Colon cancer is something that two people in my life have had and have also died from. They were completely different in every way. One of the people was a 24-year-old female that worked as a firefighter for two years at the time of her diagnosis. She had no family history of colon cancer and did not drink alcohol or use tobacco products. Her only symptom was unexpected weight loss. The other was a 50-year-old male with no family history of the disease but drank alcohol and smoked cigarettes regularly. He was diagnosed shortly after having his first routine colonoscopy. He was asymptomatic. They both died within two years after their diagnosis.

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Genetics: Alterations and Symptoms

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), Colon Cancer discussion

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).

References

Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, NY: McGraw-Hill Education.

Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.

Zhang, L., & Hagen, K. G. T. (2018). Pleiotropic effects of o-glycosylation in colon cancer. Journal of Biological Chemistry, 294(4), 1315–1316. https://doi-org.ezp.waldenulibrary.org/10.1074/jbc.H117.812826