TP53 and esophageal adenocarcinoma: Of particular biologic interest was the observation that patterns of TP53 mutation in esophageal adenocarcinomas were predominantly G:C to A:T transitions at CpG dinucleotides, suggesting that TP53 mutations result from endogenous mechanisms that likely involve spontaneous deamination into thymine of the 5′-methylated cytosine that frequently occurs at CpG di-nucleotides.