Genetics can play a role in having colon cancer because “hereditary nonpolyposis colorectal cancer is the methylation of a gene whose protein product repairs damaged DNA” (Huether & McCance, 2017, p. 52). The damaged DNA leads to the presence of tumors in the colon (Huether & McCance, 2017). Certain behaviors can alter a patient’s DNA over time like continuous predisposal to alcohol and tobacco products, along with many other risk factors (Huether & McCane, 2017). Someone that has ulcerative colitis is also more likely to acquire colon cancer (Huether & McCane, 2017).
Symptoms of colon cancer include weight loss, diarrhea, gastrointestinal bleeding, fever, abdominal pain, bowel obstructions, and/or bowel perforation (Hammer & McPhee, 2019). Patients can have all these symptoms or few (Hammer & McPhee, 2019).
Pathophysiology of the Disease and Cellular Function
When a patient acquires colon cancer many mutations in the DNA begin to accumulate, altering colon cells (Huether & McCane, 2017). The first mutation that begins to take place is when the Adenomatous polyposis coli (APC) gene is changed (Hammer & McPhee, 2019). This gene suppresses tumors and is present in the colon of those with mutation-free DNA (Huether & McCane, 2017). Protein glycosylation is altered when a tumor is formed (Zhang & Hagen, 2018). “O-linked glycosylation (GalNAc-T6) in the cellular transformations typically (is) seen in cancerous cells and tissues” (Zhang & Hagen, 2018, p. 1315). Zhang and Hagen performed a study where they discovered the O-linked protein was absent in cancer-free colons but was present in most colons infected with cancer (2018),
In a patient with colon cancer, somatic changes take place in the APC gene, and once polyps in the colon are formed, other pathways are alerted making the polyps begin to grow larger (Hammer & McPhee, 2019). The cell cycle allows cancer to progress because certain genes and apoptosis have been inactivated (Hammer & McPhee, 2019). In the normal cellular function of the colon, apoptosis kills off mutated DNA because it is not recognized, but with colon cancer, mutations multiply without any cell death (Hammer McPhee, 2019). Metastasis of colon cancer then takes place (Hammer & McPhee, 2019).