TOPIC COLON CANCER CHAPTER I INTRODUCTION 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. ometimes 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.

!hen 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. o what is the difference% The answer

is that a benign tumor grows only in the tissue from which it arises. &enign tumors sometimes can grow 'uite large or rapidly and cause severe symptoms, even death, although most do not. (or 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. (ibroids, 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. * 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. +ancer often is referred to as a single entity, but in fact, it is a group of more than ,-- different diseases, much like infectious diseases. +ancers are named by the tissues from which the first tumor arises. .ence, 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 uni'ue disease, and the relative success or lack thereof of treatment among patients with the same diagnosis may be very different. *s a result, it is important to treat each person with a diagnosis of cancer as an individual regardless of the type of cancer. SIGNIFICANCE OF THE STUDY The study is signifiant due to the understanding of colon cancer. This will provide us information about colon cancer and how to prevent it. STATEMENT OF THE PROBLEM !hat are the causes of colon cancer% !hat is the Diet and colorectal cancer !hat are the +olon polyps and colorectal cancer% !hat is /lcerative colitis and colorectal cancer% !hat is 0enetics and colorectal cancer%

CHAPTER II FACTS OF THE STUDY What are the causes of co o! ca!cer% Doctors are certain that colorectal cancer is not contagious "a person cannot catch the disease from a cancer patient#. ome people

are more likely to develop colorectal cancer than others. (actors 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. D"et a!# co orecta ca!cer 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 cancer1causing chemicals "carcinogens#. Diets high in vegetables and high1fiber foods such as whole1grain breads and cereals contain less fat that produces these carcinogens and may counter the effects of the carcinogens. &oth effects would help reduce the risk of cancer. What are the Co o! $o %$s a!# co orecta ca!cer&

Doctors believe that most colorectal cancers develop in colorectal polyps. Therefore, removing benign "but precancerous# colorectal polyps can prevent colorectal cancer. 2recancerous 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 locali3ed within the polyp. !hen 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 ac'uire additional chromosome damage to become cancerous. What "s U cerat"'e co "t"s a!# co orecta ca!cer& +hronic ulcerative colitis causes inflammation of the inner lining of the colon. (or further information, please read the /lcerative +olitis article. +olon cancer is a recogni3ed complication of chronic ulcerative colitis. The risk for cancer begins to increase after 4 to ,- 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. +urrent estimates of the cumulative incidence of colon cancer associated with ulcerative colitis are 5.67 at ,- years, 8.97 at :years, and ,-.47 at 6- years. 2atients 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. ince 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 4 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. !hen precancerous changes are found, removal of the colon may be necessary to prevent colon cancer. What "s Ge!et"cs a!# co orecta ca!cer& * person)s genetic background is an important factor in colon cancer risk. *mong first1degree relatives of colon cancer patients, the lifetime risk of developing colon cancer is ,47 "a threefold increase over the general population in the /nited tates#.

Even though a family history of colon cancer is an important risk factor, a ma;ority "4-7# of colon cancers occur sporadically in patients with no family history of colon cancer. *pproximately 5-7 of cancers are associated with a family history of colon cancer. .ereditary colon cancer syndromes are disorders where affected family members have inherited cancer1causing genetic defects from one or both parents. In

only 67 of colon cancers due to hereditary, however, have the exact chromosomal abnormalities been identified. +hromosomes 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 ac'uired "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. &ut in hereditary colon cancer syndromes, the chromosomal defects are inherited at birth and are present in every cell in the body. 2atients 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.

(amilial

adenomatous

polyposis

"(*2#

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. /nless the condition is detected and treated early "treatment involves removal of the colon#, a person affected by (*2 is almost sure to develop colon cancer from these

polyps. +ancers almost certainly develop by the time a person is in their <-s. 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. (*2 arises from a mutation in a specific gene called the *2+ gene. The specific mutation can be identified in most people with appropriate testing, and such testing is recommended for individuals diagnosed with (*2 as well as their family members.

*ttenuated familial adenomatous polyposis "*(*2# is a milder version of (*2. *ffected members develop fewer than ,-- colon polyps. =evertheless, 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.

.ereditary nonpolyposis colon cancer "also known as >ynch yndrome or .=2++# is a hereditary colorectal cancer syndrome where affected family members can develop colon polyps and cancers, usually in the right colon, in their :-s to <-s. 2atients with .=2++ 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 fre'uently in patients with .=2++, these cancers may be more easily cured than ?sporadic? colon cancers. The specific genetic abnormalities associated with .=2++ have been identified, and patients and family members can be tested to determine if .=2++ is present and if family members carry the abnormality and are likely to develop cancer.

M@. polyposis syndrome is a recently discovered hereditary colorectal cancer syndrome. *ffected members typically develop ,- to ,-- polyps occurring at around <- years of age and are at high risk of developing colon cancer. .ere, too, the genetic abnormality has been identified.

*s time goes by, it is likely that additional hereditary syndromes leading to colon cancer will be identified. =evertheless, it is important to remember that the overwhelming ma;ority 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.

CHAPTER III SUMMARY There is no one magic dietary bullet, no one simple step to take. It is very difficult for scientists to tease out an isolated lifestyle or dietary factor on any health 'uestion within a free living population. .owever, one thing is now rather clear. The western type of diet with large portions of animal meat, little fiber, low intake of vegetables, and possible low intake of vitamin D and calcium all seem to be ma;or factors. The amount of solid information percolating into the medical literature has reached a point where a reasonable balanced colon cancer and polyp prevention program can be outlined. *s hard as it is, control your weight. Averweight people have more colon cancer. Beduce red meat, saturated and trans1fats in the diet. Take ,5-- mg of calcium each day using milk or calcium carbonate supplements. Take vitamin D at least 4-- I/Cday. +heck with your physician. Eat cruciferous vegetables. Daily aspirin, but only if discussed with your physician. Daily multiple vitamin with ade'uate folate. =o smoking or excessive alcohol. ome experts say ,5-- I/Cday.

2rebiotics D eat these in food or take a dietary supplement, preferably ours "products#. +olon and rectal cancer develop in the digestive tract, which is also called the gastrointestinal, or 0I, tract. The digestive system processes food for energy and rids the body of solid waste matter "fecal matter or stool#. +olon cancer and rectal cancer have many features in common. colorectal cancer. Aver E67 of colorectal cancers are ad enocarcinomas. These are cancers of the glandular cells that line the inside of the colon and rectum. Ather, less common type of tumors may also develop in the colon and rectum. +arcinoid tumors develop from hormone1producing cells of the intestine. 0astrointestinal stromal tumors develop in the connective tissue and muscle layers in the wall of the colon and rectum. >ymphomas are cancers of immune system cells that typically develop in lymph nodes but may also start in the colon and rectum or other organs. +olorectal cancers are thought to develop slowly over a period of several years. &efore a true cancer develops, there usually are precancerous changes in the lining of the colon or rectum. These changes might be dysplasia or adenomatous polyps. * polyp is a growth of tissue into the center of the colon or rectum. ome types of ometimes they are referred to together as

polyps

"hyperplastic

polyps

and

inflammatory

polyps#

are

not

precancerous. .owever, having adenomatous polyps, also known as adenomas, does increase a person)s risk of developing cancer, especially if there are many polyps or they are large. In contrast to the inward growth of a polyp, a true cancer can grow inward toward the hollow part of the colon or rectum, andCor outward through the wall of these organs. If not treated, cells from the tumor may break away and spread through the bloodstream or lymph system to other parts of the body. There, they can form ?colony? tumors. This process is called metastasis. CONCLUSION 2hysical activity is another area that people can control. Even small amounts of exercise on a regular basis can be helpful, at least :minutes of physical activity on most days. *lso, achieving and maintaining a healthy weight. ome studies suggest that taking a daily multivitamin containing folic acid or folate can lower colorectal cancer risk. Ather studies suggest that increasing calcium intake via supplements or low1fat dairy products may lower risk. tudies of vitamin *, +, D, and E

supplements have yielded conflicting results, and additional research is needed.

RECOMMENDATION +olorectal cancers are thought to develop slowly over a period of several years. &efore a true cancer develops, there usually are precancerous changes in the lining of the colon or rectum. These changes might be dysplasia or adenomatous polyps. * polyp is a growth of tissue into the center of the colon or rectum. polyps "hyperplastic polyps and inflammatory ome types of are not

polyps#

precancerous. .owever, having adenomatous polyps, also known as adenomas, does increase a personFs risk of developing cancer, especially if there are many polyps.