Colorectal cancer (CRC) progresses from precursor lesions or polyps via two main pathways – the traditional and serrated pathway. The traditional pathway is the conventional type, while the serrated neoplastic pathway has been recently identified and is not well characterised. The aim of this study was to evaluate molecular factors associated with the serrated pathway and study its progression from a serrated polyp to colorectal cancer using patient samples and mouse models. The first part of the study was to evaluate CIMP status of all the serrated polyp subtypes and its association with functionally important genes such as MLH1, p16 and IGFBP7 in patient samples. The mouse models were then utilized to assess the contribution of BRAF V600E mutation along with the cell cycle regulators and tumour suppressor genes, p16Ink4a and p19Arf in the initiation and progression of CRC. The CIMP study was a prospective study in which the real-time based MethyLight assay was employed to evaluate CIMP and methylation status of p16, IGFBP7 and MLH1 in 154 serrated polyps and 63 adenomas. Samples were subjected to bisulfite modification and methylation levels were assessed using the Weisenberger et al panel of methylation markers (IGF2, SOCS1, NEUROG1, RUNX3 and CACNA1G) with ALU as the reference gene.