TP53 and neoplasm: After a > 2-year follow-up, all lines, brca2+/+; tp53+/M214K, brca2+/Q658X; tp53+/M214K and brca2Q658X/Q658X; tp53+/M214K, had a tumor incidence of 80–100% and tp53 LOH was observed nearly universally in the brca2+/+; tp53+/M214K tumors while it was only observed in 30% of the brca2Q658X/Q658X; tp53+/M214K tumors, suggesting that brca2 homozygous mutants undergo other genetic changes that drive tumorigenesis (Shive et al., 2014).