TP53 and neoplasm: Driver alterations in SNVs and indels are well characterized in OAC, as are distinct copy number (CN) amplification of oncogenes (e.g. ERBB2, EGFR, RB1, GATA4/6, CCND1 and MDM2) and loss of tumour suppressors (e.g. TP53, CDKN2A, CDKN2B)9,10,14.