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• Gene expression profiles in paediatric ETV6-RUNX1 leukemia

  Study EGAS00001007097

• Common and rare germline variants in Japanese prostate cancer patients

  Study JGAS000487

• Single cell genomic variation induced by mutational processes in cancer

  How cell-to-cell copy number alterations that underpin genomic instability in human cancers drive genomic and phenotypic variation, and consequently cancer evolution, remains understudied. Here, applying scaled single cell whole genome sequencing to wildtype, TP53-deficient and TP53/BRCA1/2-deficient mammary epithelial cells (n=13,818 genomes) and primary triple negative breast (TNBC) and high grade serous ovarian cancers (HGSC) (n=22,057 genomes), we identified three distinct ‘foreground’ mutational patterns defined by cell-to-cell copy number and structural variation properties occurring in the ‘background’ of cancer-associated genomic instability. Cell and clone-specific high level amplifications (HLAMPs), parallel allele-specific copy number alterations and copy number segment length variation (serrate structural variations) exhibited measurable phenotypic and evolutionary consequences. Clone-specific HLAMPs in known oncogenes were highly prevalent in fold back inversion (FBI)-bearing tumors and associated with increased clone-to-clone phenotypic variation in gene expression inferred from matched single cell RNASeq. Parallel allele-specific alterations were linked with phylogenetically determined evolutionary diversity and clone-specific mono-allelic expression. Serrate patterns present across all clones were increased in FBI tumors, most prominently on a tetraploid background and were highly correlated with increased genomic diversity of cellular populations. Taken together, we show that cell-to-cell structural-copy number variation significantly impacts the phenotypes and evolutionary diversity of TNBC and HGSC, revealing previously hidden genomic states of cancer cells.

  Study EGAS00001006343

• SCANDARE MACARON project

  Among gynecological cancers, high-grade serous ovarian cancer has the highest prevalence and more than 75% of patients have advanced stage at diagnosis with a 5-year survival of 40%. When the initial complete surgical removal is not possible (60% of patients), an interval surgery can be considered after three to four cycles of neoadjuvant chemotherapy to reduce the tumor mass. However, in approximately 50% of cases the tumor has little or no response to neoadjuvant chemotherapy. Therefore, identification of potential drug targets, biomarkers and/or pathways whose modulation can help in the prevention, interception, or curing of the disease is essential to address the unmet need. Therefore, MACARON project aims to address these issues through the identification of shared neoantigens arising out of somatic alterations and aberrant transcriptional programs in ovarian cancer DNA/RNA datasets.

  Dac EGAC50000000104

• Detection of Enhancer-Associated Rearrangements Reveals Mechanisms of Oncogene Dysregulation in B-cell Lymphoma

  Lymphomas are a prevalent and heterogeneous family of cancers arising in cells of the immune system. Drivers of lymphomagenesis include genomic rearrangements that juxtapose active regulatory elements with specific oncogene targets, as well as mutations affecting specific transcription factors and chromatin regulatory proteins. This study seeks to combine genome-wide genetic and epigenetic datasets to better understand mechanisms of oncogene dysregulation across distinct lymphoma types.

  Study phs000939

• Non-Coding Mutations Cause Enhancer Targeting Resulting in Protein Synthesis Dysregulation During B-Cell Lymphoma Progression

  In this study, we performed whole-genome sequencing of longitudinal tumor pairs, representing transformation of follicular lymphoma (FL) to high grade B-cell lymphoma with MYC and BCL2 rearrangements (known as "double hit lymphoma" or DHL), a very aggressive class of non-Hodgkin B cell lymphoma (B-NHL). We identified coding and noncoding genomic alterations acquired during the course of lymphoma progression.

  Study phs003398

• Molecular underpinnings of dedifferentiation and aggressiveness in chromophobe renal cell carcinoma

  This study expands our understanding of aggressive chromophobe renal cell carcinoma (ChRCC), provides insight into molecular mechanisms of tumor progression, and informs pathologic classification and diagnostics. Tumor and adjacent normal samples were collected from 11 patients treated in affiliated hospitals of the University of Texas Southwestern Medical Center (UTSW), including Parkland Hospital. Seven of the eleven patients consented to depositing their genomic data to public repository.

  Study EGAS50000000287

• Olink Explore Protein Expression

  Serum samples (DC, CRSsNP, CRSwNP, N-ERD, n=20 each) were subjected to the Olink Explore 3072 analysis including the following panels: Olink Explore 384 Cardiometabolic and Cardiometabolic II, Olink Explore 384 Inflammation and Inflammation II, Olink Explore 384 Neurology and Neurology II, Olink Explore Oncology and Oncology II. The latter had 4 failed samples. From the originally 2925 unique proteins determined, 84 proteins had missing values in all samples and were removed. Further 164 proteins had >50% of values below LOD across all four groups and were removed with remaining values below threshold adjusted to LOD. This data cleaning left 2695 unique assays (2677 unique proteins) in serum to be analysed. Additionally, six assays (LMOD1, IDO1, SCRIB, CXCL8, IL6, TNF) were measured four times each in different panel.

  Dataset EGAD50000001327

• A distinct monocyte cellular state links systemic immune dysregulation to pulmonary impairment in long COVID

  Long COVID is a debilitating disease with a very heterogeneous disease aetiology. In this study, we collected blood from Long COVID patients and generated single-cell multiomics datasets. The samples collected were both longitudinal and cross-sectional cohorts. The aim of the study involved examining the transcriptomic and epigenetic landscape of circulating immune cells from these samples to better understand the disease imprints.

  Study EGAS50000001215

• The genomic landscape of large and small tumors in early-onset prostate cancer patients

  This study characterizes the genomic landscape of prostate cancer (PCA) cells in patients below or at the age of 50 years. Tumors of such early onset patients already show a broad spectrum of sizes. To test if the size differences are indicative of special cancer subgroups, we sequenced the genome of the tumor cells and matched control samples from blood.

  Study EGAS00001000383