Colorectal cancer, also called colon cancer or rectal cancer, is cancer of the large intestine or bowel. Most cases start from polyps on the lining of the intestine. Polyps are small, mushroom-shaped growths, which most of the time are harmless. However, certain kinds, called adenomatous polyps, have the potential to become cancerous.
Colon cancer is among the most common types of cancer, with more than 104,000 new diagnoses each year. An additional 40,000 people are diagnosed annually with cancer of the rectum. Genetics plays a role: Up to 1 in 4 people with colon cancer have family members who have had the disease. Lifestyle is also a factor: People who aren't physically active and who eat a high-fat or low-fiber diet are at increased risk.
The good news is that there are reliable tests to screen for precancerous polyps, and when detected early, both colon cancer and rectal cancer have high cure rates. Compliance with these screening guidelines may prevent cancer from occurring in the first place.
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The colon and rectum are part of the digestive system, which takes the food you eat, removes the nutrients—including proteins, fats, carbohydrates, and vitamins—and eliminates the wastes. The key component of this system is the digestive tract, a 28-foot-long hollow tube that includes the mouth, esophagus, stomach, small intestine, large intestine, and anus.
The last 5 to 6 feet of the intestine form the colon or large intestine. This structure has six major divisions: cecum, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum. The last 5 or 6 inches of the large intestine make up the rectum.
Colorectal cancer generally begins as a polyp—a growth or a tumor that is not cancerous. Some stay benign, but others, known as adenomatous polyps or adenomas, may become cancerous if not removed. Nearly all colorectal cancer begins as one of these adenomas. (Growth is slow, so if detected as a benign polyp, colorectal cancer can be arrested before it begins.) Chronic inflammation, as found in inflammatory bowel diseases like ulcerative colitis and Crohn's disease, can also set the stage for colorectal cancer through a process known as dysplasia. Dysplasia involves changes within cells that may lead to cancer.
When a polyp becomes cancerous, it can, like all cancers, invade the surrounding tissues and spread malignant cells through the body via blood or lymph vessels.
People who have cancer, including women with uterine and ovarian cancers are at increased risk of colorectal cancer. Individuals who have been previously treated for colorectal cancer are at risk for recurrence.
Those with ulcerative colitis and Crohn's disease, among other inflammatory bowel diseases, are at increased risk of developing colorectal cancer.
Those with family members who have had colon cancer are at increased risk. Several genes are known to cause colon cancer, and there may be others not yet identified. Doctors say that a family has hereditary colorectal cancer when the exact gene causing the disease in that family has been pinpointed.
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Also known as Lynch syndrome or cancer family syndrome, HNPCC syndrome was first described over 100 years ago. It is the most common of the recognized inherited colorectal cancer syndromes and accounts for approximately 3 to 5 percent of all colon cancer cases. HNPCC is usually characterized by a predisposition to cancer in the third and fourth decades of life, although it is not unusual to have earlier or later onset. People with HNPCC have a 50 percent chance of passing the HNPCC gene to each of their children. Genetic counseling is recommended for families affected by HNPCC. Counselors are trained to explain the advantages and disadvantages of genetic testing.
"Nonpolyposis" means that colorectal cancer can occur when only a small number of polyps are present (or no polyps are present at all). In families with HNPCC, cancer usually occurs on the right side of the colon. Endometrial, ovarian, urinary tract, biliary tract, small intestine, and gastric cancers are seen more often in families with HNPCC than in the general population.
FAP is an inherited condition caused by a mutation on chromosome 5. It is characterized by the growth of hundreds or thousands of polyps—abnormal, mushroom-like growths—inside the colon and rectum (and occasionally the stomach and small intestine, too). Other names for this condition include familial polyposis and Gardner's syndrome. People with a mutation in the gene associated with FAP, known as APC, have a nearly 100 percent lifetime risk of developing colon cancer.
The polyps begin to appear during teen years and often become cancerous by age 40. They vary in size from less than one tenth of an inch to 1 to 2 inches. Indeed, some may be large enough to block part of the intestine. FAP may also be associated with benign tumors of the skin, soft connective tissue, and bones.
People with FAP have a 50 percent chance of passing the condition on to each of their children. The condition can be passed on even if the patient has had his or her own colon removed. Children of FAP sufferers who are lucky enough not to inherit the condition cannot pass it on to their own children. About one third of people with FAP do not have an affected parent but have a new or spontaneous mutation and can pass FAP on to their children. Genetic counseling is available and recommended for individuals with FAP and for their family members.
Some families are affected with attenuated FAP (AFAP). This is a mild form of FAP in which individuals develop fewer polyps at a later age than those with typical FAP. Although people with AFAP tend to develop colon cancer at a later age than individuals with typical FAP, they still have a near 100 percent lifetime risk of colon cancer. If AFAP is suspected within a family, it is important that family members be screened with colonoscopy rather than flexible sigmoidoscopy because polyps are not evenly distributed throughout the colon. The number of polyps and age of onset can vary greatly from one family member to another in a family with AFAP.
Regular screening is important because the symptoms of colon cancer may not occur until the disease is advanced. Examinations should begin by age 11 even in children who do not have symptoms. With FAP, abnormalities in other areas of the body may give early clues to its presence: bumps or lumps on the bones of the legs, arms, skull, and jaw; cysts of the skin; teeth that do not erupt when they should; and freckle-like spots on the inside lining of the eyes.
This genetic mutation is found primarily in people of Ashkenazi Jewish heritage (Jews of eastern European or Russian ancestry). Researchers believe that 6 percent of Ashkenazi Jews carry this gene mutation, which gives them an approximately 18 to 30 percent lifetime risk of developing colon cancer.
Both the APC I1307K mutation and mutations that cause FAP (familial adenomatous polyposis) occur in the APC (adenomatous polyposis coli) gene, a tumor-suppressing gene that fails to inhibit colon cancer's development when it is defective. The APC I1307K mutation is different from other APC mutations in that it does not directly cause colorectal cancer. Instead, this particular mutation creates an unstable spot in the gene that makes the gene more susceptible to additional genetic changes that may, in turn, lead to colorectal cancer.
Any person of Ashkenazi heritage who has a personal or family history of colorectal cancer or colorectal polyps may wish to consider genetic testing. A family history means having at least one close family member with colorectal cancer or polyps. Ashkenazi Jews without a family history of colorectal cancer may still wish to obtain genetic counseling to learn the value of gene testing in their own circumstances.
Ulcerative colitis and Crohn's disease are inflammatory conditions of the intestines. Both are known risk factors for colorectal cancer. A patient's risk of developing colorectal cancer is related to the duration of the disease.
Patients with either condition should undergo colonoscopic surveillance for epithelial dysplasia, a precursor to cancer, at routine intervals. Surveillance should be performed every one to two years in patients who have had either illness for eight to 10 years and annually in those who have been afflicted for more than 15 years.
Last reviewed on 7/22/09
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