989ac3fb-0152-4cb1-8d9d-957b7ef365be - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001011813 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed whole exome sequencing (WES) of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.
2025-10-11 | GSE307529 | 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:H3K27ac ChIP-seq of 79 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). In addition, 4 samples derived from CD34+ cord blood cells of healthy donors were included. 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); EGAD00001011060 (dataset).
2023-08-31 | E-MTAB-13119 | biostudies-arrayexpress
Project description:Embryonic genome activation (EGA) marks the onset of embryonic program and enables the transition toward the first lineage specification. However, the molecular features of EGA and the transcription factors (TFs) orchestrating this process remain unclear. Here, by performing single-cell RNA-seq on bovine embryos, we reveal that major EGA is asynchronously initiated among blastomeres at the 8-cell stage. Integrative analyses reveal distinctive protein accumulation compared to transcription and translation activation during bovine EGA. Furthermore, we investigate the role of SP1, a TF activated at the minor EGA stage, with motifs enriched in accessible chromatin during major EGA stage in bovine and human embryos. SP1 deficiency leads to morula arrest in bovine and impairs EGA in human embryos. Multi-omics analysis demonstrates that SP1 promotes early lineage gene expression by modulating nearby chromatin states in bovine and directly targets key EGA genes in human embryos. Together, our study delineates the dynamics of bovine EGA and uncovers the conserved and species-specific roles of SP1 in regulating EGA and early development in mammals.
2026-02-12 | GSE304792 | GEO
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:Lung adenocarcinoma (LUAD) remains the leading cause of cancer-related mortality worldwide. Unlike patients harboring epidermal growth factor receptor (EGFR) mutations, those with wild-type EGFR lack effective targeted therapeutic options. We established a super-SILAC-based proteomic dataset (PXD046807) comprising LUAD tissues stratified by EGFR mutation status and clinical stages. Notably, myeloid-derived growth factor (MYDGF) was identified as a potential key regulator in patients with wild-type EGFR LUAD. To further investigate the role of MYDGF in LUAD, we applied gene knockdown combined with tandem mass tag (TMT)-based quantitative proteomic analysis to search for the specific biological processes regulated by MYDGF in normal lung fibroblasts and LUAD cells with different EGFR status.
2025-06-22 | PXD064751 | Pride
Project description:We find that malignant LUAD tumor cells grown in the brain microenvironment display significantly altered transcriptomic profiles when compared to tumor cells grown in monolayer or subcutaneously. Additionally, we characterize the reciprocal neuroinflammatory response of the surrounding brain stroma to metastatic LUAD. This dataset can be utilized to explore the mechanisms of LUAD cell plasticity as well as the co-adaptation of the brain microenvironment to metastatic disease.
2019-04-08 | GSE115700 | GEO
Project description:We find that malignant LUAD tumor cells grown in the brain microenvironment display significantly altered transcriptomic profiles when compared to tumor cells grown in monolayer or subcutaneously. Additionally, we characterize the reciprocal neuroinflammatory response of the surrounding brain stroma to metastatic LUAD. This dataset can be utilized to explore the mechanisms of LUAD cell plasticity as well as the co-adaptation of the brain microenvironment to metastatic disease.
2019-04-08 | GSE115699 | GEO
Project description:Genome wide DNA methylation profiling of peripheral blood mononuclear cells(PBMCs) in normal and LUAD samples. The Illumina Infinium 850k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 820,000 CpGs in PBMC samples. Samples included 35 LUAD patients and 50 normal controls.
2024-12-14 | GSE275371 | GEO
Project description:Mutations in isocitrate dehydrogenase 2 (IDH2) occur in many cancers including Acute Myeloid Leukemia (AML). In preclinical models mutant IDH2 causes partial hemopoietic differentiation arrest. Recently, we showed that single agent Enasidenib, a first-in-class, selective mutant IDH2 inhibitor, produces a 40% response in relapsed/refractory AML patients by promoting differentiation. Yet, the rate, extend and duration of the clinical benefits of Enasidenib vary from one patient to another. To investigate how the genetic mutational landscape, at baseline or at relapse, contributes in modulating response to Enasidenib, WES analyses on FACS-sorted blasts from baseline, best response and/or relapse samples from 16 Enasidenib-treated patients were performed. WES analyses were also performed on the CD3+ cells from the same patients, which may be used as germinal control samples.
2018-08-13 | E-MTAB-6299 | biostudies-arrayexpress