High-PTMRS tumors carried a heavier genomic alteration burden: frequent mutations in canonical CRC drivers (APC, TP53, KRAS, PIK3CA) co-occurred with recurrent segmental CNV gains and losses, and copy-number changes were biased toward gains, with elevated arm-level and focal amplifications compared with relatively weaker losses (Supplementary Figures 3C, D). Here, KRAS is linked to colorectal carcinoma.