Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606061 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11071400_1.fastq.gz | Fastqsanger.gz | |||
| SRR11071400_2.fastq.gz | Fastqsanger.gz | |||
| SRR11071401_1.fastq.gz | Fastqsanger.gz | |||
| SRR11071401_2.fastq.gz | Fastqsanger.gz | |||
| SRR11071402_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 140 |
Similar Datasets
Project description:Gut microbiome predicts efficacy and immune-related toxicities of advanced non-small cell lung cancer patients treated with anti-PD-1/PD-L1 Ab-based immunotherapy
| PRJEB36730 | ENA
Project description:Background: Immune checkpoint inhibitors combined with antiangiogenic therapy has become the standard of care for advanced hepatocellular carcinoma, albeit with limited therapeutic benefit. Our previous studies demonstrated the immunomodulatory and antitumor effects of polyIC, a synthetic double-stranded RNA. Here, we compared the efficacy of anti-programmed death ligand 1 (?PD-L1) plus polyIC versus ?PD-L1 plus anti-vascular endothelial growth factor (?VEGF) in primary liver tumor models.Conclusion: This preclinical study identifies polyIC as a better enhancer of ?PD-L1 efficacy than ?VEGF in liver cancer, providing a novel strategy for improving immunotherapy outcomes. Further clinical investigation is warranted.
2025-08-27 | GSE296090 | GEO
Project description:Immunotherapy has revolutionized cancer treatment, however, a reliable biomarker is missing. MGAT5-mediated PD-L1 glycosylation is critical for its interaction with PD-1. MGAT5 expression is a functional biomarker that predicts immunotherapy responses.
2025-05-06 | PXD045506 | Pride
Project description:Immune checkpoint inhibitors (ICIs) in cancer therapy are challenged for immune-related adverse events (irAEs), such as inflammatory arthritis induced by ICI therapy (ICI-arthritis) and exacerbation of rheumatoid arthritis (RA). As well as activating T cells by inhibiting programmed cell death protein 1 (PD-1)/ programmed death ligand 1 (PD-L1) signal, anti-PD-L1 antibody (αPD-L1 ab) activate intracellular pathway through PD-L1 binding. However, the effects of αPD-L1 ab on synovial fibroblasts, which are important in the pathogenesis of arthritis, are unknown.
2025-07-11 | GSE272100 | GEO
Project description:Patients with advanced melanoma have shown an improved outlook after receiving anti-PD1 therapy, but the low response rate restricts clinical benefit; therefore, enhancing anti-PD1 therapy efficacy remains a major challenge. Here, our findings show significantly higher abundance of α-KG in healthy controls, anti-PD1-sensitive melanoma-bearing mice, and anti-PD1-sensitive melanoma patients; moreover, supplementation with α-KG enhanced the efficacy of anti-PD1 immunotherapy and increased PD-L1 expression in melanomas via STAT1/3. We also found that supplementation with α-KG significantly increased methylcytosine dioxygenase TET2/3, which led to an increased 5-hydroxymethylcytosine (5-hmC) level in the PD-L1 promoter. As a consequence, STAT1/3 had been recognized and stabilized in PD-L1 promoter to upregulate PD-L1 expression. Importantly, single-cell sequencing of preclinical samples and analysis of clinical data revealed that the TET2/3-STAT1/3-CD274 signaling was associated with sensitivity to anti-PD1 treatment in melanoma. Taken together, we provide a novel insight into α-KG's function in melanoma anti-PD1 treatment and supplement of α-KG is a novel promising strategy to improve the efficacy of anti-PD1 therapy.
2023-03-08 | GSE223110 | GEO
Project description:Immunotherapy has improved the prognosis of patients with advanced non-small cell lung
cancer (NSCLC), but only a small subset of patients achieved clinical benefit. The purpose of our study was to integrate multidimensional data using a machine learning method to predict the therapeutic efficacy of immune checkpoint inhibitors (ICIs) monotherapy in patients with advanced NSCLC.The authors retrospectively enrolled 112 patients with stage IIIB-IV NSCLC receiving ICIs monotherapy. The random forest (RF) algorithm was used to establish efficacy prediction models based on five different input datasets, including precontrast computed tomography (CT) radiomic data, postcontrast CT radiomic data, combination of the two CT radiomic data, clinical data, and a combination of radiomic and clinical data. The 5-fold cross-validation was used to train and test the random forest classifier. The performance of the models was assessed according to the area under the curve (AUC) in the receiver operating characteristic (ROC) curve. Among these models(RF MLP LR XGBoost), our reproduced onnx models have better performance, especially for random forest. The response variable with a value (1/0) indicates the (efficacy/inefficacy) of PD-1/PD-L1 monotherapy in patients with advanced NSCLC
2023-07-11 | BIOMD0000001074 | BioModels
Project description:Immune checkpoint blockade (ICB), particularly programmed death 1 (PD-1) and its ligand (PD-L1), has shown considerable clinical benefits in patients with various cancers. Many studies show that PD-L1 expression may be biomarkers to help select responders for anti-PD-1 treatment. Therefore, it is necessary to elucidate the molecular mechanisms that control PD-L1 expression. As a potential chemosensitizer and anticancer drug, copper combined with disulfiram (DSF) kills tumor cells by regulating multiple signaling pathways and transcription factors in vitro and in vivo. Here, we showed that DSF increased PD-L1 expression in triple negative breast cancer (TNBC) cells. Through TCGA data analysis, we found that DNMT1 and IRF7 were highly expressed and the hypermethylation states in the IRF7 gene body promoter region in TNBC vs normal breast tissue (NBT). Then, we demonstrated that DSF affected PD-L1 expression via DNMT1-mediated IRF7 hypomethylation in two TNBC cell lines. In vivo experiments, DSF significantly enhanced the response to PD-1 antibody (Ab) in the triple-negative 4T1 BC mouse model. By analyzing the results of the tumor tissue sequencing, the DSF joint anti-PD-1 Ab could be a significant activation of anti-tumor immunity. And the inactive state of immune associated pathways was found to be reversed, such as Th1 and Th2 cell differentiation, antigen processing and presentation, natural killer cell-mediated cytotoxicity and T cell receptor signal transduction. In conclusion, we found that DSF could up-regulate PD-L1 in TNBC cells and elucidated its mechanism. Our findings revealed that the combination of DSF and anti-PD-1 Ab could activate the tumor immune microenvironment (TIME) to show much better antitumor efficacy than monotherapy.
2021-11-05 | GSE186885 | GEO
Project description:The identification of circulating predictors of response to ICB therapy is vital as very few of them meet the demands of the clinic. Herein, by using high-dimensionality mass cytometry, we designed a blood immunomap in metastatic NSCLC individuals who underwent anti-PD-1 treatment. We identified heightened frequencies of CD8+PD-L1+ T cells in non-responders compared responders. Notably, Imaging Mass Cytometry data revealed that CD8+PD-L1+ T cells were enriched in tumor biopsies, pleural infusions and BAL of early-stage NSCLC individuals, proposing this cells subset as candidate not only for the advanced but also for early disease detection. Transcriptomic analysis unveiled that CD8+PD-L1+ T cells displayed an exhausted phenotype related to their increased frequencies to non-responders to immunotherapy, and gene signatures correlated with the overall survival of an independent cohort. Overall, our study pinpoints immune-related events which may benefit the quest for detection of predictive biomarkers of immunotherapy responses.
2025-05-31 | GSE295969 | GEO
Project description:Chemotherapy in combination with immunotherapy offers limited benefit in advanced Small Cell Lung Cancer (SCLC). This study explores the potential of combining MET pathway inhibition with chemo-immunotherapy for treating advanced SCLC. MET pathway activation triggers epithelial-mesenchymal transition, fostering chemoresistance and potentially undermining the efficacy of immunotherapy. In a SCLC mouse model, MET inhibition added to chemo-immunotherapy (anti-PD-L1) reduced tumor growth and extended survival by reshaping the tumor microenvironment, decreasing suppressive myeloid cells, and promoting an effective immune response. Analysis of patient samples revealed that myeloid-enriched immune infiltrates during chemo-immunotherapy might contribute to treatment resistance. Notably, elevated serum hepatocyte growth factor (HGF) levels were associated with a mesenchymal and inflamed phenotype, indicating that this subgroup of patients could potentially benefit from MET inhibitor (METi)-based therapeutic strategies.
2025-06-20 | GSE262975 | GEO
Project description:Programmed death-ligand 1, PD-L1 (CD274) facilitates immune evasion and exerts pro-survival functions in cancer cells. Here, we report a new mechanism whereby internalization of PD-L1 in response to alterations of bioactive lipid/ceramide metabolism by ceramide synthase 4 (CerS4) induces sonic-hedgehog (Shh) and TGF- receptor signaling to enhance tumor metastasis in triple-negative breast cancers (TNBC), exhibiting immunotherapy resistance. Mechanistically, data showed that internalized PD-L1 interacts with an RNA-binding protein Caprin-1 to stabilize Shh/TGFBR1/Wnt mRNAs to induce -catenin signaling and TNBC growth/metastasis, consistent with increased infiltration of FoxP3+ T regs and resistance to immunotherapy. While mammary tumors developed in MMTV-PyMT/CerS4-/- were highly metastatic, targeting the Shh/PD-L1 axis using Sonidegib and anti-PD-L1 antibody vastly decreased tumor growth and metastasis, consistent with the inhibition of PD-L1 internalization and Shh/Wnt signaling, restoring anti-tumor immune response. These data, validated in clinical samples and databases, provide a mechanism-based therapeutic strategy to improve immunotherapy responses in metastatic TNBCs.
2025-05-07 | PXD053108 | Pride