When comparing cancer to dysplastic tissue, there were fewer significantly over-expressed genes, but these also included genes involved in extra-cellular matrix remodelling (COL1A1, COL1A2, CEACAM6, ACTA2) and carcinogenesis (MYC, CTNNB1, CCND1), indicating a progression of cellular remodelling from normal through dysplastic to cancer tissue (Figure 4B). This evidence concerns the gene ACTA2 and cancer.