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

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.