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• A Functional Network of Gastric-Cancer-Associated Splicing Events Controlled by Dysregulated Splicing Factors

  Except for a few genes known to have oncogenic spliceforms in gastric cancer, the full scope of aberrant splicing in gastric oncogenesis remains unclear. In this study, we elucidated the alternative splicing events associated with gastric carcinogenesis and identified upstream regulators governing these events. We performed RNA-seq on 19 matched tumor/normal pairs and a panel of gastric cancer cell lines, and identified 361 tumor associated (TA) alternative splicing events (ASEs), which included known oncogenic ASEs in genes such as INSR, FGFR2, CD44 and KRAS. We further identified 8 splicing factors dysregulated in gastric tumors, the expression of which are correlated to the splice ratio of the TA ASEs. We thereby constructed a dysregulated splicing network in gastric cancer, consisting of alternative splicing changes correlated to their potential regulators. This network featured three potential regulatory modules centered around the splicing factors ESRP2, MBNL1 and PTPB1. Knockdown of each splicing factor led to the expected changes in splicing of approximately half of the ASEs assayed. Thus, dysregulation of the splicing factors indeed was the cause of many of the TA ASEs. Pathway enrichment analysis showed that genes affected by tumor associated splicing were pre-dominantly involved in cytoskeletal organization. Concordant with this, knockdown of the splicing factors regulating the TA ASEs led to the expected changes in trans-well migration activity. Thus, we have established for the first time a comprehensive splicing network that likely drives gastric tumor progression, based on which novel therapeutic targets can be identified for further evaluation.

  Study EGAS00001002256

• CRISPR screen M14, NCI-H3122 (2019-08-28)

  Genome wide CRISPR screen was performed to find resistance to targeted drugs for melanoma and lung . This dataset contains all the data available for this study on 2019-08-28.

  Dataset EGAD00001005296

• Engineered cartilage: deriving design principles from human developmental: RNA (2025-07-30)

  Engineered cartilage: deriving design principles from human developmental pathways . This dataset contains all the data available for this study on 2025-07-30.

  Dataset EGAD00001015664

• Engineered cartilage: deriving design principles from human developmental pathways (2025-10-02)

  Engineered cartilage: deriving design principles from human developmental pathways . This dataset contains all the data available for this study on 2025-10-02.

  Dataset EGAD00001015724

• Epigenetics/genetics of the patient-derived xenografts of pediatric T-cell leukemia

  We compared 12 pediatric T cell acute lymphoblastic leukemias collected at initial diagnosis and relapse with their corresponding PDX models. The analysis was performed on genomic level (whole genome sequencing (WGS), whole exome sequencing (WES), multiplex ligation probe amplification (MLPA), targeted sequencing) and the epigenetic level (DNA methylation, Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq)). In sum, this study underlines the remarkable genomic stability, and for the first time documents the preservation of the epigenomic landscape in T-ALL-derived PDX models.

  Study EGAS00001003248

• LCCC 1108: Development of a Tumor Molecular Analyses Program and Its Use to Support Treatment Decisions (UNCseqTM)

  The primary objective of this specimen correlative study was two-fold: to provide a mechanism for the association of known molecular alterations with clinical outcomes, and to provide rapid genetic profiling of alterations with known clinical utility using tumor and germline specimens to support treatment decisions.

  Study phs001713

• Piloting exome resequencing in consanguineous families with homozygosity mapping intervals

  This pilot study aims to generate pilot data to inform future study designs in consanguineous families or inbred populations by resequencing the exome of six individuals from five families with neurodevelopmental diseases. For all of these families a single mapping interval containing the causal variant has previously been identified.

  Study EGAS00001000024

• Repeated sampling

  Repeated sampling experiment – sample acquisition A repeated sampling experiment was set up to specifically evaluate the effect of increasing time after death on sample quality. Selected non-tumor and large tumor tissues (with enough material available to collect for this experiment beside routine sampling) were sampled repeatedly at 1.5-hour time intervals during the autopsy.

  Study EGAS50000000224

• MPN_Tissue_WGS_NanoSeq

  An exploration of the somatic mutational landscape of a patient with myeloproliferative neoplasm (MPN) and squamous cell carcinoma (SCC). In particular this study aims to identify mutational signatures present in SCC lesion compared to a region of healthy skin, especially searching for the presence of signatures specific to hydroxycarbamide from previous chemotherapy treatment.

  Study EGAS00001007761

• Childhood Cancer Data Initiative (CCDI): Identification and Targeting of Treatment Resistant Progenitor Populations in T-cell Acute Lymphoblastic Leukemia

  Our goal with this study was to identify the mechanisms of treatment resistance in T-cell acute lymphoblastic leukemia (ALL) using single-cell genomics. We profiled 40 T-ALL cases from the Children's Oncology Group AALL0434 clinical trial using CITE-seq/snATAC-seq, capturing a breadth of immunophenotypes, including early T-cell precursor (ETP) and near-ETP/non-ETP subtypes. By integrating analyses of T-ALL cells with the normal T-cell developmental trajectory, the study identified a specific subgroup of leukemia cells resembling bone marrow progenitors (BMP-like cells). These BMP-like cells were associated with treatment failure and poor overall survival in T-ALL patients. Overall, this study reveals comprehensive multiomic signatures for rapidly assessing risk and tailoring targeted treatment for high-risk T-ALL patients.

  Study phs003432