This study investigates the patterns of somatic copy number alterations (SCNAs) in 4,934 cancers from the Cancer Genome Atlas Pan-Cancer dataset. Whole-genome doubling, observed in 37% of cancers, was associated with higher rates of other types of SCNAs, TP53 mutations, CCNE1 amplifications, and alterations of the PPP2R complex. Internal SCNAs tended to be shorter than telomere-bounded SCNAs, suggesting different mechanisms of generation. Significantly recurrent focal SCNAs were identified in 140 regions, including 102 without known oncogene or tumor suppressor gene targets and 50 with significantly mutated genes. Amplified regions without known oncogenes were enriched for genes involved in epigenetic regulation. When accounting for genomic disruption levels, 7% of region pairs showed anticorrelations, indicating functional redundancies or synergies. These findings provide insights into the mechanisms and functional consequences of cancer-related SCNAs.This study investigates the patterns of somatic copy number alterations (SCNAs) in 4,934 cancers from the Cancer Genome Atlas Pan-Cancer dataset. Whole-genome doubling, observed in 37% of cancers, was associated with higher rates of other types of SCNAs, TP53 mutations, CCNE1 amplifications, and alterations of the PPP2R complex. Internal SCNAs tended to be shorter than telomere-bounded SCNAs, suggesting different mechanisms of generation. Significantly recurrent focal SCNAs were identified in 140 regions, including 102 without known oncogene or tumor suppressor gene targets and 50 with significantly mutated genes. Amplified regions without known oncogenes were enriched for genes involved in epigenetic regulation. When accounting for genomic disruption levels, 7% of region pairs showed anticorrelations, indicating functional redundancies or synergies. These findings provide insights into the mechanisms and functional consequences of cancer-related SCNAs.