Colorectal cancer is a malignant tumor arising from the inner wall of the large intestine.
Colorectal cancer is the third leading cause of cancer in males and fourth in females in the U.S.
Risk factors for colorectal cancer include heredity, colon polyps, and long-standing ulcerative colitis.
Most colorectal cancers develop from polyps. Removal of colon polyps can prevent colorectal cancer.
Colon polyps and early cancer can have no symptoms. Therefore regular screening is important.
Diagnosis of colorectal cancer can be made by barium enema or by colonoscopy with biopsy confirmation of cancer tissue.
Treatment of colorectal cancer depends on the location, size, and extent of cancer spread, as well as the health of the patient.
Surgery is the most common treatment for colorectal cancer.
Chemotherapy can extend life and improve quality of life for those living with colorectal cancer.
What is cancer?
Every day within our bodies, a massive process of destruction and repair occurs. The human body is comprised of about fifteen trillion cells, and every day billions of cells wear out or are destroyed. In most cases, each time a cell is destroyed the body makes a new cell to replace it, trying to make a cell that is a perfect copy of the cell that was destroyed because the replacement cell must be capable of performing the same function as the destroyed cell. During the complex process of replacing cells, many errors occur. Despite remarkably elegant systems in place to prevent errors , the body still makes tens of thousands of mistakes daily while replacing cells either because of random errors or because there are outside pressures placed on the replacement process that promote errors. Most of these mistakes are corrected by additional elegant systems or the mistake leads to the death of the newly made cell, and another normal new cell is produced. Sometimes a mistake is made, however, and is not corrected. Many of the uncorrected mistakes have little effect on health, but if the mistake allows the newly made cell to divide independent of the checks and balances that control normal cell growth, that cell can begin to multiply in an uncontrolled manner. When this happens a tumor (essentially a mass of abnormal cells) can develop.
Tumors fall into two categories; there are benign tumors and malignant (cancerous) tumors. So what is the difference? The answer is that a benign tumor grows only in the tissue from which it arises. Benign tumors sometimes can grow quite large or rapidly and cause severe symptoms, even death, although most do not. For example, a fibroid tumor in a woman's uterus can cause bleeding or pain, but it will never travel outside the uterus and grow as a new tumor elsewhere. Fibroids, like all benign tumors, lack the capacity to shed cells into the blood and lymphatic system, so they are unable to travel to other places in the body and grow. A cancer, on the other hand, can shed cells that can float like dandelion seeds in the wind through the blood or lymphatic system, landing in tissues distant from the primary tumor and growing into new tumors in these distant tissues. This process of spreading to distant tissues, called metastasis, is the defining characteristic of a cancerous tumor.
Cancer often is referred to as a single entity, but in fact, it is a group of more than 100 different diseases, much like infectious diseases. Cancers are named by the tissues from which the first tumor arises. Hence, a lung cancer that travels to the liver is not a liver cancer but is described as lung cancer metastatic to the liver, and a breast cancer that spreads to the brain is not described as a brain tumor but rather as breast cancer metastatic to the brain. Each cancer is a different disease with different treatment options and varying prognoses (likely outcomes). In fact, each individual with cancer has a unique disease, and the relative success or lack thereof of treatment among patients with the same diagnosis may be very different. As a result, it is important to treat each person with a diagnosis of cancer as an individual regardless of the type of cancer.
What is cancer of the colon and rectum?
Picture of colon (colorectal) cancer.
The colon and the rectum are the final portions of the tube that extends from the mouth to the anus. Food enters the mouth where it is chewed and then swallowed. It then travels through the esophagus and into the stomach. In the stomach, the food is ground into smaller particles and then enters the small intestine in a carefully controlled manner. In the small intestine, final digestion of food and absorption of the nutrients contained in the food occurs. The food that is not digested and absorbed enters the large intestine or colon and finally the rectum. The large intestine is about six feet long and acts primarily as a storage facility for waste; however, additional water, salts, and some vitamins are further removed. In addition, some of the undigested food, for example, fiber, is digested by colonic bacteria and some of the products of digestion are absorbed from the colon and into the body. (It is estimated that 10% of the energy derived from food comes from these products of bacterial digestion in the colon.) The remaining undigested food, dying cells from the lining of the intestines, and large numbers of bacteria are stored in the colon and then periodically passed into the rectum. Their arrival into the rectum initiates a bowel movement that empties the colonic contents from the body as stool.
Most of the large intestine rests inside a cavity in the abdomen called the peritoneal cavity. Parts of the colon are able to move quite freely within the peritoneal cavity as the undigested food is passing through it. As the colon heads towards the rectum, it becomes fixed to the tissues behind the peritoneal cavity, an area called the retroperitoneum. The end portion of the large intestine, the part that resides in the retroperitoneum, is the rectum. Unlike much of the rest of the colon, the rectum is fixed in place by the tissues that surround it. Because of its location, treatment for rectal cancer often is different than treatment for cancer of the rest of the colon, as we'll explain later.
Picture of colon cross section.
Although the large intestine is a tube, it is structurally a complicated tube, more like a steel belted radial tire than a garden hose. The tube is comprised of four layers. The first is an inner layer of cells that line the cavity through which the undigested food travels, called the mucosa. The mucosa is attached to a thin second layer, the submucosa, that is attached itself to a layer of muscle, the muscularis. The entire tube is surrounded by fibrous (scar-like) tissue called the serosa. The most common cancers of the large intestine (the type called adenocarcinoma) arise from the mucosa, the inner layer of cells. These cells are exposed to toxins from food and bacteria as well as mechanical wear and tear and are constantly dying off and being replaced. Mistakes (usually a series of mistakes involving genes within the replacement cells) lead to abnormal cells and uncontrolled proliferation of the abnormal cells that give rise to cancer.
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.
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 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. Hereditary colon cancer syndromes are disorders where affected family members have inherited cancer-causing genetic defects from one or both parents. In only 5% of colon cancers due to hereditary, however, have the exact chromosomal abnormalities been identified.
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.
Cancers of the colon and rectum (colorectal cancer) start when the process of the normal replacement of lining cells goes awry. Mistakes in mucosal cell division occur frequently. For reasons that are poorly understood, sometimes mistakes occur that escape our editing systems. When this occurs, these cells begin to divide independently of the normal checks and balances that control growth. As these abnormal cells grow and divide, they can lead to growths within the colon called polyps. Polyps vary in type, but many are precancerous tumors that grow slowly over the course of years and do not spread. As polyps grow, additional genetic mutations further destabilize the cells and can make the cells more bizarre. When these precancerous tumors change direction (growing through the tube rather than into the middle of it) and invade other layers of the large intestine (such as the submucosa or muscular layer), the precancerous polyp has become cancerous. In most cases this process is slow, taking at least 8 to 10 years to develop from those early aberrant cells to a frank cancer.
Once a colorectal cancer forms, it begins to grow in two ways. First, the cancer can grow locally and extend through the wall of the intestine and invade adjacent structures, making the mass (called the primary tumor) more of a problem and harder to remove. Local extension can cause additional symptoms such as pain or fullness, or cause blockages of the colon or nearby structures. Second, as the cancer grows it begins the process of metastasis, shedding thousands of cells a day into the blood and lymphatic system that can cause cancers to form in distant locations. Colorectal cancers most commonly spread first to local lymph nodes before traveling to distant organs. Once local lymph nodes are involved, spread to the liver, the abdominal cavity, and the lung are the next most common destinations of metastatic spread.
What are the symptoms of colon cancer?
Symptoms of colorectal cancer are numerous and nonspecific. They include fatigue, weakness, shortness of breath, change in bowel habits, narrow stools, diarrhea or constipation, red or dark blood in stool, weight loss, abdominal pain, cramps, or bloating. Other conditions such as irritable bowel syndrome (spastic colon), ulcerative colitis, Crohn's disease, diverticulosis, and peptic ulcer disease can have symptoms that mimic colorectal cancer. For more information on these conditions, please read the following articles: Irritable Bowel Syndrome, Ulcerative Colitis, Crohn's Disease, Diverticulosis, and Peptic Ulcer Disease.
Colorectal cancer can be present for several years before symptoms develop. Symptoms vary according to where in the large intestine the tumor is located. The right colon is spacious, and cancers of the right colon can grow to large sizes before they cause any abdominal symptoms. Typically, right-sided cancers cause iron deficiency anemia due to the slow loss of blood over a long period of time. Iron deficiency anemia causes fatigue, weakness, and shortness of breath. The left colon is narrower than the right colon. Therefore, cancers of the left colon are more likely to cause partial or complete bowel obstruction. Cancers causing partial bowel obstruction can cause symptoms of constipation, narrowed stool, diarrhea, abdominal pains, cramps, and bloating. Bright red blood in the stool may also indicate a growth near the end of the left colon or rectum.
How can colon cancer be prevented?
The most effective prevention for colorectal cancer is early detection and removal of precancerous colorectal polyps before they turn cancerous. Even in cases where cancer has already developed, early detection still significantly improves the chances of a cure by surgically removing the cancer before the disease spreads to other organs. Multiple world health organizations have suggested general screening guidelines. For more specific recommendations, please contact the American Cancer Society at www.cancer.org.
Digital rectal examination and stool occult blood testing
It is recommended that all individuals over the age of 40 have yearly digital examinations of the rectum and their stool tested for hidden or "occult" blood. During digital examination of the rectum, the doctor inserts a gloved finger into the rectum to feel for abnormal growths. Stool samples can be obtained to test for occult blood (see below). The prostate gland can be examined at the same time for evidence of prostate cancer.
An important screening test for colorectal cancers and polyps is the stool occult blood test. Tumors of the colon and rectum tend to bleed slowly into the stool. The small amount of blood mixed into the stool usually is not visible to the naked eye. The commonly used stool occult blood tests rely on chemical color conversions to detect microscopic amounts of blood. These tests are both convenient and inexpensive. A small amount of stool is smeared on a special card for occult blood testing. Usually, three consecutive stool cards are collected. A person who tests positive for stool occult blood has a 30% to 45% chance of having a colon polyp and a 3% to 5% chance of having a colon cancer. Colon cancers found under these circumstances tend to be small and not to have spread and have a better long-term prognosis.
It is important to remember that having stool tested positive for occult blood does not necessarily mean a person has colon cancer. Many other conditions can cause occult blood in the stool. However, patients with a positive stool occult blood test should undergo further evaluations involving barium enema X-rays, colonoscopies, and other tests to exclude colon cancer and to explain the source of the bleeding. It is also important to realize that stool which has tested negative for occult blood does not mean that colorectal cancer or polyps do not exist. Even under ideal testing conditions, at least 20% of colon cancers can be missed by stool occult blood screening. Many patients with colon polyps do not have positive stool occult blood. In patients suspected of having colon tumors and in those at higher risk for developing colorectal polyps and cancer, screening flexible sigmoidoscopies or colonoscopies are performed even if the stool occult blood tests are negative.
Flexible sigmoidoscopy and colonoscopy
Beginning at age 50, a flexible sigmoidoscopy screening test is recommended every 3 to 5 years. Flexible sigmoidoscopy is an exam of the rectum and the lower colon using a viewing tube (a short version of colonoscopy). Recent studies have shown that the use of screening flexible sigmoidoscopy can reduce mortality from colon cancer. This is a result of the detection of polyps or early cancers in people with no symptoms. If a polyp or cancer is found, a complete colonoscopy is recommended. The majority of colon polyps can be completely removed at the time of colonoscopy without surgery. Recommendations now are that screening colonoscopies instead of screening flexible sigmoidoscopies should be done for healthy individuals starting at ages 50 to 55. Please read the Colon Cancer Screening article.
Patients with a high risk of developing colorectal cancer may undergo screening colonoscopies starting at earlier ages than 50. For example, patients with family history of colon cancer are recommended to start screening colonoscopies at an age 10 years before the earliest colon cancer diagnosed in a first-degree relative or 5 years earlier than the earliest precancerous colon polyp discovered in a first-degree relative. Patients with hereditary colon cancer syndromes such as FAP, AFAP, HNPCC, and MYH are recommended to begin colonoscopies early. The recommendations differ depending on the genetic defect. For example, in FAP colonoscopies may begin during teenage years to look for the development of colon polyps. Patients with a prior history of polyps or colon cancer may also undergo colonoscopies to exclude recurrence. Patients with a long history (greater than 10 years) of chronic ulcerative colitis have an increased risk of colon cancer, and should have regular colonoscopies to look for precancerous changes in the colon lining.
Genetic counseling and testing
Blood tests are now available to test for FAP, AFAP, MYH, and HNPCC hereditary colon cancer syndromes. Families with multiple members having colon cancers, multiple colon polyps, cancers at young ages, and other cancers such as cancers of the ureters, uterus, duodenum, and more, should be referred for genetic counseling, followed possibly by genetic testing. Genetic testing without prior counseling is discouraged because of the extensive family education that is involved and the complicated nature of interpreting the test results.
The advantages of genetic counseling followed by genetic testing include: (1) identifying family members at high risk of developing colon cancer to begin colonoscopies early; (2) identifying high-risk members so that screening may begin to prevent other cancers such as ultrasound tests for uterine cancer, urine examinations for ureter cancer, and upper endoscopies for stomach and duodenal cancers; and (3) alleviating concern for members who test negative for the hereditary genetic defects.
Diet and colon cancer to prevent colon cancer
People can change their eating habits by reducing fat intake and increasing fiber (roughage) in their diet. Major sources of fat are meat, eggs, dairy products, salad dressings, and oils used in cooking. Fiber is the insoluble, nondigestible part of plant material present in fruits, vegetables, and whole-grain breads and cereals. It is postulated that high fiber in the diet leads to the creation of bulky stools which can rid the intestines of potential carcinogens. In addition, fiber leads to the more rapid transit of fecal material through the intestine, thus allowing less time for a potential carcinogen to react with the intestinal lining.