Pathway analyses using a combined set of single-nucleotide and copy number data across the whole cohort of cervical carcinomas revealed that ERBB- and PI3K/AKT/mTOR signaling were enhanced within mutated and/or amplified oncogenes (Supplementary Table 8), while p53 signaling and interferon signaling were enriched among deleted and mutated tumor suppressors (Supplementary Table 9). This evidence concerns the gene TP53 and cervical carcinoma.