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。

• Baseline immune transcriptional states predict future HIV-1 acquisition in individuals at risk of sexual infection
  GSE352331Homo sapiens104 个样本2026-10-31

  Natural resistance to HIV-1 acquisition in highly exposed seronegative (HESN) individuals suggests the existence of pre-existing host states associated with reduced susceptibility. However, the baseline molecular determinants of susceptibility remain poorly understood. We analyzed PBMC transcriptomes by RNA sequencing in 104 HIV-1-seronegative men who have sex with men (MSM) at high risk of sexual exposure, including 65 HESN and 39 who subsequently seroconverted. Differential expression, functional enrichment, and spatial genomic clustering analyses were integrated with Elastic Net regularized logistic regression. HESN individuals showed enrichment of sensory receptor (p.adj=2×10⁻¹⁶) and cell-adhesion pathways (p.adj=9×10⁻³), together with non-random genomic clustering (p.adj=1×10⁻⁴) of differentially expressed genes at immune-related loci, including TCR, IGH, KIR, and MHC/HLA regions. In contrast, future seroconverters exhibited increased mRNA metabolism (p.adj=1.5×10⁻¹⁴), immune activation (p.adj=0.01), and type I interferon signaling (p.adj=0.02). A 14-gene risk score showed an out-of-fold AUC of 0.888. Cross-cohort transportability was evaluated in an independent ectocervical RNA-seq dataset. Applied without refitting, the signature showed moderate discrimination between long-term HESN and HIV-negative women at high risk of acquisition (AUC=0.689). The out-of-fold molecular risk score was also associated with time to HIV-1 seroconversion in MSM (log-rank p=7.1×10⁻¹¹; score×time interaction p=0.0086). These findings identify distinct pre-infection transcriptional states associated with HIV-1 acquisition and support partially transportable transcriptional architecture across blood and genital mucosal compartments.

  空间转录组
• Longitudinal Gene Expression Profiling Reveals Molecular Evolution and Transcriptional Reprogramming During Multiple Myeloma Relapse
  GSE352244Homo sapiens105 个样本2026-10-31

  This study aims to characterize gene expression alterations associated with multiple myeloma (MM) relapse by performing longitudinal gene expression profiling (GEP) of CD138+ plasma cells isolated from bone marrow mononuclear cells collected from 35 patients at baseline, first relapse, and second relapse.
• Immune activation during broadly neutralizing antibody-mediated HIV suppression prior to post-intervention control
  GSE344609Homo sapiens52 个样本2026-10-31

  Broadly neutralizing antibodies (bNAbs) have been associated with enhancement of HIV-specific T or B cell responses and sustained partial control of HIV replication in some people with HIV (PWH). The mechanisms through which bNAbs may potentiate host immunity in this context are not known. We previously reported the outcomes of a clinical trial in which ten PWH on antiretroviral therapy (ART) received a combination of immunotherapies including two bNAbs administered immediately preceding an analytic treatment interruption (ATI). After bNAb levels waned, seven participants exhibited varying degrees of post-intervention control of HIV linked to a robust expansion of activated CD8+ T cells in response to rebounding virus. To investigate the role of the bNAbs in enhancing endogenous immune responses, we looked for evidence of HIV-specific or broader immune activation during the period after ART was paused and prior to rebound when bNAbs were controlling HIV replication. At a timepoint early post-ART interruption and at least one month before virus emerged in plasma, we detected an increase in levels of plasma inflammatory proteins as well as phenotypic and transcriptional activation of innate and adaptive immune cells. Compared to non-controllers, post-intervention controllers demonstrated unique transcriptional activation patterns as well as differential longitudinal plasma inflammatory protein trends. No enhancement of HIV-specific T cell or antibody responses was observed in this window. This study identifies activated cell types and inflammatory pathways that are recruited early during bNAb-mediated HIV suppression and that may play a role in potentiating long-lasting HIV immune control after bNAb therapy.
• Adaptive transcriptional responses to KRAS(G12C) inhibition in cancer cells
  GSE352065Homo sapiens60 个样本2026-10-30

  KRAS(G12C) inhibitors have demonstrated promising antitumor activity, but adaptive resistance remains a major therapeutic challenge. To characterize transcriptional adaptations to KRAS(G12C) inhibition, we performed bulk RNA sequencing of four human KRAS(G12C)-mutant cancer cell lines (H358, Calu-1, H23, and H1792) following treatment with RMC-6291. Transcriptomic analyses were conducted to identify treatment-associated gene expression changes and biological pathways, with particular emphasis on metabolic reprogramming and glutathione-associated responses. This dataset provides insights into the transcriptional responses of cancer cells to KRAS(G12C)-targeted therapy.
• Mycobacterium abscessus inhibits IFNg activation, impairing control of intracellular infection
  GSE339253Homo sapiens80 个样本2026-10-30

  Mycobacterium abscessus (Mab) is an emerging pathogen among the nontuberculous mycobacteria (NTM), causing infections in individuals with lung conditions (e.g. cystic fibrosis) or immunodeficiency (e.g. impaired interferon gamma (IFNg) production or response pathway). Mab infections are difficult to treat, and adjunctive therapy with IFNg is sometimes used for refractory infections. However, the reasons that endogenous IFNg fails to control infections remain unknown. Using a THP-1 macrophage-mycobacteria infection model, we studied the combined effects of IFNg and imipenem (IPM) on intracellular M. abscessus. Through flow cytometry, RNAseq and cytokine measurements in infected cells treated for over 24 hours with IPM and IFNg alone or in combination, we identified distinct cellular response pathways at different stages of infection. In early stages of infection, IFNg pathway signaling, as assessed by STAT1 phosphorylation level, was preserved, while there were changes in TNFa, IL1b and IL6 inflammatory pathways in response to the infection. However, after 24 hrs of infection the IFNg signaling was impaired. Addition of imipenem abolished the impairment in IFNg signaling and led to a significant decrease in intracellular bacterial load. At 48 hrs, treatment with IFNg alone or combined with IPM significantly reduced the IFNg receptor1 surface display, while total cellular IFNgR1 and IFNgR2 levels remained unchanged. Mycobacterium abscessus reduces STAT1 phosphorylation and blunts IFNg signaling, thereby limiting macrophage activation and facilitating intracellular mycobacterial growth. Imipenem counteracts this suppression, reactivates antimicrobial pathways, enhances IFNg-mediated killing, and promotes bacterial clearance. Understanding M. abscessus immune subversion and how to counter it is crucial for developing effective antimicrobial therapies.
• Diagnostic value of a panel of serum exosomal miRNAs as potential biomarkers for pancreatic cancer
  GSE332591Homo sapiens96 个样本2026-10-30

  Exosomes and exosomal miRNAs were isolated from the serum of patients with pancreatic cancer, cholangiocarcinoma, duodenal cancer, pancreatic benign tumor and healthy individuals. Exosomal miRNAs were analyzed using next-generation sequencing (NGS) to identify miRNA candidates for diagnosis.
• RNA-seq of human meningioma samples
  GSE351918Homo sapiens59 个样本2026-10-29

  Meningiomas are frequently diagnosed tumors of intracranial location. In the WHO classification, tumor aggressiveness is assessed by assigning increasing grades, with WHO grade I tumors considered benign and WHO grade III tumors the most aggressive. In our study, we aimed to identify biological features associated with meningioma aggressiveness by profiling gene expression in FFPE tumor samples of different WHO grades (I, II, and III).
• Microregional RNA sequencing reveals layer-specific smooth muscle cell heterogeneity in human bicuspid aortic valve-associated aortic dilatation
  GSE329454Homo sapiens60 个样本2026-10-28

  BAV is associated with aortic dilatation that can progress to aneurysm. To detect layer-specific transcriptomic profiles in the human aortic media with BAV, we performed microregional RNA sequencing analysis.
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [endoBID]
  GSE314423Homo sapiens96 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [incellBIDPool1]
  GSE314389Homo sapiens66 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

  扰动筛选
• Genomic and Immune Profiling Characterizes Immune Heterogeneity and a TIGIT-Associated Subtype in Intrahepatic Cholangiocarcinoma
  GSE350183Homo sapiens164 个样本2026-10-27

  Background and Aims: Intrahepatic cholangiocarcinoma (iCCA) is characterised by marked molecular and microenvironmental heterogeneity and moderate response to immunotherapy. We aimed to define the genomic and spatial determinants of immune checkpoint activity in iCCA and their association with clinical outcome. Approach and Results: We performed integrated transcriptomic, DNA panel sequencing, and multiplex immunohistochemistry analyses in a cohort of 144 patients with iCCA. Tumors were classified according to STIM-defined microenvironmental subtypes. Spatially resolved immune profiling was conducted across tumor core, stroma, invasive margin, and adjacent liver. Immune checkpoint expression, cellular proximity, and clinical outcome were analysed using Cox regression and Kaplan-Meier methods. TIGIThigh tumors were further characterised by differential gene expression and pathway enrichment analyses. STIM classification stratified tumors into inflamed (47%) and non-inflamed (53%) subtypes with distinct survival outcomes and genomic profiles. Recurrent alterations in CDKN2A/B, TP53, MTAP, and BAP1 showed subtype-specific enrichment and prognostic relevance. Spatial immune profiling revealed compartment-specific distributions of T cells and immune checkpoints, with predominance of TIGIT and PD-1 expression in stromal and marginal regions. Most tumor-infiltrating T cells lacked inhibitory receptor expression, while co-expression of multiple checkpoints was uncommon. TIGIThigh tumors displayed coordinated activation of immune effector, antigen presentation, and interferon signalling pathways, alongside enrichment of distinct genomic alterations, defining an immune-activated molecular subtype. Conclusions: Integrated genomic and spatial immune profiling reveals pronounced context-dependent heterogeneity of immune checkpoint regulation in iCCA. TIGIT delineates an immune-activated subtype with distinct molecular features, providing a potential biomarker framework for patient stratification and rational immunotherapeutic targeting.

  空间转录组
• T and B cells recognize splicing-derived neutrophil neoantigens in lupus
  GSE327018Homo sapiens100 个样本2026-10-27

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Bulk RNA-seq of neutrophils from systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, and healthy control samples
  GSE326777Homo sapiens78 个样本2026-10-27

  This study profiled bulk RNA-seq from human neutrophil samples derived from individuals with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, and healthy controls. Total RNA was extracted and sequenced to characterize transcriptomic features across disease groups. Raw and normalized gene-level count matrices, gene annotation, and sample-level metadata are provided.
• Pervasive ERBB2 amplification and immune exclusion characterize esophageal adenocarcinoma brain metastases with divergent clinical outcomes
  GSE346866Homo sapiens74 个样本2026-10-26

  Esophageal adenocarcinoma (EAC) is an aggressive malignancy with increasing incidence in younger adults. Brain metastases occur in a clinically significant subset of patients and carry a median survival of 14 months, yet the genomic drivers, mechanisms of seeding, and the basis for rare long-term survival remain undefined. Overall, our work establishes ERBB2 amplification architecture as a major determinant of survival in EAC brain metastasis and demonstrates that HER2 IHC alone is insufficient for risk stratification. We propose DNA-level ERBB2 assessment, including in HER2 IHC 3+ cases, and early brain surveillance in HER2-positive primary EAC to guide therapy selection and enable timely intervention.
• Recordanelles for transcriptome-wide single-cell RNA recording in human cells [dataset_3 RNA-Seq]
  GSE344736Homo sapiens50 个样本2026-10-26

  Transcriptomic measurement technologies provide powerful approaches to understand biology but are limited to providing either a high-resolution snapshot at a moment in time or a low-resolution history of transcription constrained to a few genes over a narrow time range. Here, we introduce the “recordanelle”, a single-component synthetic organelle capable of recording the transcriptome in human cells. Recordanelles are composed of a mitochondrial membrane anchor, a condensate assembler and a poly-A-binding protein. We demonstrate that the recordanelle can be engineered to recruit engineered RNAs or a sampling of up to 90% of all endogenous mRNAs and protect them over several days. We further show that transient and dynamic transcriptional responses resulting from inducible promoters or interferon signaling are preserved throughout time within the recordanelle at the single-cell level. This work provides a non-disruptive and unbiased transcriptome-wide single-cell RNA recording technology to enable a deeper understanding of biology.

  单细胞
• Recordanelles for transcriptome-wide single-cell RNA recording in human cells [dataset_1 RNA-Seq]
  GSE344731Homo sapiens60 个样本2026-10-26

  Transcriptomic measurement technologies provide powerful approaches to understand biology but are limited to providing either a high-resolution snapshot at a moment in time or a low-resolution history of transcription constrained to a few genes over a narrow time range. Here, we introduce the “recordanelle”, a single-component synthetic organelle capable of recording the transcriptome in human cells. Recordanelles are composed of a mitochondrial membrane anchor, a condensate assembler and a poly-A-binding protein. We demonstrate that the recordanelle can be engineered to recruit engineered RNAs or a sampling of up to 90% of all endogenous mRNAs and protect them over several days. We further show that transient and dynamic transcriptional responses resulting from inducible promoters or interferon signaling are preserved throughout time within the recordanelle at the single-cell level. This work provides a non-disruptive and unbiased transcriptome-wide single-cell RNA recording technology to enable a deeper understanding of biology.

  单细胞
• 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.
• 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.
• 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