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• RNA-seq data of Metabolic profiling of patient-derived organoids reveals nucleotide synthesis as a metabolic vulnerability in malignant rhabdoid tumors

  Patient-matched normal kidney organoid (103H) and MRT tumoroid (103T2) models were treated for 24h with either DMSO (ctrl), 400nM MTX, or 50nM BAY to investigate the direct effects of drug treatment on the expression of key metabolic enzymes in the nucleotide biosynthesis pathways.

  Dataset EGAD00001015391

• 47 urothelial cancer patients WES and 38 RNAseq

  We performed a global mutational landscape analysis using tumor samples from the 47 urothelial cancer patients included in MATCH-R or MOSCATO studies, with advanced metastatic disease and WES available (RNAseq is included for 38 patient samples).

  Dataset EGAD00001011063

• Spatially resolved cellular and molecular drivers of cardiac remodelling in healthy and failing human hearts: Adult RNA (2025-07-31)

  Cell Atlas of the diseased human heart. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ . This dataset contains all the data available for this study on 2025-07-31.

  Dataset EGAD00001015668

• Predictors of Immune Checkpoint Blockade Response in dMMR Colorectal Cancer Using an Integrated Immune-Enhanced Multi-Omics Platform

  To identify candidate tumor- and immune-related biomarkers associated with clinical outcomes following anti–PD-1 therapy in dMMR colorectal cancer, we conducted a comprehensive genomic profiling using ImmunoID NeXT platform, including whole exome, whole transcriptome and TCR/BCR sequencing.

  Dataset EGAD50000002504

• Metadata Submission

  Metadata Submission Welcome to the EGA Metadata Submission landing page. Here, we provide you with essential resources to facilitate a seamless submission process. Before starting your submission, please make sure you check the following pages: Submission FAQ Submission Quickguide Submission account terms EGA metadata schema If you want to submit sequencing and/or phenotypic data check these pages: Submitter Portal Submitter Portal API If you want to submit array data check these pages: Array documentation Webin Webin API

  Documentation submission/metadata/submission

• Primary Prostate Tumor Tissue DNA Methylation Profiles

  The study cohort includes 525 Caucasian and African American prostate cancer (PCa) patients who underwent radical prostatectomy (RP) as primary therapy for clinically localized adenocarcinoma of the prostate. These patients were previously enrolled in one of two population-based studies: 1) men 40-64 years of age, diagnosed between January 1993 and December 1996; and, 2) men 35-74 years of age, diagnosed between January 2002 and December 2005. Gleason grade and sum, diagnostic PSA, and pathological tumor stage were obtained from the SEER cancer registry. Formalin-fixed paraffin-embedded prostate tumor tissue blocks were obtained from RP specimens and used to make hematoxalin and eosin stained slides, which were reviewed by pathologists to confirm the presence/location of adenocarcinoma. For each patient two 1-mm tumor tissue cores from the dominant lesion that were enriched with >=75% tumor cells were taken for DNA purification. The RecoverAll Total Nucleic Acid Isolation Kit (Ambion/Applied Biosciences, Austin, TX) was used to extract DNA, which was then quantified (PicoGreen), aliquoted onto 96-well plates and shipped to Illumina for DNA methylation profiling using the Infinium® HumanMethylation450 BeadChip.

  Study phs001921

• Systems Analysis of Single-Cell Heterogeneity Underlying Glioma Drug Resistance

  This study characterizes the transcriptional regulatory mechanisms that drive responses of two patient-derived glioblastoma multiforme (GBM) stem-like cells (PD-GSCs) that have distinct phenotypes - one sensitive and another resistant to the drug pitavastatin. This study investigates the differing mechanisms driving drug response in the two PD-GSCs at the single-cell level, and provides an approach that can be used to infer transcriptional regulatory network models, which can then be used to identify mechanisms driving cell-state transitions, e.g., proneural-to-mesenchymal transitions (PMT), which has been observed experimentally and clinically in GBM. The use of these network models enabled the identification of transcription factor and gene targets that perturbed drug-induced PMT through 1) simulations of network dynamics network, and 2) characterization of gene program activities over the time-course response to drug treatment. These results enabled the identification of multiple siRNAs and the drug vinflunine as secondary components that potentiate the efficacy of pitavastatin. This work demonstrates an approach to uncover the transcriptional network topology (TRN) topology of PD-GSCs, and use it to rationally predict combinatorial treatments that block treatment escape and acquired resistance to drugs in GBM.

  Study phs003501

• Transcriptomes of human CD4+ T lymphocytes - Metabolic project

  Human CD4+ T cells are essential mediators of immune responses. By altering the mitochondrial and metabolic states, we defined metabolic requirements of human CD4+ T cells for in vitro activation, expansion, and effector function. T cell activation and proliferation were reduced by inhibiting oxidative phosphorylation, while early cytokine production was maintained by either OXPHOS or glycolytic activity. Glucose deprivation in the presence of mild mitochondrial stress markedly reduced all three T cell functions, contrasting the exposure to resveratrol, an antioxidant and sirtuin-1 activator, which specifically inhibited cytokine production and T cell proliferation, but not T cell activation. Conditions that inhibited T cell activation were associated with the downregulation of 2′,5′-oligoadenylate synthetase genes via interferon response pathways. Our findings indicate that T cell function is grossly impaired by stressors combined with nutrient deprivation, suggesting that correcting nutrient availability, metabolic stress and/or the function of T cells in these conditions will improve the efficacy of T cell-based therapies.

  Study EGAS00001005565

• Long-Term Outcome in Offspring and Mothers of Dexamethasone-Treated Pregnancies at Risk for Classical Congenital Adrenal Hyperplasia Owing to 21-Hydroxylase Deficiency

  Summary The purpose of this study is to perform the first long-term follow up study both of adolescents and young adults with a history of prenatal treatment with dexamethasone and of their mothers and to test for adverse medical or behavioral side effects. The emphasis will be on the outcome of this prenatal treatment in those fetuses who are not affected with steroid 21-hydroxylase deficiency (21OHD) form of congenital adrenal hyperplasia (CAH) and are either heterozygotes or homozygote-unaffected. Prenatal treatment of 46,XX fetuses with 21OHD (via administration of dexamethasone to the pregnant mother) has been shown to reduce the masculinization of the genitalia and, thereby, the later need for 'corrective' feminizing genital surgery and potential impairment of sexual functioning. Along with the suppression of excess prenatal androgen production and reduction of prenatal masculinization of the genitalia in 46,XX fetuses with 21OHD, prenatal dexamethasone treatment may reduce the behavioral masculinization that is well documented in untreated 46, XX patients with 21OHD. Those fetuses who are partially treated until diagnosis of an unaffected status (heterozygous or homozygous-unaffected) will be studied as well. This latter group is of importance because these fetuses are being unnecessarily treated, but we have no way of diagnosing the unaffected status before the 8th week of gestation when treatment must begin for the female fetus who is affected. As treatment is necessary only until term in the female fetus affected with classical CAH, male fetuses and unaffected or heterozygous female fetuses do not require treatment. Thus, only one out of eight fetuses will require prenatal treatment until term. Findings of adverse effects of glucocorticoid treatment in non-human mammals [1, 2] have raised concerns among other clinicians and investigators about potential adverse side effects of such treatment on the developing human. Thus, this study will address this concern and investigate the potential adverse side effects of prenatal treatment. Detailed Description Females with classical CAH owing to 21-hydroxylase deficiency are born with ambiguous genitalia due to the production of excess androgens in utero. Prenatal treatment with dexamethasone was inaugurated in 1978 by Maguelone Forest and has been the standard of practice in the United States since 1986. Dexamethasone, which crosses the placental barrier, suppresses the fetal adrenal gland production of androgens, thus preventing ambiguous genitalia in the affected female. Children of both sexes are prenatally treated as soon as pregnancies at risk are confirmed. Treatment in females with 21OHD continues to term, but is discontinued in males and unaffected females. To date, 685 pregnancies have been diagnosed, of which 366 fetuses were treated. These investigators will study prenatally treated adolescents and adults 12 years and older with respect to medical and behavioral outcomes (see Table 5). In addition, mothers of children prenatally treated for varying periods of time for suspected 21OHD will be studied for long-term side effects of dexamethasone treatment administered during pregnancy. The long-term outcome in these children and their mothers has never before been studied.

  Study phs001317

• Effect of ETS2 modulation on chromatin accessibility and enhancer activity in inflammatory (TPP) macrophages

  This dataset consists of H3K27ac ChIP-seq and ATAC-seq in primary human macrophages following modulation of ETS2 expression. There are three datasets: H3K27ac ChIP-seq in ETS2-edited and unedited inflammatory (TPP) macrophages, H3K27ac ChIP-seq in ETS2-overexpressing and control M0 macrophages, and ATAC-seq in ETS2-edited and unedited inflammatory macrophages. For editing experiments, monocytes were transfected with CRISPR-Cas9 ribonucleoproteins containing a gRNA that was validated to edit ETS2, or a non-targeting control gRNA. Inflammatory macrophage differentiation was performed using conditions that model chronic inflammation (TPP): 3 days GM-CSF (50ng/mL) followed by 3 days GM-CSF, TNFa (50ng/mL), PGE2 (1mg/mL), and Pam3CSK4 (1mg/mL). For overexpression experiments, controlled overexpression of ETS2 mRNA or control mRNA (an equivalent amount of mRNA encoding the reverse complement of ETS2 – thereby controlling for the quantity, length and purine/pyrimidine composition of the transfected RNA but with a transcript that would not be translated) was induced in resting, non-activated (M0) macrophages by transfecting 500ng mRNA. To minimise non-specific activation due to the transfected RNA, in vitro transcription was performed using co-transcriptional capping (to minimise uncapped products), and incorporating modified, minimally immunogenic nucleotides (replacing uridine with N1-methyl-pseudouridine and cytidine with methylcytidine). After 18 hours, transfected cells were were activated with low dose LPS and harvested 6 hours later. For H3K27ac ChIP-seq, cells were harvested, cross-linked, quenched, lysed, and sheared. Immunoprecipitation of histone-DNA complexes was performed overnight at 4C with rotation using an anti-H3K27ac antibody and the SimpleChIP Plus Sonication ChIP kit (Cell Signaling Technology). Following reverse cross-linking, 50ng of immunoprecipitated DNA or input DNA were used to prepare sequencing libraries using the iDeal Library Preparation kit (Diagenode), according to manufacturer instructions. 10 PCR cycles were used for the amplification step and size selection was not performed. The quality and molarity of all libraries was assessed using a BioAnalyzer 2100 (Agilent) and the libraries were sequenced on an Illumina NovaSeq 6000. Raw data are provided as raw and aligned sequencing reads from H3K27ac-bound DNA and the input chromatin. ATAC-seq in TPP macrophages was performed using the Omni-ATAC protocol (Corces et al 2017) with the following modifications: cell number was increased to 75,000 cells, cell lysis time was increased to 5 minutes; volume of Tn5 transposase in the transposition mixture was doubled; duration of the transposition step was extended to 40 minutes. Sequencing libraries were prepared by PCR with the NEBNext Ultra II Q5Master Mix (NEB) as described previously (Corces et al 2017). Amplified libraries were cleaned using AMPure XP beads (Beckman Coulter). Sequencing reads were trimmed using TrimGalore! (Phred score 24), filtered to remove reads < 20 bp and aligned to the human genome (hg19) using Burrows-Wheeler Aligner (BWA). Aligned reads were converted to BAM files, sorted and indexed using SAMtools (Li et al, 2009). PCR duplicates and unmapped reads were removed, and the resulting BAM files were re-sorted and indexed. Raw data are provided as 100 bp paired-end Illumina reads from n = 3 donors for each experiment. BAM files are also provided.

  Study EGAS50000000109