Pathogenesis of colorectal cancer
Colorectal cancer is commonly an adenocarcinoma affecting the viscera, which initially starts as a benign polyp and may become malignant, invading and causing destruction on normal tissues of the colon or rectum in the gastrointestinal tract and after that destroying the adjacent and surrounding tissues and cells. The cancerous cells may travel from the primary tumour to other body parts such as the liver, lungs, and peritoneum. Common in people experiencing inflammatory bowel disease. According to (Rosa, 2015), cancer commonly originates from mutation of the Wnt signalling pathway, which precipitates the signalling activity, which could be an inherited or acquired process. When the colorectal adenocarcinoma develops, the GIT’s epithelial cells develop sequential genetic mutation on specified oncogenes and the tumour suppressor genes, which results in proliferation of the mucosal epithelium that develops as a benign adenoma and eventually becomes a carcinoma. APC mutation/ Beta-catenin mechanism suggests that there is loss of tumour suppressor adenomatous polyposis coli which is related to the beta-catenin leading to the translocation of the beta-catenin to the nucleus of the cell resulting in transcription of other proto-oncogenes such as the MYC and cyclin D leading to uncontrolled proliferation of cells. There is also point mutation of K-RAS gene that results from the loss of APC gene, deletion of DCC gene on chromosome 18…………………………………………………………….