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• Integrative analysis of non-small cell lung cancer patient-derived xenografts identifies unique proteotypes associated with patient outcomes

  Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. Only a fraction of NSCLC harbour actionable driver mutations and there is an urgent need for patient-derived model systems that will enable the development of new targeted therapies. NSCLC and other cancers display profound proteome remodelling compared to normal tissue that is not predicted by DNA or RNA analyses. We generated NSCLC patient-derived xenografts (PDXs) that recapitulate the histology and molecular features of primary NSCLC. Here, we completed whole exome sequencing on 122 NSCLC PDXs.

  Study EGAS00001006068

• Multiple Tissue Monitoring in Huntington disease - RNAseq skeletal muscle

  We examined whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in Huntington disease (HD) patients. Under the MTM-HD study we generated large, high-quality human datasets from skeletal muscle, skin and adipose tissue, as well as primary human fibroblast lines to probe molecular changes in human pre-manifest and early manifest HD patients. We document the involvement of inflammation, energy metabolism and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials.

  Study EGAS00001006474

• NOTCH-mutations drive immune-escape mechanisms in B cell malignancies

  Here we provide access to MCL expression data that were used for interrogating the molecular functions of NOTCH1 and NOTCH2, which are two of the most commonly mutated genes in CLL and MCL and associated with a poor clinical outcome. The mechanisms underlying how NOTCH1 contributes to disease progression, resistance to treatment and Richter’s transformation remain largely unknown. The main goal of this study is to compare the gene expression profile of primary MCL cells transduced with the intracellular part of NOTCH1 or NOTCH2 lacking of the PEST domain vs cells transduced with an empty vector.

  Study EGAS00001005793

• Discovery and capture of novel dynamic DNA methylation in human sperm with preferential links to altered folate metabolism

  The sperm DNA methylation landscape is unique and critical for offspring health. If gamete-derived DNA methylation escapes reprogramming in early embryos, epigenetic defects in sperm may be transmitted to the next generation. Current techniques to assess sperm DNA methylation show bias towards CpG dense regions and do not target areas of dynamic methylation, those predicted to be environmentally sensitive and tunable regulatory elements. Thus, this study aim to assess variation in human sperm DNA methylation and design a targeted capture panel to interrogate the human sperm methylome.

  Study EGAS00001003617

• Multiple Tissue Monitoring in Huntington disease - RNAseq fibroblasts

  We examined whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in Huntington disease (HD) patients. Under the MTM-HD study we generated large, high-quality human datasets from skeletal muscle, skin and adipose tissue, as well as primary human fibroblast lines to probe molecular changes in human pre-manifest and early manifest HD patients. We document the involvement of inflammation, energy metabolism and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials.

  Study EGAS00001006472

• Multiple Tissue Monitoring in Huntington disease - RNAseq adipose tissue

  We examined whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in Huntington disease (HD) patients. Under the MTM-HD study we generated large, high-quality human datasets from skeletal muscle, skin and adipose tissue, as well as primary human fibroblast lines to probe molecular changes in human pre-manifest and early manifest HD patients. We document the involvement of inflammation, energy metabolism and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials.

  Study EGAS00001006473

• Spatial and temporal intra-tumoural heterogeneity in advanced High-Grade Serous Ovarian Cancer: implications for surgical and clinical outcomes

  Limited evidence exists on the extent and impact of spatial and temporal heterogeneity of high grade serous ovarian cancer (HGSOC) on tumour evolution and patients surgical and clinical outcome. We investigated this through systematic mapping of multi-site tumours at initial presentation and matched relapse from 49 chemo-naïve HGSOC patients with high tumour load, operated upfront. Our data provides a unique insight into the tumour evolution and metastatic pathways of HGSOC across time and space, how this complexity relates to surgical and clinical outcome and its consequences on clinical decision-making.

  Study EGAS00001007164

• Single-cell proteogenomics of MDS upon AZA

  To study the evolution of the clonal molecular and cellular architecture of MDS upon the treatment with AZA, we performed scDNA-seq of an amplicon panel of 53 genes recurrently mutated in myeloid malignancies, as well as typically lost or gain DNA regions, and scProt-seq of 42 cell-surface proteins to provide a simultaneous landscape of the genetic setting and immunophenotype using the Tapestri platform (MissionBio). We sequenced thousands of cells from 14 MDS patients, where paired bone marrow samples were obtained at the timepoint of diagnosis and after AZA treatment.

  Study EGAS00001007427

• AML FLT3 TCR study

  We identified a T-cell receptor (TCR) reactive to the recurrent FLT3 D835Y mutation in the tyrosine-kinase domain frequently expressed in acute myeloid leukemia (AML). To validate the TCRs' elimination efficacy of leukemic cells, we transplanted human AML cells with FLT3 D835Y mutation into NSG-SGM3 mice and treated either with TCR FLT3 D835Y redirected T cells, or control TCR (TCR 1G4). After treatment, we performed flow sorting of human AML cells from the mice (mCD45-hCD45+hCD3-hCD19-) and compared to primary AML blasts (hCD3-hCD19-) and primary T cells (hCD3+hCD8+orhCD4+hCD19-hCD33-) by whole-exome sequencing.

  Study EGAS00001007467

• Subclonal somatic copy number alterations emerge and dominate in recurrent osteosarcoma

  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.

  Study EGAS00001007486