S100A10 and neoplasm: Direct analysis of expression in tumours was not possible, as RNA was not available for the majority of the cohort; however, the hypermethylation of S100A10 observed in primary tumours is of a comparable level to that seen in the cell lines, consistent with its epigenetic transcriptional inactivation and candidate tumour suppressor role in disease pathogenesis (Figures 2A, D and 3).