Fig. 7: Cell-intrinsic inflammation in high-risk UM. | Nature Communications

Fig. 7: Cell-intrinsic inflammation in high-risk UM.

From: Loss of polycomb repressive complex 1 activity and chromosomal instability drive uveal melanoma progression

Fig. 7

a Expression of key cytosolic nucleic acids sensors, intermediate signaling adapters, executioners, interferon stimulated genes (ISGs) and CIN-induced non-canonical NF-kB targets (shown in red)56 for all patient tumor cells ranked by average imputed expression of the GEP2 gene signature (gene signatures annotated in Supplementary Data File 1) in ascending order from left to right; genes are clustered using an Euclidean distance metric. For each gene, imputed expression was z-normalized across all cells and smoothed using a 20-cell moving average window. Top, filled area plot showing average expression of the GEP2 signature across ranked tumor cells. b Immunofluorescence of STING (green) and DAPI (blue) in MSK-UM03 (greatest proportion of GEP1 tumor cells in the cohort) and MSK-UM01 (greatest proportion of GEP2 tumor cells in the cohort). Representative images from six biological specimens. c Overall survival (left) and UM-related metastasis (right) of (n = 80) TCGA-UM patients with primary tumors stratified by expression of high (top 50th percentile, n = 40) and low (bottom 50th percentile, n = 40) STING. Statistical significance tested using two-sided log-rank test; p (left) = 2.2 × 10−5.

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