TP53 and neoplasm: Esteller et al. (2000) first proposed this mechanism in colorectal cancer, and its basis was the over-representation of p14ARF hyper-methylation in tumours with wild-type p53, in comparison to tumours harbouring p53 mutations. Tumour type greatly influences the methylation profiles of tumour suppressor genes, and each tumour is designated with a distinct “DNA hypermethylome” (Estellar, 2005).