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Spatial Transcriptomics Inc geomx dsp platform
Digital spatial profiling reveals transcriptional programs and tumor–immune interactions in SCC. (A) Example of a representative SCC sample stained with H&E. Inset shows a higher magnification of a selected ROI. (B) Representative <t>GeoMx</t> spatial transcriptomics images from squamous cell carcinoma (SCC), and pemphigus vulgaris (PV) skin lesions. In SCC samples ( n = 2), regions of interest (ROIs) were selected to capture PanCK + tumor areas in close proximity to immune cell infiltrates. ROIs were segmented into SCC_Tumor and SCC_TME based on PanCK expression. In PV and PSO lesions, epithelial and immune compartments were delineated using CD45/CD31 and PanCK markers. (C) UMAP plot displaying spatial transcriptomic profiles from SCC ( n= 8 tumor, n = 8 TME), and PV ( n = 10 epithelial, n = 9 immune) regions. Each point represents an individual area of interest (AOI), color‐coded by lesion type and tissue compartment. (D) Boxplots illustrating genes associated with SCC progression and previously identified in the Carcinoma 3 cluster, the majority of which were significantly upregulated in SCC_Tumor compared to PV and PSO epithelial regions. (E) Heatmap showing paired Spearman correlation analysis of ligand–receptor gene pairs in SCC. Each row represents a ligand expressed in SCC_Tumor regions, and each column represents its corresponding receptor in SCC_TME regions. Ligand–receptor pairs were pre‐selected based on top‐ranked interactions predicted from Carcinoma 3 in Figure , and only those with Spearman correlation coefficient ≥ 0 are shown. Cell color represents the strength of correlation, and values within each cell indicate the associated p value. The red‐highlighted ligand–receptor pairs were previously identified as key components of the Carcinoma 3—Treg interaction network. (F) Scatter plots showing the expression of selected ligands (CXCL16, TNFSF9) and their corresponding receptors (CXCR6, TNFRSF9) in SCC and PV samples. Ligands were measured in SCC_Tumor and PV epithelial regions, while receptors were measured in SCC_TME and PV immune regions. Among these, CXCL16 and TNFRSF9 showed significant upregulation in SCC samples. p < 0.05 suggested significant differences. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 and ns, not significant.
Geomx Dsp Platform, supplied by Spatial Transcriptomics Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/geomx+dsp+platform/pmc12331524-55-6-0?v=Spatial+Transcriptomics+Inc
Average 86 stars, based on 1 article reviews
geomx dsp platform - by Bioz Stars, 2026-07
86/100 stars

Images

1) Product Images from "CXCL16 Producing Tumor Clones Are Shaping Immunosuppressive Microenvironment in Squamous Cell Carcinoma via CXCR6 Regulatory T Cell"

Article Title: CXCL16 Producing Tumor Clones Are Shaping Immunosuppressive Microenvironment in Squamous Cell Carcinoma via CXCR6 Regulatory T Cell

Journal: Cancer Medicine

doi: 10.1002/cam4.71060

Digital spatial profiling reveals transcriptional programs and tumor–immune interactions in SCC. (A) Example of a representative SCC sample stained with H&E. Inset shows a higher magnification of a selected ROI. (B) Representative GeoMx spatial transcriptomics images from squamous cell carcinoma (SCC), and pemphigus vulgaris (PV) skin lesions. In SCC samples ( n = 2), regions of interest (ROIs) were selected to capture PanCK + tumor areas in close proximity to immune cell infiltrates. ROIs were segmented into SCC_Tumor and SCC_TME based on PanCK expression. In PV and PSO lesions, epithelial and immune compartments were delineated using CD45/CD31 and PanCK markers. (C) UMAP plot displaying spatial transcriptomic profiles from SCC ( n= 8 tumor, n = 8 TME), and PV ( n = 10 epithelial, n = 9 immune) regions. Each point represents an individual area of interest (AOI), color‐coded by lesion type and tissue compartment. (D) Boxplots illustrating genes associated with SCC progression and previously identified in the Carcinoma 3 cluster, the majority of which were significantly upregulated in SCC_Tumor compared to PV and PSO epithelial regions. (E) Heatmap showing paired Spearman correlation analysis of ligand–receptor gene pairs in SCC. Each row represents a ligand expressed in SCC_Tumor regions, and each column represents its corresponding receptor in SCC_TME regions. Ligand–receptor pairs were pre‐selected based on top‐ranked interactions predicted from Carcinoma 3 in Figure , and only those with Spearman correlation coefficient ≥ 0 are shown. Cell color represents the strength of correlation, and values within each cell indicate the associated p value. The red‐highlighted ligand–receptor pairs were previously identified as key components of the Carcinoma 3—Treg interaction network. (F) Scatter plots showing the expression of selected ligands (CXCL16, TNFSF9) and their corresponding receptors (CXCR6, TNFRSF9) in SCC and PV samples. Ligands were measured in SCC_Tumor and PV epithelial regions, while receptors were measured in SCC_TME and PV immune regions. Among these, CXCL16 and TNFRSF9 showed significant upregulation in SCC samples. p < 0.05 suggested significant differences. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 and ns, not significant.
Figure Legend Snippet: Digital spatial profiling reveals transcriptional programs and tumor–immune interactions in SCC. (A) Example of a representative SCC sample stained with H&E. Inset shows a higher magnification of a selected ROI. (B) Representative GeoMx spatial transcriptomics images from squamous cell carcinoma (SCC), and pemphigus vulgaris (PV) skin lesions. In SCC samples ( n = 2), regions of interest (ROIs) were selected to capture PanCK + tumor areas in close proximity to immune cell infiltrates. ROIs were segmented into SCC_Tumor and SCC_TME based on PanCK expression. In PV and PSO lesions, epithelial and immune compartments were delineated using CD45/CD31 and PanCK markers. (C) UMAP plot displaying spatial transcriptomic profiles from SCC ( n= 8 tumor, n = 8 TME), and PV ( n = 10 epithelial, n = 9 immune) regions. Each point represents an individual area of interest (AOI), color‐coded by lesion type and tissue compartment. (D) Boxplots illustrating genes associated with SCC progression and previously identified in the Carcinoma 3 cluster, the majority of which were significantly upregulated in SCC_Tumor compared to PV and PSO epithelial regions. (E) Heatmap showing paired Spearman correlation analysis of ligand–receptor gene pairs in SCC. Each row represents a ligand expressed in SCC_Tumor regions, and each column represents its corresponding receptor in SCC_TME regions. Ligand–receptor pairs were pre‐selected based on top‐ranked interactions predicted from Carcinoma 3 in Figure , and only those with Spearman correlation coefficient ≥ 0 are shown. Cell color represents the strength of correlation, and values within each cell indicate the associated p value. The red‐highlighted ligand–receptor pairs were previously identified as key components of the Carcinoma 3—Treg interaction network. (F) Scatter plots showing the expression of selected ligands (CXCL16, TNFSF9) and their corresponding receptors (CXCR6, TNFRSF9) in SCC and PV samples. Ligands were measured in SCC_Tumor and PV epithelial regions, while receptors were measured in SCC_TME and PV immune regions. Among these, CXCL16 and TNFRSF9 showed significant upregulation in SCC samples. p < 0.05 suggested significant differences. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 and ns, not significant.

Techniques Used: Staining, Expressing



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Image Search Results


Digital spatial profiling reveals transcriptional programs and tumor–immune interactions in SCC. (A) Example of a representative SCC sample stained with H&E. Inset shows a higher magnification of a selected ROI. (B) Representative GeoMx spatial transcriptomics images from squamous cell carcinoma (SCC), and pemphigus vulgaris (PV) skin lesions. In SCC samples ( n = 2), regions of interest (ROIs) were selected to capture PanCK + tumor areas in close proximity to immune cell infiltrates. ROIs were segmented into SCC_Tumor and SCC_TME based on PanCK expression. In PV and PSO lesions, epithelial and immune compartments were delineated using CD45/CD31 and PanCK markers. (C) UMAP plot displaying spatial transcriptomic profiles from SCC ( n= 8 tumor, n = 8 TME), and PV ( n = 10 epithelial, n = 9 immune) regions. Each point represents an individual area of interest (AOI), color‐coded by lesion type and tissue compartment. (D) Boxplots illustrating genes associated with SCC progression and previously identified in the Carcinoma 3 cluster, the majority of which were significantly upregulated in SCC_Tumor compared to PV and PSO epithelial regions. (E) Heatmap showing paired Spearman correlation analysis of ligand–receptor gene pairs in SCC. Each row represents a ligand expressed in SCC_Tumor regions, and each column represents its corresponding receptor in SCC_TME regions. Ligand–receptor pairs were pre‐selected based on top‐ranked interactions predicted from Carcinoma 3 in Figure , and only those with Spearman correlation coefficient ≥ 0 are shown. Cell color represents the strength of correlation, and values within each cell indicate the associated p value. The red‐highlighted ligand–receptor pairs were previously identified as key components of the Carcinoma 3—Treg interaction network. (F) Scatter plots showing the expression of selected ligands (CXCL16, TNFSF9) and their corresponding receptors (CXCR6, TNFRSF9) in SCC and PV samples. Ligands were measured in SCC_Tumor and PV epithelial regions, while receptors were measured in SCC_TME and PV immune regions. Among these, CXCL16 and TNFRSF9 showed significant upregulation in SCC samples. p < 0.05 suggested significant differences. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 and ns, not significant.

Journal: Cancer Medicine

Article Title: CXCL16 Producing Tumor Clones Are Shaping Immunosuppressive Microenvironment in Squamous Cell Carcinoma via CXCR6 Regulatory T Cell

doi: 10.1002/cam4.71060

Figure Lengend Snippet: Digital spatial profiling reveals transcriptional programs and tumor–immune interactions in SCC. (A) Example of a representative SCC sample stained with H&E. Inset shows a higher magnification of a selected ROI. (B) Representative GeoMx spatial transcriptomics images from squamous cell carcinoma (SCC), and pemphigus vulgaris (PV) skin lesions. In SCC samples ( n = 2), regions of interest (ROIs) were selected to capture PanCK + tumor areas in close proximity to immune cell infiltrates. ROIs were segmented into SCC_Tumor and SCC_TME based on PanCK expression. In PV and PSO lesions, epithelial and immune compartments were delineated using CD45/CD31 and PanCK markers. (C) UMAP plot displaying spatial transcriptomic profiles from SCC ( n= 8 tumor, n = 8 TME), and PV ( n = 10 epithelial, n = 9 immune) regions. Each point represents an individual area of interest (AOI), color‐coded by lesion type and tissue compartment. (D) Boxplots illustrating genes associated with SCC progression and previously identified in the Carcinoma 3 cluster, the majority of which were significantly upregulated in SCC_Tumor compared to PV and PSO epithelial regions. (E) Heatmap showing paired Spearman correlation analysis of ligand–receptor gene pairs in SCC. Each row represents a ligand expressed in SCC_Tumor regions, and each column represents its corresponding receptor in SCC_TME regions. Ligand–receptor pairs were pre‐selected based on top‐ranked interactions predicted from Carcinoma 3 in Figure , and only those with Spearman correlation coefficient ≥ 0 are shown. Cell color represents the strength of correlation, and values within each cell indicate the associated p value. The red‐highlighted ligand–receptor pairs were previously identified as key components of the Carcinoma 3—Treg interaction network. (F) Scatter plots showing the expression of selected ligands (CXCL16, TNFSF9) and their corresponding receptors (CXCR6, TNFRSF9) in SCC and PV samples. Ligands were measured in SCC_Tumor and PV epithelial regions, while receptors were measured in SCC_TME and PV immune regions. Among these, CXCL16 and TNFRSF9 showed significant upregulation in SCC samples. p < 0.05 suggested significant differences. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001 and ns, not significant.

Article Snippet: Spatial transcriptomics was performed using the GeoMx DSP platform of the whole‐transcriptome atlas (NanoString Technologies, Seattle, WA, USA).

Techniques: Staining, Expressing

Representative GeoMx ® DSP scan of PCa specimen Gleason 3 and 4 TMA cores stained with morphology markers SYTO13, CD45 and PanCK along with H&E staining. Scale bar = 250 µm.

Journal: Frontiers in Oncology

Article Title: Digital spatial profiling identifies phospho-JNK as a biomarker for early risk stratification of aggressive prostate cancer

doi: 10.3389/fonc.2025.1572299

Figure Lengend Snippet: Representative GeoMx ® DSP scan of PCa specimen Gleason 3 and 4 TMA cores stained with morphology markers SYTO13, CD45 and PanCK along with H&E staining. Scale bar = 250 µm.

Article Snippet: The GeoMx ® DSP platform (NanoString Technologies, Seattle, Bruker Corporations, Billerica, MA, USA) was used for the spatial analysis of PCa TMAs, and the TMA cores were prepared as described previously ( , ).

Techniques: Staining