Aneuploidy meets network analysis: leveraging copy number alterations to identify molecular pathways disrupted in high-grade serous ovarian carcinomas

Cancer is a genomic disorder that often involves the accumulation of various types of genomic alterations that play roles in disease development and progression (1,2). In solid tumors, somatic mutations (herein, point mutations and short indels) and SCNAs (somatic copy number alterations as chromosomal amplifications/deletions) comprise the majority of the genomic alterations in cancer genomes in terms of abundance and genomic fraction, respectively; several to tens of thousands of somatic mutations and SCNAs occupying >50% of the genome have been observed in solid tumor genomes. Aneuploidy is defined as the presence of an abnormal number of chromosomes, and this chromosome-level SCNA has long been recognized as a hallmark of cancer genomes (3).