GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• Overlapping MHC class I/II epitopes program monocyte-derived dendritic cells toward a cDC1-like state via mTORC1 pathway inhibition [RNA-Seq]
  GSE325601Homo sapiens66 个样本2026-10-26

  Viral infection polarizes monocyte derived dendritic cells (moDC) to initiate type 1 immune responses. The availability of homologous (overlapping) MHC class I and II epitopes, an occurrence associated with viral infection, significantly enhances this process; however, the underlying mechanism(s) remain unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition among cDC1-like cells leads to NF-B-mediated expression of IL-12 and other type I immune polarizing genes. The cDC1-like signature was also significantly enhanced in clinical moDC vaccine products for glioblastoma and PDAC made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel mechanism of immune governance that may also be exploited in cancer immunotherapy.
• NFIC condensates partition NMNAT1 to limit nuclear NAD+ synthesis and promote cellular senescence
  GSE317403Homo sapiens6 个样本2026-10-26

  In this study, two groups of human-derived U2OS cells were subjected to transcriptome comparative analysis, including the control group (ctrl) and the gene knockout group (KO), with three biological replicates set for each group. Using eukaryotic UID-mRNA sequencing technology, the characteristics of transcriptomic changes in cells after gene knockout were systematically identified and analyzed.
• Spatially Decoding Interactypes of Vascular and Synaptic Remodeling in the Glioblastoma Tumor Microenvironment by Surprisal Information-Theoretic Analysis
  GSE317289Homo sapiens10 个样本2026-10-26

  Glioblastoma (GBM) is a highly heterogeneous and invasive brain cancer, where interactions between tumor cells, vasculature, and neurons shape disease progression and therapeutic resistance. To better understand the spatial organization of these processes, we profiled ten tumor samples from five patients, one sample from T1-constrast-enhanced and one from non-contrast enhanced regions using spatial transcriptomic sequencing and multiplexed protein imaging. While each patient’s tumor presents a unique landscape, together these samples capture all major histological and spatial niches of GBM, enabling a complete picture of the tumor microenvironment and cell–cell “interactypes.” By applying surprisal analysis, an information-theoretic framework, for the first time to spatial omics data, we decomposed gene expression into orthogonal constraint modes that uncovered distinct processes such as extracellular matrix remodeling, vascular-associated invasion, and neuron–tumor synaptic interactions, each with well-defined molecular mechanism. Complementing this approach, a spatial ligand–receptor interactype analysis mapped specific communication events across niches. Within the perivascular niche, we observed collagen–integrin signaling linked to a trajectory from astrocyte-like to mesenchymal-like tumor states. At neuron–tumor interfaces, synaptic remodeling emerged, characterized by NLGN1–NRXN1 and SEMA5A–MET interactions together with enrichment of neuronal gene modules including MAP2 and CALM1. These findings suggest that surprisal analysis can reveal vascular remodeling and neuron-tumor crosstalk are critical mechanisms of GBM progression. This study demonstrates the use of surprisal information-theoretic analysis of spatial omics data to expose hidden spatial programs with mechanistic insights and the interactype mapping to decode the GBM biology across all major tumor niches, pointing toward the discovery of potential therapeutic vulnerabilities mediated by cell-cell interaction and microenvironments.

  空间转录组
• Non-enzymatic functions of CBP/EP300 are harnessed by gene-targeted inducers of proximity [ChIP-seq]
  GSE313540Homo sapiens82 个样本2026-10-26

  Friedreich’s ataxia (FRDA) is a rare neurodegenerative disease caused by an expansion of GAA-trinucleotide repeats within the frataxin (FXN) gene. These GAA repeat expansions are enriched in repressive chromatin marks that accompany near complete silencing of the gene. Restoring FXN expression is thus a curative therapeutic goal. Here, we report the development of bifunctional synthetic gene regulators (SynGR-KATs) that recruit lysine acetyl transferases CBP/KAT3A and EP300/KAT3B to GAA repeat expansions. The GAA-targeted enzymes install transcriptionally conducive acetyl marks on proximal chromatin and restore FXN expression. Proximity-induced pharmacology of CBP/EP300 focuses solely on the enzymatic activity of these multi-domain proteins; however, we find that the non-enzymatic protein scaffolding functions contribute in equal measure to FXN expression. Highlighting the importance of protein scaffolding, co-treatment of patient-derived FRDA cells with BRD4/BET-binding SynGRs (SynGR-BETs) along with SynGR-KATs enhanced FXN expression beyond what can be achieved by either class of molecules on their own. Thus, SynGR-KATs serve as invaluable probes of transcriptional regulation while also providing a new path to therapeutic restoration of FXN expression.
• VisiumHD of EVOV treated GSCs
  GSE308834Homo sapiens4 个样本2026-10-26

  Humanized mice were implanted with patient-derived glioblastoma stem-like cells (GSCs) tumor and treated with control (EV) or treatment (EVOV).

  空间转录组
• DNA Methylation Patterns in Neuroendocrine Tumors from Different Primary Sites
  GSE305905Homo sapiens194 个样本2026-10-26

  Neuroendocrine tumors (NETs) represent a unique group of tumors with diverse anatomical origins but share common clinical and molecular characteristics. Despite their low mutational burden and limited number of recurrent mutations, epigenetic mechanisms play a crucial role in their biology. This study aims to establish a universal molecular classification of NETs, independent of their site of origin, by integrating gene expression and methylation data. The objective is to uncover shared vulnerabilities to support the development of improved diagnostic, prognostic, and predictive biomarkers, as well as innovative treatment strategies to enhance patient outcomes.
• Gene Expression Data of Neuroendocrine Tumors from Different Primary Sites
  GSE305904Homo sapiens194 个样本2026-10-26

  Neuroendocrine tumors (NETs) represent a unique group of tumors with diverse anatomical origins but share common clinical and molecular characteristics. Despite their low mutational burden and limited number of recurrent mutations, epigenetic mechanisms play a crucial role in their biology. This study aims to establish a universal molecular classification of NETs, independent of their site of origin, by integrating gene expression and methylation data. The objective is to uncover shared vulnerabilities to support the development of improved diagnostic, prognostic, and predictive biomarkers, as well as innovative treatment strategies to enhance patient outcomes. Transcriptomic and methylomic profiles were examined from paraffin-embedded tumor samples of 194 patients diagnosed with G1-G3 neuroendocrine tumors (NETs) originating in the gastrointestinal-pancreatic (GEP) tract and lungs. Using these integrated datasets, a Multi-Omics Factor Analysis (MOFA) model comprising eight factors was developed. This model facilitated the application of unsupervised clustering algorithms, resulting in a consensus molecular classification for neuroendocrine tumors.

  多组学计算与 AI
• Organoids and cortical tubers in Tuberous Sclerosis Complex show non-cell autonomous effects of second hit variants
  GSE294081Homo sapiens10 个样本2026-10-26

  Structural abnormalities are common causes of refractory epilepsy, and while progress has been made in understanding the genetic changes associated with these malformations, the pathogenic mechanisms often remain unclear. Dysregulation of the mechanistic target of rapamycin pathway has been found to contribute to a group of focal cortical dysplasia, and patients with Tuberous Sclerosis Complex often have several of these malformations. We used organoids generated from heterozygous patient-derived induced pluripotent stem cells and added isogenic stem cells with second hit variants to determine whether there are non-cell autonomous effects of the null cells. We found that the presence of null cells during differentiation led to abnormalities in neuronal development, which was due to secreted factors. Furthermore, null cells secreted extracellular vesicles containing proteins that inhibit the transcriptional coactivator, YAP1, and knockdown of one specific factor, AMOT, in null cells rescued neuronal differentiation and YAP1 expression. Finally, we analyzed cell type specific gene expression in malformations in patients with TSC and observed similar patterns of gene expression dysregulation. These data define a novel pathogenic mechanism underlying the development of focal brain malformations.
• EGR1 Binding to a Promoter G-Quadruplex Supports Early TNF Expression
  GSE292945Homo sapiens16 个样本2026-10-26

  G-quadruplexes (G4s) influence chromatin and transcription, but their roles in stimulus-induced rapid gene activation remain incompletely understood. Integration of public transcription-factor ChIP-seq, genome-wide G4 maps, and G4 pull-down/MS identified EGR1 as a G4-associated transcription factor. In vitro binding assays further demonstrated that EGR1 directly interacts with multiple G4 conformations, including parallel MYC G4, hybrid BCL2 G4, and antiparallel telomeric hTel21T18 G4. RNA-seq revealed an EGR1-dependent early LPS-induced inflammatory program. Integration with EGR1 ChIP-seq and G4access profiles prioritized TNF as a promoter-proximal EGR1–G4-associated target. A TNF promoter G4 showed BG4 enrichment and a parallel-like CD signature, and its mutation reduced BG4 signal, EGR1 occupancy, reporter activation, and early LPS-induced TNF expression. G4 ligands further disrupted EGR1 binding to the TNF G4 and reduced TNF expression. These findings reveal a promoter G4-dependent layer of EGR1-mediated TNF activation.