Colon Cancer (cont.)
Francis W. Nugent, MD
Francis W. Nugent, MD
Dr. F.W. Nugent is a medical oncologist specializing in gastrointestinal cancers with a special interest in pancreatic cancer. Dr. Nugent graduated from Middlebury College with a bachelors degree in religion before graduating from Albany Medical College. He presently serves as vice-chairman of medical oncology at the Lahey Clinic in Burlington, Massachusetts.
In this Article
What are the causes of colon cancer?
Doctors are certain that 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 inflammatory bowel diseases, primarily chronic ulcerative colitis.
Diet and colorectal cancer
Diets high in fat are believed to predispose people 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 digestion of fat that occurs in the small intestine and the colon leads to the formation of cancer-causing chemicals (carcinogens). Diets high in vegetables and high-fiber foods such as whole-grain breads and cereals contain less fat that produces these carcinogens and may counter the effects of the carcinogens. Both effects would help reduce the risk of cancer.
Colon polyps and colorectal cancer
Doctors believe that most colorectal cancers develop in colorectal polyps. Therefore, removing benign (but precancerous) colorectal polyps can prevent colorectal cancer. Precancerous colorectal polyps develop when chromosomal damage occurs in cells of the inner lining of the colon. The damage produces abnormal cells, but the cells have not yet developed the ability to spread, the hallmark of cancer. Instead, the growing tissue remains localized within the polyp. When chromosomal damage increases further within the polyp, cell growth becomes uncontrolled, and the cells begin to spread, that is, they become cancer. Thus, colon polyps which are initially benign acquire additional chromosome damage to become cancerous.
Ulcerative colitis and colorectal cancer
Chronic ulcerative colitis causes inflammation of the inner lining of the colon. For further information, please read the Ulcerative Colitis article. Colon cancer is a recognized complication of chronic ulcerative colitis. The risk for cancer begins to increase after 8 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.
Patients at higher risk of cancer are those with a family history of colon cancer, a long duration of colitis, extensive colon involvement with colitis, and those with an associated liver disease, sclerosing cholangitis.
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 8 years of known extensive disease. During these examinations, samples of tissue (biopsies) are taken to search for precancerous changes in the cells lining the colon. When precancerous changes are found, removal of the colon may be necessary to prevent colon cancer.
Genetics and colorectal 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 a family history of colon cancer is an important risk factor, a 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.
Chromosomes contain genetic information, and chromosomal damage causes 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 chromosomal 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 colon polyps, usually at young ages, and are at very high risk of developing colon cancer early in life; they also are at risk of developing cancers in other organs.
Familial adenomatous polyposis (FAP) is one hereditary colorectal cancer syndrome where the affected family members will develop countless numbers (hundreds, sometimes thousands) of colon polyps starting during their teens. Unless the condition is detected and treated early (treatment involves removal of the colon), a person affected by FAP is almost sure to develop colon cancer from these polyps. Cancers almost certainly develop by the time a person is in their 40s. These patients are also at risk of developing other cancers such as cancers in the thyroid gland, stomach, and the ampulla (part of the bile duct that drains into the small intestine from the liver) as well as benign tumors called desmoid tumors. FAP arises from a mutation in a specific gene called the APC gene. The specific mutation can be identified in most people with appropriate testing, and such testing is recommended for individuals diagnosed with FAP as well as their family members.
Attenuated familial adenomatous polyposis (AFAP) is a milder version of FAP. Affected members develop fewer than 100 colon polyps. Nevertheless, they are still at very high risk of developing colon cancers at a young age. They are also at risk of having gastric polyps and duodenal polyps.
Hereditary nonpolyposis colon cancer (also known as Lynch Syndrome or HNPCC) is a hereditary colorectal cancer syndrome where affected family members can develop colon polyps and cancers, usually in the right colon, in their 30s to 40s. Patients with HNPCC 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 bile ducts. Ironically, it appears that while colon cancer occurs more frequently in patients with HNPCC, these cancers may be more easily cured than "sporadic" colon cancers. The specific genetic abnormalities associated with HNPCC have been identified, and patients and family members can be tested to determine if HNPCC is present and if family members carry the abnormality and are likely to develop cancer.
MYH polyposis syndrome is a recently discovered hereditary colorectal cancer syndrome. Affected members typically develop 10 to 100 polyps occurring at around 40 years of age and are at high risk of developing colon cancer. Here, too, the genetic abnormality has been identified.
As time goes by, it is likely that additional hereditary syndromes leading to colon cancer will be identified. Nevertheless, it is important to remember that the overwhelming majority of colorectal cancers do not have a single, identifiable chromosomal abnormality that can be looked for in relatives in order to identify individuals at risk for colorectal cancer.
Medically Reviewed by a Doctor on 10/8/2014
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