EGAS00001001797-sc-20170323 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001003252 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:A BRAF V600E colorectal organoid which is sensitive to MAP kinase inhibition was mutagenised with the chemical mutagen ENU and then drug selected using a combination of Trametinib, Dabrafenib and Cetuximab. Single cell derived organoids were then manually picked and expanded in drug. Resistance was confirmed in a 14 day assay and DNA was collected. These then underwent targeted amplicon-based sequencing to confirm candidate resistance effectors from a screen in 2 2D BRAF V600E colorectal cell lines. Pools of resistant clones were also sequenced.
| EGAD00001003248 | EGA
Project description:Sequencing of drug resistant organoids
| EGAS00001001797 | EGA
Project description:This dataset contains RNA sequencing data of 48 human dorsal forebrain organoids on day 50 of differentiation. Half of the samples were treated with the antiepileptic drug valproic acid (VPA) from day 21 to day 50 of differentiation, while the remaining served as untreated controls. This dataset was generated to investigate how VPA influences early human cortical development at the transcriptional level.
2026-02-11 | E-MTAB-15191 | biostudies-arrayexpress
Project description:This study investigated mechanisms of acquired resistance to FGFR inhibitor therapy in RAS/RAF–wild-type colorectal cancer (CRC). RNA sequencing (RNA-seq) data from 47 RAS/RAF-wild-type colorectal cancer stem-cell (CRC-SC) spheroid lines previously deposited under GSE205787 were integrated with newly generated RNA-seq data from 31 additional RAS/RAF-wild-type CRC-SC spheroid lines and seven FGFR inhibitor-resistant CRC-SC derivatives. The resistant derivatives were established from parental CRC-SC spheroid lines by continuous exposure to erdafitinib or futibatinib. Comparative transcriptomic analysis between matched parental and resistant lines revealed consistent upregulation of EGFR and downregulation of PTPROt, a truncated isoform of PTPRO, in resistant derivatives. Gene set enrichment analysis further indicated activation of EGFR-related signaling pathways in FGFR inhibitor-resistant spheroids. In addition, the integrated RNA-seq dataset comprising 78 RAS/RAF-wild-type CRC-SC lines was used to validate the inverse correlation between EGFR and PTPRO mRNA expression, supporting the involvement of PTPROt downregulation and EGFR pathway activation in acquired resistance to FGFR inhibition.
2026-06-09 | GSE333925 | GEO
Project description:Tuberculosis (TB) is one of the deadliest infectious disorders in the world. To effectively TB manage, an essential step is to gain insight into the lineage of Mycobacterium tuberculosis (MTB) strains and the distribution of drug resistance. Although the Campania region is declared a cluster area for the infection, to contribute to the effort to understand TB evolution and transmission, still poorly known, we have generated a dataset of 159 genomes of MTB strains, from Campania region collected during 2018-2021, obtained from the analysis of whole genome sequence data. The results show that the most frequent MTB lineage is the 4 according for 129 strains (81.11%). Regarding drug resistance, 139 strains (87.4%) were classified as multi susceptible, while the remaining 20 (12.58%) showed drug resistance. Among the drug-resistance strains, 8 were isoniazid-resistant MTB (HR-MTB), 7 were resistant only to one antibiotic (3 were resistant only to ethambutol and 3 isolate to streptomycin while one isolate showed resistance to fluoroquinolones), 4 multidrug-resistant MTB, while only one was classified as pre-extensively drug-resistant MTB (pre-XDR). This dataset expands the existing available knowledge on drug resistance and evolution of MTB, contributing to further TB-related genomics studies to improve the management of TB infection.
2023-11-17 | E-MTAB-13058 | biostudies-arrayexpress
Project description:Cancer cell lines can provide robust and facile biological models for the generation and testing of hypothesis in the early stages of drug development and caner biology. Although clinical trials remain the ultimate scientific testing ground for anticancer therapies, the use of appropriate model systems to explore the molecular basis of drug activity and to identify predictive biomarkers during their development can have a profound effect on the design, cost and ultimate success of new cancer drug development. In order to capture the high degree of genomic diversity in cancer and to identify rare molecular subtypes, we have assembled a collection of >1000 cancer cell lines. These lines have been characterised using whole exome sequencing, genome wide analysis of copy number, mRNA gene expression profiling and DNA methylation analysis (http://cancer.sanger.ac.uk/cell_lines). To further characterise this panel of cell lines we have now compiled data for RNA sequencing. The current study represent data for ~450 of the cell lines in the panel, data for the remaining lines can be accessed via the CGHUB data browser hosted at UCSC. <br>This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of the EGA data set is EGAD00001001357 under EGA study accession EGAS00001000828.
2017-09-25 | E-MTAB-3983 | biostudies-arrayexpress
Project description:Embryonic genome activation (EGA), a pivotal transcriptional event during preimplantation development, is accompanied by post-transcriptional regulation of maternal mRNAs. Disentangling the transcriptional output of the newly activated embryonic genome from concomitant post-transcriptional processing is important for decoding EGA dynamics.Here, using optimized low-input SLAM-seq (thiol(SH)-linked alkylation for the metabolic sequencing) in mouse embryos, we delineates the temporal hierarchy of EGA nascent transcription during mouse preimplantation embryogenesis and uncovers a mechanistic link between EGA and the first lineage specification, providing new insights into the regulatory architecture of early mammalian development.
2026-01-01 | GSE297541 | GEO
Project description:CTCF ChIP-seq of 39 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011059 (dataset).
2023-08-31 | E-MTAB-13117 | biostudies-arrayexpress
Project description:Summary Single-cell RNA sequencing was performed on cardiac organoids differentiated from WTC11 hiPSCs (TTN-mEGFP) to investigate chamber-specific lineage commitment. Organoids were collected at day 7.5 of differentiation, using protocols designed to direct progenitors toward left ventricle, right ventricle, or atrium fates. This dataset enables the characterization of transcriptional programs and cellular heterogeneity underlying the early specification of the cardiac chamber. Dataset: This dataset contains single-cell RNA sequencing (scRNA-seq) data generated to compare the development of cardiac organoids differentiated from WTC11 hiPSCs (TTN-mEGFP reporter line). Organoids were harvested at day 7.5 of differentiation, a stage at which chamber-specific programs begin to emerge. Each sample corresponds to a distinct differentiation protocol designed to direct the commitment of progenitors toward a specific cardiac chamber identity: the left ventricle, the right ventricle, or the atrium. The experimental rationale, illustrated in Supplementary Figure 4 (Figure S4) of Becca et al. (2025), highlights the use of scRNA-seq to resolve the cellular heterogeneity of these chamber-directed organoids and to define transcriptional signatures associated with early cardiac chamber specification.
2025-10-14 | E-MTAB-15693 | biostudies-arrayexpress
Project description:BRAF(V600E) mutant melanomas treated with inhibitors of the BRAF and MEK kinases almost invariably develop resistance, which is frequently caused by reactivation of the Mitogen Activated Protein Kinase (MAPK) pathway. To identify novel treatment options for such patients, we searched for acquired vulnerabilities of MAPK inhibitor-resistant melanomas. We find that resistance to BRAF+MEK inhibitors is associated with increased levels of reactive oxygen species (ROS). Subsequent treatment with the histone deacetylase inhibitor (HDACi) vorinostat represses SLC7A11 that leads to a lethal increase in the already elevated levels of ROS in drug-resistant cells, thereby causing selective apoptotic death of only the drug resistant tumor cells. Consistently, treatment of BRAF inhibitor-resistant melanoma with HDACi in mice results in a dramatic tumor regression. In a study in patients with advanced BRAF+MEK inhibitor resistant melanoma, we find that HDACi can selectively ablate drug-resistant tumor cells, providing clinical proof of concept for the novel therapy identified here. DNA Seq data: biopy samples from patients pre- and post- treated with Vorinostat; check mutations related to MAPKi-resistance
2018-04-18 | GSE111140 | GEO