Moreover, combinations of specific P53-MYC defects were uniquely observed at relapse and were not observed at diagnosis in our large control cohorts, or in previously reported studies (Pfaff et al., 2010) (e.g., CDKN2A deletion and MYC amplification in a relapsed MBGroup3 tumor; TP53 mutation and MYC amplification in a relapsed MBSHH tumor; TP53 mutation and MYCN amplification in a relapsed MBGroup4 tumor; TP53 mutation and MYC amplification in a relapsed MBWNT tumor). This evidence concerns the gene CDKN2A and neoplasm.