TP53 and neoplasm: Nevertheless, most driver alterations had similar frequencies and clonal distributions between the primary and recurrent tumors across all of the patients with de novo recurrence: alterations in AXIN1 and TP53 always took place early in the evolution of the tumor, whereas TERT promoter mutations and amplification were often acquired subsequently, and CNVs affecting CCND1-FGF19 and VEGFA occurred at later points in the evolutionary cascade.