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single cell transcriptomics datasets for lgg cancer type  (Broad Institute Inc)

 
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    Structured Review

    Broad Institute Inc single cell transcriptomics datasets for lgg cancer type
    PANoptosis has a prognostic impact in cancers. ( A ) Consensus Clustering showing three distinct clusters (PANoptosis low, PANoptosis medium and PANoptosis high) based on PANoptosis gene expression <t>for</t> <t>SKCM.</t> ( B ) Heatmap depicting gene expression profiles of 27 PANoptosis markers including sensors and upstream regulators, adaptors and effectors of PANoptosis as scaled Z-scores for SKCM tumor samples. For brevity, 13 out of the 27 genes are labeled, but 27 distinct rows are shown. ( C ) Boxplot showing the distribution of PANoptosis scores in the three PANoptosis clusters for cancer subtypes of interest: <t>LGG,</t> KIRC and SKCM. ( D ) Forest plot showing N1 = number of samples in PANoptosis high cluster, N2 = number of samples in PANoptosis low cluster, P -value and hazard ratio (HR) with 95% CI for overall survival (OS) when comparing PANoptosis high versus low for each cancer type where there is significant prognostic impact ( P -value < 0.05). ( E–G ) Kaplan–Meier curves showing OS across the PANoptosis high and PANoptosis low groups in the three cancer types with significant differences in survival (PANoptosis high beneficial [HR < 1] or detrimental [HR > 1]). *** P -value < 0.001.
    Single Cell Transcriptomics Datasets For Lgg Cancer Type, supplied by Broad Institute Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Pancancer transcriptomic profiling identifies key PANoptosis markers as therapeutic targets for oncology"

    Article Title: Pancancer transcriptomic profiling identifies key PANoptosis markers as therapeutic targets for oncology

    Journal: NAR Cancer

    doi: 10.1093/narcan/zcac033

    PANoptosis has a prognostic impact in cancers. ( A ) Consensus Clustering showing three distinct clusters (PANoptosis low, PANoptosis medium and PANoptosis high) based on PANoptosis gene expression for SKCM. ( B ) Heatmap depicting gene expression profiles of 27 PANoptosis markers including sensors and upstream regulators, adaptors and effectors of PANoptosis as scaled Z-scores for SKCM tumor samples. For brevity, 13 out of the 27 genes are labeled, but 27 distinct rows are shown. ( C ) Boxplot showing the distribution of PANoptosis scores in the three PANoptosis clusters for cancer subtypes of interest: LGG, KIRC and SKCM. ( D ) Forest plot showing N1 = number of samples in PANoptosis high cluster, N2 = number of samples in PANoptosis low cluster, P -value and hazard ratio (HR) with 95% CI for overall survival (OS) when comparing PANoptosis high versus low for each cancer type where there is significant prognostic impact ( P -value < 0.05). ( E–G ) Kaplan–Meier curves showing OS across the PANoptosis high and PANoptosis low groups in the three cancer types with significant differences in survival (PANoptosis high beneficial [HR < 1] or detrimental [HR > 1]). *** P -value < 0.001.
    Figure Legend Snippet: PANoptosis has a prognostic impact in cancers. ( A ) Consensus Clustering showing three distinct clusters (PANoptosis low, PANoptosis medium and PANoptosis high) based on PANoptosis gene expression for SKCM. ( B ) Heatmap depicting gene expression profiles of 27 PANoptosis markers including sensors and upstream regulators, adaptors and effectors of PANoptosis as scaled Z-scores for SKCM tumor samples. For brevity, 13 out of the 27 genes are labeled, but 27 distinct rows are shown. ( C ) Boxplot showing the distribution of PANoptosis scores in the three PANoptosis clusters for cancer subtypes of interest: LGG, KIRC and SKCM. ( D ) Forest plot showing N1 = number of samples in PANoptosis high cluster, N2 = number of samples in PANoptosis low cluster, P -value and hazard ratio (HR) with 95% CI for overall survival (OS) when comparing PANoptosis high versus low for each cancer type where there is significant prognostic impact ( P -value < 0.05). ( E–G ) Kaplan–Meier curves showing OS across the PANoptosis high and PANoptosis low groups in the three cancer types with significant differences in survival (PANoptosis high beneficial [HR < 1] or detrimental [HR > 1]). *** P -value < 0.001.

    Techniques Used: Gene Expression, Labeling

    TCGA cancer abbreviations. Cancers of interest are highlighted in colors
    Figure Legend Snippet: TCGA cancer abbreviations. Cancers of interest are highlighted in colors

    Techniques Used:

    Multiple survival models identify key prognostic PANoptosis markers for LGG, KIRC and SKCM. ( A ) Forest plot for key PANoptosis genes whose high expression leads to a poor prognosis for LGG identified through univariate survival models. ( B ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for LGG. ( C ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for LGG. ( D ) Forest plot for key PANoptosis genes whose high expression leads to a poor prognosis for KIRC identified through univariate survival models. ( E ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for KIRC. ( F ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for KIRC. ( G ) Forest plot for key PANoptosis genes whose high expression leads to better prognosis for SKCM identified by univariate survival models. ( H ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for SKCM. ( I ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for SKCM. (A–I) Blue bars represent a negative coefficient (higher expression is beneficial for survival), and red bars represent a positive coefficient (higher expression is detrimental for survival). The orange boxes highlight the genes which are prognostic across the univariate, GLMNet and RFS survival models and were considered as the ‘Top’ PANoptosis markers. (B, C, E, F, H, I) The boxplots correspond to variable importance estimated using a subsampling approach.
    Figure Legend Snippet: Multiple survival models identify key prognostic PANoptosis markers for LGG, KIRC and SKCM. ( A ) Forest plot for key PANoptosis genes whose high expression leads to a poor prognosis for LGG identified through univariate survival models. ( B ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for LGG. ( C ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for LGG. ( D ) Forest plot for key PANoptosis genes whose high expression leads to a poor prognosis for KIRC identified through univariate survival models. ( E ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for KIRC. ( F ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for KIRC. ( G ) Forest plot for key PANoptosis genes whose high expression leads to better prognosis for SKCM identified by univariate survival models. ( H ) PANoptosis genes with non-zero coefficients and the fraction of times they appeared during the 100 random runs of the GLMnet model for SKCM. ( I ) Top 10 PANoptosis genes with highest prognostic relevance determined by the optimal RFS model for SKCM. (A–I) Blue bars represent a negative coefficient (higher expression is beneficial for survival), and red bars represent a positive coefficient (higher expression is detrimental for survival). The orange boxes highlight the genes which are prognostic across the univariate, GLMNet and RFS survival models and were considered as the ‘Top’ PANoptosis markers. (B, C, E, F, H, I) The boxplots correspond to variable importance estimated using a subsampling approach.

    Techniques Used: Expressing

    Survival models built using key PANoptosis markers predict survival on independent test sets. ( A ) Comparison of AUC metric at t ∈ {2,4,5} years between Coxnet, GLMnet and RFS survival models for LGG. ( B ) Comparison of AUC metric at t ∈ {2,3,5} years between Coxnet, GLMnet and RFS survival models for KIRC. ( C ) Comparison of AUC metric at t ∈ {1,2,3} years between Coxnet, GLMnet and RFS models for SKCM.
    Figure Legend Snippet: Survival models built using key PANoptosis markers predict survival on independent test sets. ( A ) Comparison of AUC metric at t ∈ {2,4,5} years between Coxnet, GLMnet and RFS survival models for LGG. ( B ) Comparison of AUC metric at t ∈ {2,3,5} years between Coxnet, GLMnet and RFS survival models for KIRC. ( C ) Comparison of AUC metric at t ∈ {1,2,3} years between Coxnet, GLMnet and RFS models for SKCM.

    Techniques Used: Comparison

    Single cell transcriptomics provides evidence for PANoptosis in individual cells in LGG and SKCM datasets. ( A ) Expression profiles of PANoptosis genes across different cell types in the LGG dataset. ( B ) PANoptosis activity across different cell types in the LGG dataset estimated using ssGSEA. ( C ) Expression profiles of PANoptosis genes across different cell types for the SKCM dataset. ( D ) PANoptosis activity across different cell types in the SKCM dataset estimated using ssGSEA.
    Figure Legend Snippet: Single cell transcriptomics provides evidence for PANoptosis in individual cells in LGG and SKCM datasets. ( A ) Expression profiles of PANoptosis genes across different cell types in the LGG dataset. ( B ) PANoptosis activity across different cell types in the LGG dataset estimated using ssGSEA. ( C ) Expression profiles of PANoptosis genes across different cell types for the SKCM dataset. ( D ) PANoptosis activity across different cell types in the SKCM dataset estimated using ssGSEA.

    Techniques Used: Single-cell Transcriptomics, Expressing, Activity Assay



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    Single‐cell transcriptome landscape in aging cohort. (A) UMAP visualization of cell‐type‐specific annotation among the aging cohort, showing 9 cell groups in different colors. (B) UMAP visualization of immune cell subpopulation annotation across different age groups, displaying 21 subpopulations in different colors. (C) The proportion of 21 different cell types across age groups.

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    doi: 10.1111/acel.70431

    Figure Lengend Snippet: Single‐cell transcriptome landscape in aging cohort. (A) UMAP visualization of cell‐type‐specific annotation among the aging cohort, showing 9 cell groups in different colors. (B) UMAP visualization of immune cell subpopulation annotation across different age groups, displaying 21 subpopulations in different colors. (C) The proportion of 21 different cell types across age groups.

    Article Snippet: Single‐cell transcriptomic data from 56 healthy individuals aged from birth to over 90 years were acquired from the Shanghai Pudong Cohort ( NCT05206643 ) (Synapse: syn61609846) (Wang, Li, et al. ).

    Techniques: Single Cell

    Centenarian phenotype‐associated immune cell type analysis at single‐cell resolution. (A) UMAP visualization of cell‐type‐specific annotation among immune cells, showing 9 cell groups in different colors. (B) UMAP visualization of subcellular annotation among immune cell subpopulations, showing 21 subpopulations in different colors. (C) UMAP visualization of Scissor + and Scissor − cells. (D, E) Proportional fractions of identified cell types across Scissor +/− conditions among extracted immune cells.

    Journal: Aging Cell

    Article Title: The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

    doi: 10.1111/acel.70431

    Figure Lengend Snippet: Centenarian phenotype‐associated immune cell type analysis at single‐cell resolution. (A) UMAP visualization of cell‐type‐specific annotation among immune cells, showing 9 cell groups in different colors. (B) UMAP visualization of subcellular annotation among immune cell subpopulations, showing 21 subpopulations in different colors. (C) UMAP visualization of Scissor + and Scissor − cells. (D, E) Proportional fractions of identified cell types across Scissor +/− conditions among extracted immune cells.

    Article Snippet: Single‐cell transcriptomic data from 56 healthy individuals aged from birth to over 90 years were acquired from the Shanghai Pudong Cohort ( NCT05206643 ) (Synapse: syn61609846) (Wang, Li, et al. ).

    Techniques: Single Cell

    PTHrP expression in IPF and BLM-induced PF in humans. a Procedure for bioinformatics-based transcriptome analysis. b Identification of 714 commonly up- or downregulated genes in human IPF lungs using publicly available transcriptome datasets. c Top 9 activated gene sets identified by KEGG pathway analysis based on 714 common genes. d Identification of 5 genes through the intersection of genes related to soluble mediators, PTH synthesis, secretion, and action and 714 common genes. e Heatmap of PTHLH expression in normal and IPF samples. f PTHLH mRNA in normal and IPF samples. g Representative images of IF staining of PTHrP and quantification of the intensity of expression of PTHrP in human pulmonary interstitial fibrosis tissue microarrays from patients with IPF ( n = 23) and healthy donors ( n = 4). A magnified view of the region highlighted in the red box is shown. Scale bar: 50 μm and 100 μm (low magnification). a , b , d were created with BioRender.com. Data are shown as the mean ± SEM. P values were determined by two-tailed Student’s t test ( f , g ). *** P < 0.001

    Journal: Signal Transduction and Targeted Therapy

    Article Title: Parathyroid hormone–related protein is a therapeutic target in idiopathic pulmonary fibrosis

    doi: 10.1038/s41392-026-02578-8

    Figure Lengend Snippet: PTHrP expression in IPF and BLM-induced PF in humans. a Procedure for bioinformatics-based transcriptome analysis. b Identification of 714 commonly up- or downregulated genes in human IPF lungs using publicly available transcriptome datasets. c Top 9 activated gene sets identified by KEGG pathway analysis based on 714 common genes. d Identification of 5 genes through the intersection of genes related to soluble mediators, PTH synthesis, secretion, and action and 714 common genes. e Heatmap of PTHLH expression in normal and IPF samples. f PTHLH mRNA in normal and IPF samples. g Representative images of IF staining of PTHrP and quantification of the intensity of expression of PTHrP in human pulmonary interstitial fibrosis tissue microarrays from patients with IPF ( n = 23) and healthy donors ( n = 4). A magnified view of the region highlighted in the red box is shown. Scale bar: 50 μm and 100 μm (low magnification). a , b , d were created with BioRender.com. Data are shown as the mean ± SEM. P values were determined by two-tailed Student’s t test ( f , g ). *** P < 0.001

    Article Snippet: To confirm the predominance of tissue-specific expression of PTHLH in human tissues, we reanalyzed publicly available single-cell transcriptome data provided by The Human Protein Atlas.

    Techniques: Expressing, Staining, Two Tailed Test

    Identification of core genes associated with macrophage immune training and heart failure. (A) Schematic overview of human-derived macrophage trained immunity model and transcriptomic profiling workflow ( GSE235897 ). (B) The volcano plot and (C) DEGs heatmap of hMDMs from trained (n=3) and untrained (n=3) samples in the macrophage-trained immunity dataset GSE235897 (|log2FC| ≥ 0.585, p < 0.05). (D) Sample clustering dendrogram of GSE135055 dataset based on gene expression profiles. (E) Scale-free topology fit index and (F) mean connectivity analysis across a range of soft-thresholding powers. (G) Cluster dendrogram of genes showing co-expression modules identified by WGCNA in database GSE135055 . (H) Module-trait heatmap values represent correlation coefficients between healthy controls and HF samples (* p < 0.05, ** p < 0.01). (I) Venn diagram showing the overlap among heart failure DEGs, trained-immunity DEGs, and WGCNA module genes.

    Journal: Frontiers in Immunology

    Article Title: Identification of MTURN as a trained immunity-related biomarker for heart failure via integrative transcriptomic machine learning analysis and experimental validation

    doi: 10.3389/fimmu.2026.1739660

    Figure Lengend Snippet: Identification of core genes associated with macrophage immune training and heart failure. (A) Schematic overview of human-derived macrophage trained immunity model and transcriptomic profiling workflow ( GSE235897 ). (B) The volcano plot and (C) DEGs heatmap of hMDMs from trained (n=3) and untrained (n=3) samples in the macrophage-trained immunity dataset GSE235897 (|log2FC| ≥ 0.585, p < 0.05). (D) Sample clustering dendrogram of GSE135055 dataset based on gene expression profiles. (E) Scale-free topology fit index and (F) mean connectivity analysis across a range of soft-thresholding powers. (G) Cluster dendrogram of genes showing co-expression modules identified by WGCNA in database GSE135055 . (H) Module-trait heatmap values represent correlation coefficients between healthy controls and HF samples (* p < 0.05, ** p < 0.01). (I) Venn diagram showing the overlap among heart failure DEGs, trained-immunity DEGs, and WGCNA module genes.

    Article Snippet: For single-cell transcriptomic data, we accessed the SCP1303 project from the Broad Institute ( https://singlecell.broadinstitute.org/single_cell ), which includes raw scRNA-seq data from failing human hearts with dilated and hypertrophic cardiomyopathy.

    Techniques: Derivative Assay, Gene Expression, Expressing

    Five heart failure transcriptomic datasets were integrated with a macrophage-trained immunity model to identify immune-related biomarkers. Through DEGs analysis, WGCNA, CIBERSORT, and six machine learning algorithms, hub genes were prioritized with MTURN emerging as the top candidate. Its potential was further validated by scRNA-seq analysis, which confirmed MTURN enrichment in cardiac macrophages. Finally, MTURN expression was validated using previously published heart failure transcriptomic data and in vitro experiments.

    Journal: Frontiers in Immunology

    Article Title: Identification of MTURN as a trained immunity-related biomarker for heart failure via integrative transcriptomic machine learning analysis and experimental validation

    doi: 10.3389/fimmu.2026.1739660

    Figure Lengend Snippet: Five heart failure transcriptomic datasets were integrated with a macrophage-trained immunity model to identify immune-related biomarkers. Through DEGs analysis, WGCNA, CIBERSORT, and six machine learning algorithms, hub genes were prioritized with MTURN emerging as the top candidate. Its potential was further validated by scRNA-seq analysis, which confirmed MTURN enrichment in cardiac macrophages. Finally, MTURN expression was validated using previously published heart failure transcriptomic data and in vitro experiments.

    Article Snippet: For single-cell transcriptomic data, we accessed the SCP1303 project from the Broad Institute ( https://singlecell.broadinstitute.org/single_cell ), which includes raw scRNA-seq data from failing human hearts with dilated and hypertrophic cardiomyopathy.

    Techniques: Expressing, In Vitro

    Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    Article Title: Platelets in the tumor microenvironment: potential mediators of immune exclusion and resistance to immune checkpoint inhibitor therapy

    doi: 10.1007/s13402-025-01129-7

    Figure Lengend Snippet: Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

    Article Snippet: Our analysis of pan-tissue single-cell transcriptomic data from the Human Protein Atlas identifies platelets as a dominant cellular source of TGF-β and among the highest expressors of PDGFB across human cell types (Fig. A), providing a strong molecular basis for their impact on CAF activation and differentiation.

    Techniques: Activation Assay, Expressing, RNA Sequencing, Derivative Assay