The causes of colon cancer

The causes of colon cancer

Colorectal cancer is not contagious (a person cannot catch the disease from a cancer patient). Some people are more likely to develop colorectal cancer than others. Factors that increase a person's risk of colorectal cancer include high fat intake, a family history of colorectal cancer and polyps, the presence of polyps in the large intestine, and chronic ulcerative colitis.

Diet and colon cancer 

Diets high in fat are believed to predispose humans to colorectal cancer. In countries with high colorectal cancer rates, the fat intake by the population is much higher than in countries with low cancer rates. It is believed that the breakdown products of fat metabolism lead to the formation of cancer-causing chemicals (carcinogens). Diets high in vegetables and high-fiber foods such as whole-grain breads and cereals may rid the bowel of these carcinogens and help reduce the risk of cancer. 

Colon polyps and colon cancer 

Doctors believe that most colon cancers develop in colon polyps. Therefore, removing benign colon polyps can prevent colorectal cancer. Colon polyps develop when chromosome damage occurs in cells of the inner lining of the colon. Chromosomes contain genetic information inherited from each parent. Normally, healthy chromosomes control the growth of cells in an orderly manner. When chromosomes are damaged, cell growth becomes uncontrolled, resulting in masses of extra tissue (polyps). Colon polyps are initially benign. Over years, benign colon polyps can acquire additional chromosome damage to become cancerous.

Ulcerative colitis and colon cancer 

Chronic ulcerative colitis causes inflammation of the inner lining of the colon. Colon cancer is a recognized complication of chronic ulcerative colitis. The risk for cancer begins to rise after eight to 10 years of colitis. The risk of developing colon cancer in a patient with ulcerative colitis also is related to the location and the extent of his or her disease.

Current estimates of the cumulative incidence of colon cancer associated with ulcerative colitis are 2.5% at 10 years, 7.6% at 30 years, and 10.8% at 50 years. Patients at higher risk of cancer are those with a family history of colon cancer, a long duration of colitis, extensive colon involvement, and those with primary sclerosing cholangitis (PSC).

Since the cancers associated with ulcerative colitis have a more favorable outcome when caught at an earlier stage, yearly examinations of the colon often are recommended after eight years of known extensive disease. During these examinations, samples of tissue (biopsies) can be taken to search for precancerous changes in the lining cells of the colon. When precancerous changes are found, removal of the colon may be necessary to prevent colon cancer.

Genetics and colon cancer

A person's genetic background is an important factor in colon cancer risk. Among first-degree relatives of colon cancer patients, the lifetime risk of developing colon cancer is 18% (a threefold increase over the general population in the United States).

Even though family history of colon cancer is an important risk factor, majority (80%) of colon cancers occur sporadically in patients with no family history of colon cancer. Approximately 20% of cancers are associated with a family history of colon cancer. And 5 % of colon cancers are due to hereditary colon cancer syndromes. Hereditary colon caner syndromes are disorders where affected family members have inherited cancer-causing genetic defects from one or both of the parents.

Chromosomes contain genetic information, and chromosome damages cause genetic defects that lead to the formation of colon polyps and later colon cancer. In sporadic polyps and cancers (polyps and cancers that develop in the absence of family history), the chromosome damages are acquired (develop in a cell during adult life). The damaged chromosomes can only be found in the polyps and the cancers that develop from that cell. But in hereditary colon cancer syndromes, the chromosome defects are inherited at birth and are present in every cell in the body. Patients who have inherited the hereditary colon cancer syndrome genes are at risk of developing large number of colon polyps, usually at young ages, and are at very high risk of developing colon cancer early in life, and also are at risk of developing cancers in other organs.

FAP (familial adenomatous polyposis) is a hereditary colon cancer syndrome where the affected family members will develop countless numbers (hundreds, sometimes thousands) of colon polyps starting during the teens. Unless the condition is detected and treated (treatment involves removal of the colon) early, a person affected by familial polyposis syndrome is almost sure to develop colon cancer from these polyps. Cancers usually develop in the 40s. These patients are also at risk of developing other cancers such as cancers in the thyroid gland, stomach, and the ampulla (the part where the bile ducts drain into the duodenum just beyond the stomach).

AFAP (attenuated familial adenomatous polyposis) is a milder version of FAP. Affected members develop less than 100 colon polyps. Nevertheless, they are still at very high risk of developing colon cancers at young ages. They are also at risk of having gastric polyps and duodenal polyps.

HNPCC (hereditary nonpolyposis colon cancer) is a hereditary colon cancer syndrome where affected family members can develop colon polyps and cancers, usually in the right colon, in their 30s to 40s. Certain HNPCC patients are also at risk of developing uterine cancer, stomach cancer, ovarian cancer, and cancers of the ureters (the tubes that connect the kidneys to the bladder), and the biliary tract (the ducts that drain bile from the liver to the intestines).

MYH polyposis syndrome is a recently discovered hereditary colon cancer syndrome. Affected members typically develop 10-100 polyps occurring at around 40 years of age, and are at high risk of developing colon cancer.