur after re-challenge with an alternative drug of the same class.

  Study EGAS50000000015

• Efficacy of two different FGFR-inhibitors in a patient with extrahepatic cholangiocarcinoma harboring an FGFR2 mutation

  Cholangiocarcinomas (CCAs) is a type of cancer with few effective systemic therapies. Elucidation of the molecular landscape of the disease from genomic studies based on next generation sequencing (NGS) has contributed to the introduction of new targeted therapies. One of these treatments consists of a class of small molecules that target members of the FGFR family of receptor tyrosine kinases. These drugs are effective and have been approved for cholangiocarcinomas with fusions or rearrangements of FGFR genes. In contrast, the role of these inhibitors in cholangiocarcinomas with mutations in FGFR genes is less well defined. We report here a patient with a cholangiocarcinoma bearing a FGFR2 p.Ser252Trp mutation. The patient was treated with two different FGFR inhibitors, as the first caused ocular toxicity. She obtained clinical benefit from both. This case illustrates the efficacy of FGFR inhibitors on cholangiocarcinoma with specific point mutations. This is the first case to report the clinical benefit of these drugs in FGFR2 p.Ser252Trp mutation. Clinical benefit can be sustained, as seen in our patient. Our case also shows that FGFR inhibitors-induced adverse effects, such as ocular toxicities, may not recur after re-challenge with an alternative drug of the same class.

  Dataset EGAD50000000021

• The Precision Medicine in Liver Cancer across an Asia-pacific NETwork (PLANET)

  Hepatocellular carcinoma (HCC) is the 2nd most important cause of cancer deaths in the world. The outcomes of treatment in HCC are poor compared to other common cancers because there are no good systemic therapy drugs. We designed a prospective study that will involve 5 different sites within the established Asia-Pacific Hepatocellular Carcinoma Trials Group to study both the genetics as well as immune profiles of HCC in different ethnicities. In this study, patients will be followed-up and at recurrence the tissues to understand the evolution of disease progression. Here, we presented both the genomic (DNA) and phenotypic (RNA) evolution for the first batch of 56 patients. The detailed findings will be listed in the corresponding publication soon.

  Study EGAS00001003813

• Tracing early predictors of glioma evolution under therapy

  Clonal evolution drives cancer progression and therapeutic resistance. Recent studies revealed divergent longitudinal trajectories in gliomas, but early molecular traits steering post-treatment cancer evolution remain unclear. We analyzed sequencing data of 544 initial-recurrent adult diffuse glioma pairs to identify genomic and transcriptomic early predictors of tumor evolution in each molecular subtype.

  Study EGAS00001006894

• Sequencing of longitudinal glioma pairs

  Clonal evolution drives cancer progression and therapeutic resistance. Recent studies revealed divergent longitudinal trajectories in gliomas, but early molecular traits steering post-treatment cancer evolution remain unclear. We analyzed sequencing data of 544 initial-recurrent adult diffuse glioma pairs to identify genomic and transcriptomic early predictors of tumor evolution in each molecular subtype.

  Dataset EGAD00001009845

• The Leeds Melanoma Cohort gene expression data access committee

  Dac EGAC00001000893

• Sequencing data for oesophageal and related samples - Abbas et al (WGS)

  Data supporting: "Mutational signature dynamics shaping the evolution of oesophageal adenocarcinoma" Abbas et al (WGS for 1397 samples)

  Dataset EGAD00001011196

• Sequencing data for oesophageal and related samples - Abbas et al (RNA)

  Data supporting: "Mutational signature dynamics shaping the evolution of oesophageal adenocarcinoma" Abbas et al (RNA for 197 samples)

  Dataset EGAD00001011269

• Single-cell RNA-seq and spatial transcriptomics data for the sarcoidosis baseline project

  Granulomas are lumps of immune cells that can form in various organs. Most granulomas appear unstructured, yet they have some resemblance to lymphoid organ formation. To better understand granuloma formation, we performed single-cell sequencing and spatial transcriptomics on granulomas from patients with sarcoidosis and bioinformatically reconstructed the underlying gene-regulatory networks. We discovered an immune stimulatory environment in granulomas that repurposed transcriptional programs associated with lymphoid organ development. Granuloma formation followed characteristic spatial patterns and involved genes linked to immunometabolism, cytokine and chemokine signaling, and extracellular matrix remodeling. Three cell types emerged as key players in granuloma formation: metabolically reprogrammed macrophages, cytokine-producing Th17.1 cells, and fibroblasts with inflammatory and tissue remodeling phenotypes. Pharmacological inhibition of one of the identified processes attenuated granuloma formation in a sarcoidosis mouse model. We show that human granulomas adopt characteristic aspects of normal lymphoid organ development in aberrant combinations, indicating that granulomas constitute aberrant lymphoid organs.

  Study EGAS00001006970

• Methylome profiling of Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) and a patient derived cell-line model

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. This study established and characterized a novel SFT/HPC patient-derived cell line called SFT-S1 using the twist human methylome panel.

  Study EGAS50000000026

• Evaluating potential drug candidates for the treament of Henamgiopericytoma on patient derived cell line models

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. This study established and characterized a novel SFT/HPC patient-derived cell line called SFT-S1. Potential drug candidates that could be repurposed for the treatment of SFT/HPC were screened.

  Study EGAS50000000027

• Whole genome sequencing of Sinonasal hemangiopericytoma and patient derived cell line model

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. This study established and characterized a novel SFT/HPC patient-derived cell line called SFT-S1 using whole genome sequencing.

  Study EGAS50000000025

• Methylome profiling of Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) and a patient derived cell-line model

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. This study established and characterized a novel SFT/HPC patient-derived cell line called SFT-S1 using the twist human methylome panel.

  Dataset EGAD50000000040

• Evaluating potential drug candidates for the treament of Henamgiopericytoma on patient derived cell line models

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. This study established and characterized a novel SFT/HPC patient-derived cell line called SFT-S1. Potential drug candidates that could be repurposed for the treatment of SFT/HPC were screened. Screening was performed through RNA-Seq

  Dataset EGAD50000000039

• Whole genome sequencing of Sinonasal hemangiopericytoma and patient derived cell line model

  Solitary fibrous tumor/Hemangiopericytoma (SFT/HPC) is a rare subtype of soft tissue sarcoma associated with NAB2-STAT6 gene fusions. In this study, a novel SFT/HPC was characterized using whole genome sequencing.

  Dataset EGAD50000000038

• Single-cell multi-omic analysis of control and glioblastoma samples from the brain and border regions.

  Single-cell RNA-sequencing. Some samples were analyzed using CITE-Seq and samples were multiplexed and run on the same 10X reaction

  Dataset EGAD50000000045

• Origination of Ovarian Cancer is Dependent on Specific Aneuploidy Landscape

  Ovarian high-grade serous carcinoma (HGSC), a highly chromosomally instable malignancy, develops through sequential stages of precursors in fallopian tubes including histologically unremarkable but TP53 mutated clones (p53 signature) and serous tubal intraepithelial carcinoma (STIC). Here, we applied RealSeqS to assess aneuploidy in 127 microdissected tubal regions. We found nearly all p53 signatures lost the entire Chr17 chromosome, offering a “two-hit” mechanism of both TP53 and BRCA1 in BRCA1 germline mutation carriers. Proliferatively active STICs harbor gains of 19q12 (CCNE1), 19q13.2, 8q24 (MYCyc), or 8q arm, while proliferatively dormant STICs show 22q loss. Based on aneuploidy patterns in a training set (n= 67), we developed an algorithm, REAL-FAST, to classify NFTE and STICs into 5 clusters. In an independent validation set (n= 72), REAL-FAST was able to detect STIC/HGSC with high sensitivity and specificity. Taken together, REAL-FAST promises a molecular test for diagnosing HGSC precursor lesions based on specific aneuploidy patterns.

  Study EGAS00001007220

• Biallelic HMBS Inactivation Defines a Homogenous Clinico-Molecular Subtype of Hepatocellular Carcinoma

  Acute intermittent porphyria (AIP), caused by heterozygous germline mutations of the heme synthesis pathway enzyme HMBS (hydroxymethylbilane synthase), confers high risk of hepatocellular carcinoma (HCC) development. Yet, the role of HMBS in liver tumorigenesis remains unclear. Here we explore HMBS alterations in a large series of 758 HCC. We identify recurrent bi-allelic HMBS inactivation, both in AIP patients acquiring a second somatic HMBS mutation and in sporadic HCC with two somatic hits. HMBS alterations are enriched in truncative mutations, in particular in splice regions, leading to abnormal transcript structures. Bi-allelic HMBS inactivation results in a massive accumulation of its toxic substrate porphobilinogen and synergizes with CTNNB1 activating mutations, leading to the development of well differentiated tumors with a transcriptomic signature of Wnt/ß-catenin pathway activation and a DNA methylation signature related to ageing. HMBS-inactivated HCC mostly affect females, in absence of fibrosis and classical HCC risk factors. These data identify HMBS as a tumor suppressor gene whose bi-allelic inactivation defines a homogenous clinical and molecular HCC subtype.

  Study EGAS00001005986

• Single cell multi-omic study of H3-K27M mutant diffuse midline glioma across age and location

  Histone 3 lysine27-to-methionine (H3-K27M) mutations most frequently occur in childhood diffuse midline gliomas (DMGs) of the pons, but are also increasingly recognized in adult DMGs. Their potential heterogeneity at different ages and midline locations are vastly understudied. Here, through dissecting the single-cell transcriptomic, epigenomic and spatial architectures of a comprehensive cohort of patient H3-K27M DMGs, we delineate how age and anatomical location shape glioma cell-intrinsic and -extrinsic features in light of the shared driver mutation. We conducted multi-omic profiling of 50 H3-K27M mutant patient tumors. We performed deep full-length Smart-seq2 fresh single-cell (n=18) or frozen single-nucleus (n=25) RNA-sequencing (sc/snRNA-seq) of 43 tumors). We additionally analyzed the open chromatin profiles of 8 tumors utilizing the single-cell/nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq)

  Study EGAS00001006994

• Biallelic HMBS Inactivation Defines a Homogenous Clinico-Molecular Subtype of Hepatocellular Carcinoma

  Dataset EGAD00001009745

• Single-cell RNA-sequencing of H3-K27M diffuse midline glioma.

  Fastq files are deposited for single-cell transcriptomes of patient H3-K27M diffuse midline gliomas, generated using the SMART-seq2 method.

  Dataset EGAD00001011339

• MutWP1: CRUK Grand Challenge Mutographs of Cancer: Kidney (1)

  The Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Different patterns of somatic mutation are generated by the different environmental, lifestyle and genetic factors that cause cancer, many of them are still unknown. Within Mutographs, the International Agency for Research on Cancer is coordinating the recruitment of 5000 individuals with cancer (colorectal, renal, pancreatic, oesophageal adenocarcinoma or oesophageal squamous cancers) across 5 continents to explore whether different mutational signatures explain marked variation in incidence. In brief, through an international network of collaborators around the world, biological materials are collected, along with demographic, histological, clinical and questionnaire data. Whole genome sequences of tumour-germline DNA pairs are generated at the Wellcome Trust Sanger Institute. Somatic mutational signatures are subsequently extracted by non-negative matrix factorisation methods and correlated with risk factors data. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development.

  Dataset EGAD00001006427

• Mutational signatures in esophageal squamous cell carcinoma from eight countries of varying incidence – patient metatdata (Mutographs)

  Mutational signatures in esophageal squamous cell carcinoma from eight countries of varying incidence – patient metatdata (Mutographs)

  Dataset EGAD00001006732

• MutWP1 CRUK Grand Challenge Mutographs of Cancer Colorectal

  The Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Different patterns of somatic mutation are generated by the different environmental, lifestyle and genetic factors that cause cancer, many of them are still unknown. Within Mutographs, the International Agency for Research on Cancer is coordinating the recruitment of 5000 individuals with cancer (colorectal, renal, pancreatic, oesophageal adenocarcinoma or oesophageal squamous cancers) across 5 continents to explore whether different mutational signatures explain marked variation in incidence. In brief, through an international network of collaborators around the world, biological materials are collected, along with demographic, histological, clinical and questionnaire data. Whole genome sequences of tumour-germline DNA pairs are generated at the Wellcome Trust Sanger Institute. Somatic mutational signatures are subsequently extracted by non-negative matrix factorisation methods and correlated with risk factors data. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development.

  Dataset EGAD00001007510

• Whole genome, exome and RNA sequencing of TFCP2-rearranged rhabdomyosarcoma

  Whole genome, exome and RNA sequencing of TFCP2-rearranged rhabdomyosarcoma, 86 samples of paired fastq files, sequenced on: Illumina HiSeq 2500 using Agilent SureSelect WGS, Illumina HiSeq 2500 using Illumina TruSeq RNA, Illumina HiSeq 2500 using Agilent SureSelect v5 WES (+UTRs), Illumina HiSeq 4000 using Agilent SureSelect WGS, Illumina HiSeq 4000 using Illumina TruSeq stranded mRNA Kit, Illumina HiSeq 4000 using Agilent SureSelect v5 WES stranded mRNA Kit, Illumina NovaSeq 6000 using Illumina TruSeq Stranded mRNA, Illumina NovaSeq 6000 using Illumina TruSeq Nano DNA, Illumina HiSeq X Ten using TruSeq Nano DNA.

  Dataset EGAD00001010108

• Methylation profiling of sarcoma and TFCP2-rearranged rhadomyosarcoma samples

  Methylation profiling of 345 sarcoma and TFCP2-rearranged rhadomyosarcoma samples, using the approach described "Genomic, transcriptomic, functional, and mechanistic characterization of rhabdomyosarcoma with FUS-TFCP2 or EWSR1-TFCP2 fusions"

  Dataset EGAD00010002451

• CGMH-OCCC-WES

  CGMH-OCCC-WES data (tumor-normal paired) from 104 patients with ovarian clear cell carcinoma.

  Dataset EGAD50000000048