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• A Human Lymphoma Organoid Model for Evaluating and Targeting the Follicular Lymphoma Tumor Immune Microenvironment

  Heterogeneity in the tumor microenvironment (TME) of follicular lymphoma (FL) can affect clinical outcomes. We developed a new organoid culture method for cultivating patient-derived lymphoma organoids (PDLOs), which include cells from the native FL TME. We generated organoids from 12 FL patients at diagnosis, clinical progression, or relapse. These organoids were profiled with targeted DNA sequencing and mRNA sequencing. We evaluated the stability of organoids in culture at serial weekly timepoints (D0, D7, D14, D21). We treated organoids with CD19:CD3 or CD20:CD3 bispecific antibodies or unconjugated anti-CD20, anti-CD19, and anti-CD3 as a control, and profiled DNA/RNA at D11 to evaluate treatment response. This system is intended as a platform for advancing precision medicine efforts in FL through patient-specific modeling, high-throughput screening, TME signature identification, and treatment response evaluation.

  Study phs003410

• scRNAseq of colonic organoids derived from biopsies taken from healthy human individuals treated with IL22

  scRNAseq dataset of colonic organoids derived from epithelium from biopsies taken from three healthy human individuals. The organoids have either been grown in standard conditions (control) or treated with IL22 (treated). Includes 6 samples in total, one control from each individual (ctrl1, ctrl2, ctrl3) and one treated from each (treat1, treat2, treat3). The samples have been multiplexed using the antibody hashing technique. The 6 samples have been pooled into the one organoids sample. In order to analyse the raw files, they have to be demultiplexed first. Information necessary for demultiplexing, as well as which files belong to which sample, can be found in the map_file.csv, attached to each sample. Dataset includes raw Fastq files and processed csv count matrices. Fastq files are divided into HTO (hashtag) and RNA (transcriptome) files. HTO has one index (I1) and two read (R1, R2) files and RNA has two index (I1, I2) and two read (R1, R2) files. The fastq files are for the pooled (organoids) sample and need to be demultiplexed. Count matrices contain comma-separated values with cell barcodes as column names and gene names as row names. Since count matrices have been created after the demultiplexing step, there’s one matrix for each of the 6 individual samples. scRNA-seq data from human colon organoids was analysed in the same manner as for the Colitis dataset, apart from the following changes. Data was generated with the Cell Hashing technique, which uses oligo-tagged antibodies against surface proteins to barcode single cells. This allows for samples to be multiplexed together and run in a single experiment. The data was demultiplexed using the HTODemux() function from Seurat (Hao et al., 2021).

  Dataset EGAD00001010168

• RNA-seq as a tool for evaluating human embryo competence

  The majority of embryos that are created through IVF do not implant. It seems plausible that rates of implantation would improve if we had a better understanding of molecular factors affecting embryo competence. Currently, the process of selecting an embryo for uterine transfer utilizes an ad-hoc combination of morphological criteria, the kinetics of development, and genetic testing for aneuploidy. However, no single criterion can ensure selection of a viable embryo. In contrast, RNA-sequencing of embryos could yield highly dimensional data, which may provide additional insight and illuminate the discrepancies among current selection criteria. Indeed, recent advances enabling the production of RNA-sequencing (RNA-seq) libraries from single cells have facilitated the application of this technique to the study of some transcriptional events in early human development. However, these studies have not assessed the quality of their constituent embryos relative to commonly used embryological criteria. Here, we perform proof-of-principle advancement to clinical selection procedures by generating high quality RNA-seq libraries from a trophectoderm biopsy as well as the remaining whole embryo. We combine state-of-the-art embryological methods with low-input RNA-seq to develop the first transcriptome-wide approach for use in future predictive embryology studies. Specifically, we demonstrate the capacity of RNA-seq as a promising tool in preimplantation screening by showing that biopsies of an embryo can capture valuable information content available in the whole embryo from which they are derived. Furthermore, we show that this technique can be used to generate a RNA-based digital karyotype, and to identify candidate competence-associated genes. Together, these data establish the foundation for a future RNA-based diagnostic in IVF.

  Dataset EGAD00001005044

• A Genome-Wide Association Study of Fuchs' Endothelial Corneal Dystrophy (FECD)

  Fuchs' Endothelial Corneal Dystrophy (FECD) is a common disease that results in loss of vision associated with progressive corneal edema and loss of corneal transparency. In the initial stages of the disease, excrescences on Descemet's membrane with the appearance of an abnormal posterior collagenous layer, result in the clinical and pathologic appearance of guttae. Corneal edema ensues as endothelial function is compromised that may result in stromal edema, epithelial edema, and painful bullous keratopathy. Penetrating or endothelial keratoplasty is the only definitive treatment, with palliative care the only option prior to surgery. The pathophysiology underlying FECD, particularly in the common cases that affect older individuals, remains unknown, with a genetic predisposition being reported as the single best predictor of disease. Three independent groups funded by the National Eye Institute (NEI), with well-established programs in the genetics of FECD, conducted a genome-wide association study of FECD. The collaboration comprised investigators from Case Western University (CWRU), Duke University (DUEC), and Johns Hopkins University (JHU). CWRU and DUEC contributed samples that were genotyped at CIDR for the GWAS. Johns Hopkins University (JHU) provided samples for the replication phase of the study, where their data are not listed in dbGaP. Cohorts of FECD cases and controls were assembled. Synchronization of clinical and coded data was performed to unify the information across centers. The family history, clinical, demographic information, and genome-wide genotype data for samples from CWRU and DUEC were deposited in dbGaP.

  Study phs000421

• Genetic Modifiers of Duchenne Muscular Dystrophy

  The primary determinant of disease severity in patients with severe Duchenne muscular dystrophy (DMD) or milder Becker muscular dystrophy (BMD) is whether their dystrophin gene (DMD) mutation disrupts the mRNA reading frame or permits the expression of a partially functional protein. However, even in the complete absence of dystrophin, variability in disease severity is observed, with candidate gene studies implicating several genes as potential DMD modifiers. This study undertakes a comprehensive genome-wide search for modifier loci influencing disease severity in DMD patients. The availability of subjects for such studies remains limited, resulting in modest sample sizes that challenge the GWAS design. To address this, we have implemented measures to minimize heterogeneity within the dataset at the dystrophin (DMD) gene itself, adopting a conservative approach to DMD mutation classification to limit the possibility of residual dystrophin expression. Additionally, the study employed statistical methods that are well-suited to smaller sample sizes, including the use of a novel linear regression-like residual for time to ambulatory loss and the application of evidential statistics, specifically the Posterior Probability of Linkage Disequilibrium (PPLD), to assess trait-SNP associations in the GWAS framework. With a sample size of 419 patients, this study has identified multiple candidate genetic modifier loci. The molecular data available in dbGaP includes 2,562,265 directly genotyped variants in 419 people using the Illumina Infinium Omni2.5Exome-8 Beadchip assay, achieving a genotyping rate of 0.998. The phenotypic data comprises age at ambulatory loss, steroid status, DMD gene mutation, and the PPLD value from the time-to-event (TE) phenotype.

  Study phs003680

• Biallelic loss of function PAX4 variants are a Novel Cause of Transient Neonatal Diabetes

  The identification of genes in which loss of function (LoF) variants cause neonatal diabetes mellitus (NDM) can provide unique insights into the development and function of human pancreatic beta cells. We describe the identification of biallelic PAX4 LoF variants in 2 unrelated individuals with transient NDM: one due to a homozygous p.(Arg126*) PAX4 stop gain variant and a second due to a homozygous c.-352_104del 2.65kb deletion affecting the first 4 exons and promoter of the PAX4 Matched Annotation from NCBI and EMBL-EBI select transcript. We confirmed reduced transcript expression due to nonsense mediated decay for the e p.(Arg126*) variant in CRISPR-edited iPSC-derived pancreatic endoderm cells. Analysis of PAX4 binding through integration of CUT&RUN and RNA-sequencing in PAX4 depleted endocrine cells identified genes directly regulated by PAX4 involved in both pancreatic islet development and glucose-sensitive insulin secretion. The remitting and relapsing diabetes in both probands demonstrates that in contrast to mice PAX4 is not essential for the development of pancreatic beta-cells and supports differences in the requirements of functional beta-cell mass across the life-course.

  Study EGAS50000000857

• Kids First: Genomic Etiologies of CHARGE Syndrome, Related Conditions and Structural Anomalies

  Developmental disorders with structural birth defects account for the majority of morbidity and mortality in children's hospitals, and the genetic bases of many clinical phenotypes remain unknown. Genetic testing for individuals with structural malformations has uncovered the basis of many such birth defects; however, many more cases remain unsolved, posing challenges for diagnosis, treatment, and prevention. Multiple anomaly conditions are particularly challenging to diagnose, since they often present with unique combinations of clinical features that vary widely between affected individuals, even in the same family. CHARGE Syndrome (Coloboma of the eye, Heart Defects, Atresia of the choanae, Retardation of growth and development, Genital abnormalities including pubertal delay and infertility, Ear abnormalities with deafness and vestibular disorders) is a multiple anomaly condition that affects a wide variety of organ systems. CHARGE Syndrome is caused in most cases by monoallelic pathogenic variants in CHD7, the gene encoding ATP-dependent helicase chromodomain DNA binding protein 7. Both de novo and inherited variants in CHD7 have been reported in CHARGE, and a growing number of families present with individuals who test positive for a pathogenic CHD7 variant yet exhibit only mild features. Similarly, individuals with CHARGE Syndrome often exhibit broad variability and reduced penetrance of clinical features, consistent with pleiotropic roles for CHD7 during development and/or additional genetic contributors or modifying alleles. Recent work has also implicated RERE, KMT2D, EP300, and PUF60 in having a role in CHARGE Syndrome.We hypothesize that (1) some cases of CHARGE are due to other genetic etiologies including oligogenicity, and (2) genetic modifiers contribute to the broad clinical variability and reduced penetrance of CHARGE features. To address these hypotheses, we have generated a cohort of 223 deeply clinically phenotyped individuals with CHARGE Syndrome and related disorders and structural anomalies who tested negative by chromosomal microarray, single gene sequencing, next generation panel sequencing, or exome sequencing. These individuals exhibit clinical CHARGE-like features including structural birth defects affecting craniofacial, ocular, neurosensory, brain, heart, mediastinal, renal, genitourinary, and skeletal organs. Our cohort includes these 223 individuals as well as affected and unaffected family members who consented to clinical and research genetic testing and donated blood samples for DNA and RNA isolation and sequencing. Building on this valuable cohort, we propose to use exome and genome sequencing to identify novel genetic etiologies of CHARGE and related developmental disorders for which alternative genetic tests have been inconclusive. Identification of novel pathogenic genetic variants and contributing modifier alleles within the coding and non-coding portion of the genome of these individuals will improve genetic diagnosis and provide important insights toward understanding the developmental mechanisms of structural birth defects.

  Study phs002592

• Colon cancer targeted sequencing study contaning WBCs, primary tumor tissue and plasma samples

  In the setting of localized colon cancer (CC), circulating tumor DNA (ctDNA) monitoring in plasma has shown potential for detecting minimal residual disease (MRD) and predicting higher risk of recurrence. With the tumor-only sequencing approach, however, germline variants may be misidentified as somatic variations, precluding the possibility of tracking in up to 11% of patients due to a lack of known somatic mutations. In this study comprising 148 prospectively recruited localized CC patients, a custom 29-gene panel was utilized to sequence both tumor tissue and matched white blood cells (WBCs) to enhance the accuracy of sequencing results. Performing targeted sequencing of paired tumor tissue and WBCs samples detected additional somatic mutations and increased the number of patients eligible for MRD tracking in plasma, although MRD detection sensitivity was not increased. Furthermore, the germline testing approach revealed the presence of pathogenic germline variants, thereby helping identify patients at elevated risk of hereditary cancer syndromes.

  Study EGAS50000000059

• Mechanisms of Extreme Genomic Instability at Large Transcribed Genes

  Inhibiting DNA replication leads to copy number variant (CNV) formation throughout the genome, especially at chromosome fragile sites (CFSs). We previously showed that these hotspots for genome instability reside in late-replicating domains associated with large transcribed genes. In this study, we compared aphidicolin (APH)-induced CNV and CFS frequency between wild-type cells and isogenic cells in which FHIT gene transcription was ablated. We further examined the impact of altering RNase H1 expression on CNV or CFS induction frequency and analyzed R-loop formation genome-wide in a human fibroblast cell line. Data sets include Bru-seq nascent RNA transcription, whole genome sequencing for replication timing, SNP microarray analysis, and DRIP-seq. Results suggest that large gene transcription is a determining factor in replication stress-induced genomic instability and that CFSs mainly result from transcription-dependent passage of unreplicated DNA into mitosis with low R-loop levels observed at these loci.

  Study phs002066

• Integrated Single-Cell Genetic and Transcriptional Analysis Suggests Novel Drivers of Chronic Lymphocytic Leukemia

  Intratumoral genetic heterogeneity has been characterized across cancers by genome sequencing of bulk tumors, including chronic lymphocytic leukemia (CLL). In order to more accurately identify subclones, define phylogenetic relationships, and probe genotype-phenotype relationships, we developed methods for targeted mutation detection in DNA and RNA isolated from thousands of single cells from five CLL samples. By clearly resolving phylogenic relationships, we uncovered mutated LCP1 and WNK1 as novel CLL drivers, supported by functional evidence demonstrating their impact on CLL pathways. Integrative analysis of somatic mutations with transcriptional states prompts the idea that convergent evolution generates phenotypically similar cells in distinct genetic branches, thus creating a cohesive expression profile in each CLL sample despite the presence of genetic heterogeneity. Our study highlights the potential for single-cell RNA-based targeted analysis to sensitively determine transcriptional and mutational profiles of individual cancer cells leading to increased understanding of driving events in malignancy. Reprinted from Genome Research, with permission from Publisher.

  Study phs001372

• Sézary Syndrome Originates from Heavily Mutated Hematopoietic Progenitors

  The pathogenesis of cutaneous T cell lymphoma (CTCL) remains unclear. To study the malignant transformation of CTCL, we collected matched hematopoietic stem cell (HSC) extracts from bone marrow, CD4+CD26- malignant T cells, CD4+CD26+ normal T cells, and CD34+ HSCs from apheresis performed on 4 patients. To establish the baseline for calling true mutations without using hematopoietic cells, we also cultured bone marrow fibroblasts from each patient to use as normal controls. Whole exome sequencing (WES) was performed on all samples for somatic mutation calling. We identified >200 mutations in CD34+ HSCs derived from either bone marrow or apheresis. Previously reported key oncodrivers in Sezary Syndrome were identified in autologous HSCs and malignant peripheral cells, but not in progenitor (bone marrow HSCs) cells. Also, we identified specific mutations shared by autologous HSCs and malignant peripheral cells in every patient. WES data of bone marrow HSCs, apheresis HSCs, CD4+CD26- T cells, CD4+CD26+ T cells, and fibroblasts will be available through dbGaP.

  Study phs003158

• Impact of Genetic Polymorphisms on Human Immune Cell Gene Expression

  While many genetic variants have been associated with risk for human diseases, how these variants affect gene expression in various cell types remains largely unknown. To address this gap, the DICE [Database of Immune Cell Expression, Expression quantitative trait loci (eQTLs) and Epigenomics] project was established. Considering all human immune cell types and conditions studied, we identified cis-eQTLs for a total of 12,254 unique genes, which represent 61% of all protein-coding genes expressed in these cell types. Strikingly, a large fraction (41%) of these genes showed a strong cis-association with genotype only in a single cell type. We also found that biological sex is associated with major differences in immune cell gene expression in a highly cell-specific manner. These datasets will help reveal the effects of disease risk-associated genetic polymorphisms on specific immune cell types, providing mechanistic insights into how they might influence pathogenesis.

  Study phs001703

• Adult granulosa cell tumor WGS data cohort with corresponding reference germline WGS data

  Adult granulosa cell tumors (AGCTs) harbor a somatic FOXL2 c.402C>G mutation in ~95% of cases and are mainly surgically removed due to limited systemic treatment effect. In this study, potentially targetable genomic alterations in AGCTs were investigated by whole genome sequencing on 46 tumor samples and matched normal DNA. Copy number variant (CNV) analysis confirmed gain  of chromosome 12 and 14, and loss of 22. Pathogenic TP53 mutations were identified in three patients with highest tumor mutational burden and mitotic activity, defining a high-grade AGCT subgroup. Within-patient tumor comparisons showed 29-80% unique somatic mutations per sample, suggesting tumor heterogeneity. FOXL2-wildtype AGCTs had DICER1, TERT(C228T) and TP53 mutations and similar CNV profiles as FOXL2-mutant tumors. Our study confirms that absence of the FOXL2 c.402C>G mutation does not exclude AGCT diagnosis. The lack of overlapping variants in targetable cancer genes, indicates the need for personalized treatment for AGCT patients 

  Study EGAS00001004249

• Autozygosity_pilot_Born_in_Bradford

  The offspring of first cousin marriages have ~6% of their genome autozygous, i.e. homozygous identical by descent, or even more if there was further consanguinity in their ancestry. In the UK there are large populations with very high first cousin marriage rates of 20-50%. Sequencing the exomes of a sample of these individuals has the potential both to support genetic health programmes in these populations, and to provide genetic research information about rare loss of function mutations. This pilot study based on existing cohort samples from the Born In Bradford study will identify homozygous individuals for almost all variants down to an allele frequency around 1%, plus individuals carrying hundreds of new homozygous rare loss-of-function variants, and will support development of community relations and ethics for a wider study currently being designed. The data deposited in the EGA consist of low coverage whole exome sequencing on these samples.

  Study EGAS00001000462

• Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets

  Genomic analyses promise to improve tumor characterization in order to optimize personalized treatment for patients with hepatocellular carcinoma (HCC). Exome sequencing analysis of 243 liver tumors revealed mutational signatures associated with specific risk factors, mainly combined alcohol/tobacco consumption, aflatoxin B1 and HBV infection. We identified 161 putative driver genes associated with 11 recurrent pathways. Associations of mutations defined 3 groups of genes related to risk factors and centered on CTNNB1 (alcohol), TP53 (HBV) and AXIN1. Analyses according to tumor stage progression revealed TERT promoter mutation as an early event whereas FGF/CCND1 amplification, TP53 and CDKN2A alterations appeared at more advanced stages in aggressive tumors. In 24% of the tumors, we identified genetic alterations potentially targetable by FDA-approved drugs. In conclusion, we identified risk factor–specific mutational signatures and defined the extensive landscape of altered genes and pathways in HCC, which will be useful to design clinical trials for targeted therapy.

  Study EGAS00001001002

• Accumulation of copy number alterations and clinical progression across advanced prostate cancer

  The burden of copy number alterations positively associated with radiologically-evident distant metastases at diagnosis (P=0.00006) and showed a non-linear relationship with clinical outcome on univariable and multivariable analysis, characterised by a sharp increase in the relative risk of progression (P=0.003) and death (P=0.045) for each unit increase, stabilising into more modest increases with higher burdens. This association between copy number burden and outcome was similar in each of the four metastatic states. Copy number loss occurred significantly more frequently than gain at the lowest copy number burden quartile (q=4.1X10-6). Loss of segments in chromosome 5q21-22 and gains at 8q21-24, respectively including CHD1 and cMYC, occurred more frequently in cases with higher copy number alteration (for either region: Kolmogorov–Smirnov distance, 0.5; adjusted P<0.0001). Copy number alterations showed variability across tumor regions in the same prostate. This variance associated with increased risk of distant metastases (Kruskal-Wallis test P=0.037).

  Study EGAS00001006251

• Comprehensive gene analysis of colorectal cancer cases

  Colorectal cancer is the third most common morbidity and the fourth leading cause of cancer death in the world.To characterize the mutation profiles of colorectal cancer with liver metastasis,we performed both whole-exosome sequencing and RNA sequencing for 12 cases of colorectal cancer with liver metastasis (group A) and 16 cases of colorectal cancer without liver metastasis (group B). As a result of driver mutation search by Mutsig pipeline, PTEN was identified as a significant mutant gene in group A alone.ADAMTS10,NELL1 and RXFP3 were identified as candidate genes for metastasis by MuTect,SID and VarScan pipeline.Furthermore, in all samples, the copy number of chromosomes 1p,4,7,8,13,15, 17p,18,20 and 22q were significantly abnormal. Chromosomes 1p,4,15,18,17p,22q were deleted and chromosomes 7, 8,13 and 20 were amplified by CNV.Pathway analysed revealed Wnt/Ca2+ and PCP pathway was involved in metastasis of cl cancer.9 kinds of fusion genes were identified in deFuse pipeline. Among them, ADAP1 fusion genes were identified in 2 samples, and ADAP1 fusion genes were further identified in 3 samples by our in-house algorithm. It is suggested that new fusion genes present in such multiple samples may be involved in the development of colorectal cancer.

  Study JGAS000128

• The Molecular Landscape of Asian Breast Cancers Reveals Clinically Relevant Population-Specific Differences

  Molecular profiles of breast cancer have contributed to an improved understanding of the disease, enabled development of molecular prognostic signatures to guide treatment decisions and unveiled new or more accurate therapeutic options for breast cancer patients. However, the extent to which differences in genetic, environmental and lifestyle factors influence molecular profiles in different populations remains poorly characterised, as relatively few large-scale molecular studies of breast tumours in non-Caucasian populations have hitherto been reported. Here, we present the molecular profiles of 560 Asian breast tumours and a comparative analysis of breast cancers arising in Asian and Caucasian women. Compared to the breast tumours in predominantly Caucasian women reported in TCGA and METABRIC, we show an increased prevalence of Her2-enriched molecular subtypes and higher prevalence of TP53 somatic mutations in ER+ Asian breast tumours. Using gene expression and immunohistochemistry, we observed elevated immune scores in Asian breast tumours, suggesting potential clinical response to immune checkpoint inhibitors. Whilst Her2-subtype and enriched immune score are associated with improved survival, presence of TP53 somatic mutations is associated with poorer survival in ER+ tumours. Taken together, these population differences unveil new opportunities to improve the understanding of this disease and lay the foundation for precision medicine in different populations.

  Study EGAS00001004518

• Hexanucleotide repeat expansions in C9orf72 alter microglial responses and prevent a coordinated glial reaction in ALS

  Neuroinflammation is an important hallmark in amyotrophic lateral sclerosis (ALS). Experimental evidence has highlighted a role of microglia in the modulation of motor neuron degeneration. However, the exact contribution of microglia to both sporadic and genetic forms of ALS is still unclear. We generated single nuclei profiles of spinal cord and motor cortex from sporadic and C9orf72 ALS patients, as well as controls. We particularly focused on the transcriptomic responses of both microglia and astrocytes. We confirmed that C9orf72 is highly expressed in microglia and shows a diminished expression in carriers of the hexanucleotide repeat expansion (HRE). This resulted in an impaired response to disease, with specific deficits in phagocytic and lysosomal transcriptional pathways. Astrocytes also displayed a dysregulated response in C9orf72 ALS patients, remaining in a homeostatic state. This suggests that C9orf72 HRE alters a coordinated glial response, which ultimately would increase the risk for developing ALS. Our results indicate that C9orf72 HRE results in a selective microglial loss-of-function, likely impairing microglial-astrocyte communication and preventing a global glial response. This is relevant as it indicates that sporadic and familial forms of ALS may present a different cellular substrate, which is of great importance for patient stratification and treatment.

  Study EGAS00001006711

• Investigation of the genetic basis of the rare syndrome Post-Transfusion Purpura (PTP)

  The Post-Transfusion Pupura (PTP) syndrome although rare has severe side effects for 5-10 cases per annum in the UK as a result of transfusion. High quality DNA has been isolated from either whole blood or from cryopreserved mononuclear cells of 4 patients in order to study our postulation that the condition is caused by a loss-of-function mutation in a specific gene.

  Study EGAS00001000053

• SALTO: chromosomal copy number alterations to predict response to bevacizumab

  Study of the correlation between vessel formation and or CMS subtypes in relation to a predictive copy number marker for bevacizumab. Shallow Whole Genome Sequencing of 92 mCRC samples.

  Study EGAS50000000711

• Dataset for "HPV integration induces gene fusions" (RNA)

  RNA-seq data for "HPV integration induces gene fusions" We performed RNA-seq analysis of five HPV+ head and neck cancer samples using Illumina short reads. Sequenced are submitted in bam format. We also sequenced one samples with pacBio long reads, and the reads are submitted in fastq format.

  Dataset EGAD50000001303

• Amplicon sequencing of duodenal adenoma

  The aim of this study is to analyze the methylation and mutation status of non-ampullary duodenal lesions in order to detect the genetic changes for predicting the progression to adenocarcinomas.

  Study JGAS000352

• GeoMx digital spatial profiling of NGS mRNA expression in pre-treatment biopsies from patients.

  This DAC is created to define the data controller (the person that determines the purposes for which and the means by which personal data is processed) for the following study: GeoMx digital spatial profiling of NGS mRNA expression in pre-treatment biopsies from patients with metastatic triple-negative breast cancer treated with PARP inhibitors.

  Dac EGAC50000000774

• singel cell RNAseq dataset for the study "Longitudinal Multi-Omics Study Reveals Molecular Drivers and Tumor Microenvironment in Extramedullary Multiple Myeloma"

  This dataset contains 16 fastq files of raw single-cell RNAsequencing data from 6 patients with Extramedullary multiple myeloma used for the study "Longitudinal Multi-Omics Study Reveals Molecular Drivers and Tumor Microenvironment in Extramedullary Multiple Myeloma"

  Dataset EGAD50000000053