A Simple Outline of the Genetic Cross Talk and the Mutations in Colorectal Cancer That Could Be a Potential Cure in Future

 One of the leading non – communicable disease that has inflicted devastative effects on millions of lives can well be pointed into the direction of cancer and out of which, the frontier in line is the colorectal cancer (CRC) affecting both gender with women showing the higher mortality in comparison to men for the age group of 65 and above. There are multiple sources including both epigenetic as well genetic mutations that may divert normal metabolic pathway to the formation of colorectal carcinoma. This very short review underlines our current knowledge on the CRC pathogenesis through genetic level along with the summarization of the role of genetic and epigenetic changes in the origin and progression of the multiple CRC pathways. Indeed, our understanding of the effect of colorectal carcinoma through molecular level and its transition from colorectal adenoma to carcinoma can be segregated into three specific pathways: (1) microsatellite instability (MSI) which is linked to the loss of DNA mismatch repair activity; (2) chromosomal instability (CIN) that results from the imperfections in the chromosomal segregation, the telomere firmness, and the biochemical/ metabolic responses against DNA damage; and finally (3) the CpG island methylator phenotype (CIMP); i.e., the global genome hypermethylation which turns off the tumour suppressor genes.