Colon cancer – signs , symptoms, causes and other risk factors

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Colon cancer

The colon cancer is a cancer of the colon (large intestine) which is the final part of our digestive tract. There are many cases when the colon cancer is beginning as small, benign (noncancerous) clumps of cells called adenomatous polyps. As the time passes, some of these polyps can become colon cancers. These polyps can be small and they can produce few, if any, symptoms. This is a reason why doctors are recommending regular screening tests to help prevent the colon cancer by identifying and removing polyps before they turn into cancer.

Colon cancer signs and symptoms

Here are signs and symptoms of the colon cancer:

  • Unexplained weight loss
  • Weakness or fatigue
  • A feeling that your bowel does not empty completely
  • Persistent abdominal discomfort, such as pain, gas or cramps
  • Rectal bleeding or blood in your stool
  • You have a change in your bowel habits, in which are included diarrhea or constipation or a change in a consistency of your stool, that lasts longer than 4 weeks. [1]

There are many people who suffer from colon cancer and they experience no symptoms in the early stages of this disease. When their symptoms appear, they can vary which is depending on the cancer’s size and location in your large intestine. If you have noticed notices some symptoms of colon cancer such as an ongoing change in bowel habits or blood in your stool, then you should not hesitate to talk with your doctor. [2]

Colon cancer

Colon cancer causes

There are many cases when the cause for colon cancer is not known. Doctors are saying that this type of cancer is happening when the healthy cells in the colon develop errors in their genetic blueprint, the DNA. It is known that healthy cells grow and divide in an orderly way to keep your body functioning normally. When the cell’s DNA is damaged and it becomes cancerous, then cells continue to divide, even when the body does not need new cells. [3] As these cells accumulate, they are forming a tumor. As the time passes, the cancer cells can grow to invade and destroy the normal tissue nearby. The cancerous cells can travel to other parts of your body to form deposits there (this is known as metastasis).

  • Inherited gene mutations that increase the risk of colon cancer: It is known that inherited gene mutations are increasing the risk of colon cancer to be passed through families. There are some studies in which are said that inherited genes are linked to only a small percentage of colon cancer. The inherited gene mutations do not make the cancer inevitable but they are increasing the risk of individual to get colon cancer. [4] Here are the most common forms of inherited colon cancer syndromes:
  • HNPCC (heredity nonpolyposis colorectal cancer): This form of colon cancer is also known as Lynch syndrome. It is known fact that the HNPCC is increasing the risk of colon cancer and other cancers. Those people who have HNPCC tend to develop colon cancer before age 50. [5]
  • FAP (familial adenomatous polyposis): This is a rare disorder which is causing you to develop thousands of polyps in the lining of the colon and rectum. Those people who have FAP have an increased risk of developing colon cancer before age 40. [6]

Genetic testing can detect FAP and HNPCC. If you have some family member who suffers from colon cancer, then talk with your doctor about the risk of getting colon cancer.

  • Association between diet and increased colon cancer risk: There are some studies of large groups of people in which are shown association between a typical Western diet and an increased risk of colon cancer. We know that a typical Western diet is low in fiber and high in fat.[7] It is known fact that when people who move from areas where the typical diet is high in fiber and low in fat to areas where the typical Western diet is most common, then their risk of getting colon cancer is increasing significantly. It is not clear why this happening is but scientists are studying whether a high – fat and low – fiber diet is affecting the microbes which live in the colon or they cause underlying inflammation which may contribute to cancer risk. It is an area of active investigation and studies are ongoing. [8]

REFERENCED ARTICLES:

[1] Sun, V., Borneman, T., Koczywas, M., Cristea, M., Piper, B. F., Uman, G., & Ferrell, B. (2012). Quality of life and barriers to symptom management in colon cancer. European Journal of Oncology Nursing, 16(3), 276–280. doi:10.1016/j.ejon.2011.06.011

[2] Kishiki, T., Kuchta, K., Matsuoka, H., Kojima, K., Asou, N., Beniya, A., … Masaki, T. (2018). The impact of tumor location on the biological and oncological differences of colon cancer: multi-institutional propensity score-matched study. The American Journal of Surgery. doi:10.1016/j.amjsurg.2018.07.005

[3] Potter, J. D., Slattery, M. L., Bostick, R. M., & Gapstur, S. M. (1993). Colon Cancer: A Review of the Epidemiology. Epidemiologic Reviews, 15(2), 499–545. doi:10.1093/oxfordjournals.epirev.a036132

[4] Rustgi, A. K. (2007). The genetics of hereditary colon cancer. Genes & development21(20), 2525-2538.

[5] Lee, W.-S., Seo, G., Shin, H. J., Yun, S. H., Yun, H., Choi, N., … Lee, W. Y. (2008). Identification of Differentially Expressed Genes in Microsatellite Stable HNPCC and Sporadic Colon Cancer. Journal of Surgical Research, 144(1), 29–35. doi:10.1016/j.jss.2007.02.005

[6] Singh, A., Steinhagen, E., & Katona, B. W. (2018). Approach to Upper Gastrointestinal Tract Lesions in Familial Adenomatous Polyposis. Seminars in Colon and Rectal Surgery. doi:10.1053/j.scrs.2018.06.003

[7] Tarasiuk, A., Mosińska, P., & Fichna, J. (2018). The mechanisms linking obesity to colon cancer: An overview. Obesity Research & Clinical Practice, 12(3), 251–259. doi:10.1016/j.orcp.2018.01.005

[8] O’Neill, A. M., Burrington, C. M., Gillaspie, E. A., Lynch, D. T., Horsman, M. J., & Greene, M. W. (2016). High-fat Western diet–induced obesity contributes to increased tumor growth in mouse models of human colon cancer. Nutrition Research, 36(12), 1325–1334. doi:10.1016/j.nutres.2016.10.005

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