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We next assessed SNV mutational signatures by computing trinucleotide signature scores and cosine similarity between each tumour–model pair (Methods, ‘Analysis methods: Mutation signature’)

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18,20,22 These processes involve key molecular mediators—including hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), p53, B-cell lymphoma 2 (Bcl-2), Bcl-2–associated X protein (Bax), and cysteine-aspartate protease-3 (Caspase-3)—which regulate oxidative stress responses, angiogenesis, and apoptosis, with their imbalance determining tissue survival or loss