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Structured Review

Broad Institute Inc single cell portal
Integrative analysis of single histone modifications and gene expression reveals dynamic and synergistic epigenetic regulation of pathways involved in glioblastoma pathogenesis. a Pearson correlation heatmaps of integrative analysis of ChIP Seq data for each HM and RNAseq dataset for genes only found in GIC (left) or iNSC (right) for at least one HM. RNAseq data are represented as log fold change of Differentially Expressed (DE) genes between GIC and iNSC: logFC DE > 1 and < − 1 when genes are up (red section) and downregulated (blue section) in GIC as compared to iNSC respectively (left). LogFC DE > 1 and < − 1 when genes are down and upregulated in iNSC as compared to GIC respectively (right). b Percentages of upregulated (red) and downregulated (blue) genes in iNSC as compared to GIC (top) and in GIC as compared to iNSC (bottom) for each HM based on <t>transcriptomic</t> dataset from the SYNGN cohort . Number of genes is also specified for each condition. c mRNA expression of GSC in iNSC, GIC and bulk tumour from the RNAseq dataset of the SYNGN cohort (left) and in bulk tumour and non-tumour samples from TCGA dataset . Results are expressed in log 2 (tpm) transcript per million (tpm). One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. d Representative immunofluorescent images for GSC (green) in iNSC and GIC from patient 52. Nuclei are counterstained with DAPI. Scale bar: 50 µm. Quantification is shown as Mean Fluorescence Intensity (MFI) standardised by the number of nuclei. One-way ANOVA test. * p value < 0.05, ** p value < 0.01, *** p value < 0.001, **** p value < 0.0001. e GSC gene expression in non-tumour and bulk primary glioblastoma tumour (left panel). t-test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. f Survival curve of glioblastoma patients with high and low expression of GSC gene (right panel). Source: TCGA Stat test: log-rank, * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. g Spatial expression of GSC in glioblastoma bulk samples, analysed on Ivy –GAP . The left panel shows an example of histological anatomic structure identified in a sub-block and the right panel represents the expression of GSC in RNAseq data from anatomic structures shown as log2 normalised gene expression. Leading Edge defined as the border of the tumour, where ratio of tumour to normal cells is 1–3 / 100. Infiltrating tumour defined as the intermediate zone between leading edge and cellular tumour, where ratio of tumour to normal cells is 10–20 /100. Cellular tumour defined as tumour core, where tumour to normal cells is 100–500 / 1. One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. h Single-cell RNAseq data showing GSC expression (left panel) in scRNAseq of glioblastoma samples in clusters defined in (right panel). Data are plotted as tSNE, with logTPM expression ranging from light orange to dark
Single Cell Portal, 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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single cell portal - by Bioz Stars, 2026-08
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1) Product Images from "Mapping chromatin remodelling in glioblastoma identifies epigenetic regulation of key molecular pathways and novel druggable targets"

Article Title: Mapping chromatin remodelling in glioblastoma identifies epigenetic regulation of key molecular pathways and novel druggable targets

Journal: BMC Biology

doi: 10.1186/s12915-025-02127-9

Integrative analysis of single histone modifications and gene expression reveals dynamic and synergistic epigenetic regulation of pathways involved in glioblastoma pathogenesis. a Pearson correlation heatmaps of integrative analysis of ChIP Seq data for each HM and RNAseq dataset for genes only found in GIC (left) or iNSC (right) for at least one HM. RNAseq data are represented as log fold change of Differentially Expressed (DE) genes between GIC and iNSC: logFC DE > 1 and < − 1 when genes are up (red section) and downregulated (blue section) in GIC as compared to iNSC respectively (left). LogFC DE > 1 and < − 1 when genes are down and upregulated in iNSC as compared to GIC respectively (right). b Percentages of upregulated (red) and downregulated (blue) genes in iNSC as compared to GIC (top) and in GIC as compared to iNSC (bottom) for each HM based on transcriptomic dataset from the SYNGN cohort . Number of genes is also specified for each condition. c mRNA expression of GSC in iNSC, GIC and bulk tumour from the RNAseq dataset of the SYNGN cohort (left) and in bulk tumour and non-tumour samples from TCGA dataset . Results are expressed in log 2 (tpm) transcript per million (tpm). One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. d Representative immunofluorescent images for GSC (green) in iNSC and GIC from patient 52. Nuclei are counterstained with DAPI. Scale bar: 50 µm. Quantification is shown as Mean Fluorescence Intensity (MFI) standardised by the number of nuclei. One-way ANOVA test. * p value < 0.05, ** p value < 0.01, *** p value < 0.001, **** p value < 0.0001. e GSC gene expression in non-tumour and bulk primary glioblastoma tumour (left panel). t-test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. f Survival curve of glioblastoma patients with high and low expression of GSC gene (right panel). Source: TCGA Stat test: log-rank, * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. g Spatial expression of GSC in glioblastoma bulk samples, analysed on Ivy –GAP . The left panel shows an example of histological anatomic structure identified in a sub-block and the right panel represents the expression of GSC in RNAseq data from anatomic structures shown as log2 normalised gene expression. Leading Edge defined as the border of the tumour, where ratio of tumour to normal cells is 1–3 / 100. Infiltrating tumour defined as the intermediate zone between leading edge and cellular tumour, where ratio of tumour to normal cells is 10–20 /100. Cellular tumour defined as tumour core, where tumour to normal cells is 100–500 / 1. One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. h Single-cell RNAseq data showing GSC expression (left panel) in scRNAseq of glioblastoma samples in clusters defined in (right panel). Data are plotted as tSNE, with logTPM expression ranging from light orange to dark
Figure Legend Snippet: Integrative analysis of single histone modifications and gene expression reveals dynamic and synergistic epigenetic regulation of pathways involved in glioblastoma pathogenesis. a Pearson correlation heatmaps of integrative analysis of ChIP Seq data for each HM and RNAseq dataset for genes only found in GIC (left) or iNSC (right) for at least one HM. RNAseq data are represented as log fold change of Differentially Expressed (DE) genes between GIC and iNSC: logFC DE > 1 and < − 1 when genes are up (red section) and downregulated (blue section) in GIC as compared to iNSC respectively (left). LogFC DE > 1 and < − 1 when genes are down and upregulated in iNSC as compared to GIC respectively (right). b Percentages of upregulated (red) and downregulated (blue) genes in iNSC as compared to GIC (top) and in GIC as compared to iNSC (bottom) for each HM based on transcriptomic dataset from the SYNGN cohort . Number of genes is also specified for each condition. c mRNA expression of GSC in iNSC, GIC and bulk tumour from the RNAseq dataset of the SYNGN cohort (left) and in bulk tumour and non-tumour samples from TCGA dataset . Results are expressed in log 2 (tpm) transcript per million (tpm). One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. d Representative immunofluorescent images for GSC (green) in iNSC and GIC from patient 52. Nuclei are counterstained with DAPI. Scale bar: 50 µm. Quantification is shown as Mean Fluorescence Intensity (MFI) standardised by the number of nuclei. One-way ANOVA test. * p value < 0.05, ** p value < 0.01, *** p value < 0.001, **** p value < 0.0001. e GSC gene expression in non-tumour and bulk primary glioblastoma tumour (left panel). t-test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. f Survival curve of glioblastoma patients with high and low expression of GSC gene (right panel). Source: TCGA Stat test: log-rank, * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. g Spatial expression of GSC in glioblastoma bulk samples, analysed on Ivy –GAP . The left panel shows an example of histological anatomic structure identified in a sub-block and the right panel represents the expression of GSC in RNAseq data from anatomic structures shown as log2 normalised gene expression. Leading Edge defined as the border of the tumour, where ratio of tumour to normal cells is 1–3 / 100. Infiltrating tumour defined as the intermediate zone between leading edge and cellular tumour, where ratio of tumour to normal cells is 10–20 /100. Cellular tumour defined as tumour core, where tumour to normal cells is 100–500 / 1. One-way ANOVA test. * p value < 0.05, ** p value < 0.01 and *** p value < 0.001. h Single-cell RNAseq data showing GSC expression (left panel) in scRNAseq of glioblastoma samples in clusters defined in (right panel). Data are plotted as tSNE, with logTPM expression ranging from light orange to dark

Techniques Used: Gene Expression, ChIP-sequencing, Expressing, Fluorescence, Blocking Assay

Comparative analysis of the functional impact of chromatin states dynamics in GIC and iNSC using automatic fragmentation analysis. a Chromatin states defined by enrichment of HM using ChromHMM . Probabilities of each HM in chromatin states are depicted as a heatmap. b Pie charts show percentages of peaks in each chromatin state in GIC (left) and iNSC (right). c Sankey diagram shows the switch of peaks from one chromatin state in iNSC to another in GIC. The thickness of the links is proportional to the number of peaks included. Flows with the highest number of peaks between two opposite state functions are highlighted in bold red (activating transition in GIC) and blue (repressing transition in GIC). d Percentages of upregulated (red) and downregulated (blue) genes in the chromatin states of interest based on transcriptomic dataset from the SYNGN Cohort . Number of genes is also specified for each condition. e Visualisation of the enriched pathways identified in GIC from genes activated in GIC as compared to iNSC and from genes inactivated in GIC as compared to iNSC. Pathways are annotated based on pathways enrichment analysis performed with Reactome and represented as circle, colours represent each histone (see legend), size of the circle is proportional to the number of genes involved in the pathway (FDR < 0.05)
Figure Legend Snippet: Comparative analysis of the functional impact of chromatin states dynamics in GIC and iNSC using automatic fragmentation analysis. a Chromatin states defined by enrichment of HM using ChromHMM . Probabilities of each HM in chromatin states are depicted as a heatmap. b Pie charts show percentages of peaks in each chromatin state in GIC (left) and iNSC (right). c Sankey diagram shows the switch of peaks from one chromatin state in iNSC to another in GIC. The thickness of the links is proportional to the number of peaks included. Flows with the highest number of peaks between two opposite state functions are highlighted in bold red (activating transition in GIC) and blue (repressing transition in GIC). d Percentages of upregulated (red) and downregulated (blue) genes in the chromatin states of interest based on transcriptomic dataset from the SYNGN Cohort . Number of genes is also specified for each condition. e Visualisation of the enriched pathways identified in GIC from genes activated in GIC as compared to iNSC and from genes inactivated in GIC as compared to iNSC. Pathways are annotated based on pathways enrichment analysis performed with Reactome and represented as circle, colours represent each histone (see legend), size of the circle is proportional to the number of genes involved in the pathway (FDR < 0.05)

Techniques Used: Functional Assay



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(a) Simplified cross-section of the human epidermis, highlighting squamous cells, melanocytes and basal cells. Coloured regions represent cSCC (green), which originates from squamous cells, melanoma (orange), which originates from melanocytes, and BCC (blue), which originates from basal cells. Two orange melanocytes are shown in the dermal region as occurs in invasive melanoma; other cells in the lower dermis layer are not depicted. (b) Overview of sample design and technologies used to generate data for this project. ROI - region of interest; FOV - field of view; S - cSCC; B - BCC; M - melanoma; HC - healthy (cancer patient); HNC - healthy (non-cancer patient donor). Technologies included are single cell RNA sequencing for fresh samples, single nuclei sequencing for formalin-fixed samples, Visium, Xenium, CosMX, GeoMX DSP for whole transcriptome, GeoMX DSP for proteins, Polaris, RNAscope, the proximal ligation assay, spatial glycomics and CODEX.

Journal: bioRxiv

Article Title: Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

doi: 10.1101/2025.07.25.666708

Figure Lengend Snippet: (a) Simplified cross-section of the human epidermis, highlighting squamous cells, melanocytes and basal cells. Coloured regions represent cSCC (green), which originates from squamous cells, melanoma (orange), which originates from melanocytes, and BCC (blue), which originates from basal cells. Two orange melanocytes are shown in the dermal region as occurs in invasive melanoma; other cells in the lower dermis layer are not depicted. (b) Overview of sample design and technologies used to generate data for this project. ROI - region of interest; FOV - field of view; S - cSCC; B - BCC; M - melanoma; HC - healthy (cancer patient); HNC - healthy (non-cancer patient donor). Technologies included are single cell RNA sequencing for fresh samples, single nuclei sequencing for formalin-fixed samples, Visium, Xenium, CosMX, GeoMX DSP for whole transcriptome, GeoMX DSP for proteins, Polaris, RNAscope, the proximal ligation assay, spatial glycomics and CODEX.

Article Snippet: Cells expressing the two genes are visualized on single-cell level resolution spatial data from STOmics and Curio-Seeker (Takara Bio, USA) melanoma samples and appear to be in spatial proximity ( ).

Techniques: RNA Sequencing, Sequencing, RNAscope, Ligation

(a) Gene specificity score (GSS) and association of spatial spots with skin cancer heritability. GSS score for each gene in a spot/cell represents the enrichment of the gene as a top rank most abundant gene in the spot/cell and its neighbour spots/cells in an anatomical region, a spatial domain, or a cell type. The p-value shows the spatial heritability enrichment significance of a spot with a trait based on SNPs mapped to the genes with high GSS scores (one-sided Z-test for stratified coefficient different to 0). The p-value is more significant if the SNPs that are mapped to the high GSS genes explain a higher proportion of heritability for the trait. (b) Cell types with the highest enrichment of heritability explained by SNPs tagged to GSS genes of cells in a cell type. The white asterisks indicate the most enriched cell-type for heritability of cutaneous melanoma, cSCC and BCC traits. (c) gsMAP significance spatial heritability enrichment is shown at single-cell resolution across the tissue (upper tissue plots) or per annotated skin regions (lower violin plots) from the cosMx data of the sample mel48974. (d) LR pairs with significant association with SNP heritability explained by the corresponding cell types. The rectangles show cases where both L and R genes had PCC >0.3 between GSS of the gene and the gsMAP P-values (the significance level for the LD stratified coefficients for the spot bigger than 0). The results suggest which LR pairs are related with the heritability of a cell type pairs. (e) GSS of two LR pairs showing specificity of the L and R genes to tissue regions at the immune-rich dermal layers and the epidermis of the skin. (f) Manhattan plot showing top significant GWAS SNPs co-localizing with genes in melanocytes (red) and T cells (blue) that had the highest Pearson correlation between GSS and the gsMAP trait association P-value or associated with SNPs with genome-wide significance. The Y-axis shows the -log(P-value) from GWAS analysis.

Journal: bioRxiv

Article Title: Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

doi: 10.1101/2025.07.25.666708

Figure Lengend Snippet: (a) Gene specificity score (GSS) and association of spatial spots with skin cancer heritability. GSS score for each gene in a spot/cell represents the enrichment of the gene as a top rank most abundant gene in the spot/cell and its neighbour spots/cells in an anatomical region, a spatial domain, or a cell type. The p-value shows the spatial heritability enrichment significance of a spot with a trait based on SNPs mapped to the genes with high GSS scores (one-sided Z-test for stratified coefficient different to 0). The p-value is more significant if the SNPs that are mapped to the high GSS genes explain a higher proportion of heritability for the trait. (b) Cell types with the highest enrichment of heritability explained by SNPs tagged to GSS genes of cells in a cell type. The white asterisks indicate the most enriched cell-type for heritability of cutaneous melanoma, cSCC and BCC traits. (c) gsMAP significance spatial heritability enrichment is shown at single-cell resolution across the tissue (upper tissue plots) or per annotated skin regions (lower violin plots) from the cosMx data of the sample mel48974. (d) LR pairs with significant association with SNP heritability explained by the corresponding cell types. The rectangles show cases where both L and R genes had PCC >0.3 between GSS of the gene and the gsMAP P-values (the significance level for the LD stratified coefficients for the spot bigger than 0). The results suggest which LR pairs are related with the heritability of a cell type pairs. (e) GSS of two LR pairs showing specificity of the L and R genes to tissue regions at the immune-rich dermal layers and the epidermis of the skin. (f) Manhattan plot showing top significant GWAS SNPs co-localizing with genes in melanocytes (red) and T cells (blue) that had the highest Pearson correlation between GSS and the gsMAP trait association P-value or associated with SNPs with genome-wide significance. The Y-axis shows the -log(P-value) from GWAS analysis.

Article Snippet: Cells expressing the two genes are visualized on single-cell level resolution spatial data from STOmics and Curio-Seeker (Takara Bio, USA) melanoma samples and appear to be in spatial proximity ( ).

Techniques: Genome Wide

Journal: Cell

Article Title: Spatiotemporal analysis of human intestinal development at single-cell resolution

doi: 10.1016/j.cell.2020.12.016

Figure Lengend Snippet:

Article Snippet: STAR-FINDer Single Cell and Spatial Transcriptomics Data Portal , This study , https://simmonslab.shinyapps.io/FetalAtlasDataPortal.

Techniques: Conjugation Assay, Recombinant, Saline, Modification, Plasmid Preparation, Gene Expression, RNAscope, Generated, Software