Colorectal Cancer Term Paper

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Colorectal Cancer

The Gastrointestinal Tract is our body's pathway where food travels from the mouth, through the esophagus, stomach, small and large intestine within where the nutrients are extracted for the needs of the body. The first part of the pathway is the esophagus. It is the conduit that guides food from the mouth, where it is prepared by chewing, down to the stomach where it is stored. Then, the stomach, which is both a storage space and a secretory organ that produces the gastric acid necessary for digestion. Then the tract is followed by the duodenum when involuntary muscle contractions (peristalsis) empties the food gradually into it, the first part of the small intestine. Other parts of the small intestine are the duodenum, the jejunum and the ileum. Each part has a certain digestive secretion which is mixed with food. Then, waste products of the process travel from the small intestine or terminal ileum, into the large intestine. This is also known as the colon. The beginning of the colon is in the right lower quadrant of the abdomen, near the appendix. The primary function of the colon is to store waste products of digestion prior to evacuation. The colon absorbs small amounts of water and electrolytes.

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Colorectal Cancer is one of the leading causes of cancer related death in the world. Although in the recent years this type of cancer has decreased in incidence and mortality rate. This most often involves men and individuals greater than or equal to 50 years of age. Colorectal cancers, no matter what etiology, come from an adenomatous polyp. This is a grossly visible protrusion from the mucosal surface. This may then be classified as nonneoplastic hamartoma or what is called juvenile polyp, a hyperplastic mucosal proliferation or the hyperplastic polyp, or an adenomatous polyp. The last mentioned is the only kind of lesion that is premalignant and only a minority of this develop into cancer.

Term Paper on Colorectal Cancer Assignment

The risk factors for developing Colorectal Carcinoma are as follows: having an a diet which mostly consists of animal fat, having hereditary symptoms which is an autosomal dominant inheritance of polyposis coli and a nonpolyposis or the Lynch syndrome, having an inflammatory bowel disease, Streptococcus bovis bacteremia, Uroterosigmoidoscopy and sometimes Tobacco use has also been related to the development of Colorectal Cancer. Let us look into these risk factors one by one.

The diet, this is said to be the etiology in most cases of cancer of the large bowel. This also appears to be related to the individual's environmental factors because the disease is mostly observed to occur in the upper socioeconomic population living in the urban areas. It was found out that the mortality rate of this kind of cancer is directly correlated with per capita consumption of calories, meat protein and dietary fat and oil, elevation of serum cholesterol concentration and deaths caused by coronary artery decease.

There are two hypothesis regarding diet as the etiology of Colorectal Cancer. First is the hypothesis of animal fat. Ingestion of animal fats leads to an increased proportion of anaerobes in the gut microflora. This then results in the conversion of normal bile acids into carcinogens. This hypothesis is also supported by several reports of increased amounts of fecal anaerobes in the stools of Colorectal Cancer patients. Diets rich in animal fats and low in vegetable are also associated with high serum cholesterol which is also in turn associated with elevated risk of developing colorectal adenomas and carcinomas. The second hypothesis is observed in South African Bantus that ingest a diet of far higher in roughage. They produce bulkier stools more frequently and have a lower incidence of large-bowel cancer compared to Americans and Europeans. This linked dietary fibers, which is poor in western diets, as a preventive factor in developing Colorectal Cancer. Dietary fibers are believed to accelerate intestinal transit time, thus reducing the exposure of colonic mucosa to potential carcinogens. This is also believed to dilute carcinogens because of enhanced fecal bulk. But this hypothesis is constantly discredited because although high fiber diets increase fecal bulk they have not been documented to increase intestinal transit time. A low fiber diet on the other hand has a higher risk of developing Colorectal Cancer because this leads to constipation and diverticulosis. But fibers do not protect individuals against developing adenomatous polyps or colorectal cancer. Second risk factor is having hereditary factor and syndromes. About 25% of patients with Colorectal Cancer have a family history of the disease. Inherited diseases of the large bowel cancers can be divided into two main groups: the polyposis syndromes and the nonpolyposis syndromes, the latter being more common.

Polyposis Coli or familial polyposis of the colon is rare. It is characterized by the appearance of thousands of adenomatous polyps throughout the large bowel. This is inherited as an autosomal dominant trait. This is associated with a deletion in the long arm of chromosome 5 and including the APC gene in both neoplastic and normal cells. This then results to the absence of tumor suppressor genes whose protein products would normally inhibit neoplastic growth in the large bowel. Gardner's Syndrome is a subset of Polyposis Coli which is characterized by the presence of soft tissue and bony tumors, congenital hypertrophy of the retinal pigment epithelium, mesenteric desmoids tumors and of ampullary cancers in addition to the colonic polyps. Turcot's syndrome is the appearance of malignant tumors of the central nervous system accompanying polyposis coli. These are generally seen in individuals by age 25. If not surgically treated it may develop into colorectal cancer for most cases before the patient reaches age 40.

Hereditary Nonpolyposis Colon Cancer or also known as the Lynch syndrome is also an autosomal dominant trait. This is characterized by the presence of three or more relatives with histologically documented colorectal cancer, one of whom is a first-degree relative of the other two. This is diagnosed mostly before age 50 in the family and involves at least two generations. This is also associated with an unusually high frequency of cancer arising in the proximal large bowel with the median age of the appearance of adenocarcinoma is less than 50 years of age, 10 to 15 years younger than the median age for the general population. The proximal colon tumors, as compared to the sporadic tumors have a better prognosis. Hereditary Nonpolyposis Colon Cancer is also associated with germline mutations of several genes, particularly hMSH2 on chromosome 2 and hMLH1 on chromosome 3. these mutations then lead to errors in DNA replication and are said to result in DNA instability because of defective repair of DNA mismatches resulting in agnormal cell growth and tumor development. Thus, testing tumor cells for "microsatellite instability" for patients under the age of 50 with colorectal cancer and a positive family history for colorectal or endometrial cancer may identify probands with Hereditary Nonpolyposis Colon Cancer.

In summary there are 6 syndromes of Hereditable Gastrointestinal Polyposis. First, the Familial adenomatous polyposis seen in the large intestine which is histologically classified as an adenoma and has a common malignant potential but with no associated lesions. The Gardner's syndrome, seen in the large and small intestines, histologically classified as an adenoma, also with a common malignant potential and is associated with osteomas, fibromas, lipomas, epidermoid cysts, ampullary cancers, congenital hypertrophy of retinal pigment epithelium. The Turcot's syndrome is seen in the large intestine is also an adenoma with common malignant potential associated with brain tumor lesions. The Nonpolyposis or Lynch syndrome is seen in the large intestine, often in the proximal part, is also an adenoma with common malignant potential associated with endometrial and ovarian tumors. The Peutz-Jeghers syndrome is seen in the large and small intestines and also the stomach. This is a hamartoma and has a rare incidence of malignancy. It is also associated with mucocutaneous pigmentation, tumors of the ovary, breast, pancreas and endometrium. And lastly, the Juvenile polyposis is also seen in the large and small intestines and also the stomach. It is classified histologically as a hamartoma but rarely progresses into an adenoma. This also has a rare potential of malignancy and is associated with various congenital abnormalities.

Other risk factors include having an inflammatory bowel disease. This increases the incidence of having Large-bowel Cancer. Cancers commonly develop in patients with ulcerative colitis as compared with those having granulomatous colitis. Although the risk of having colorectal cancer for patients with inflammatory bowel disease is relatively small during the first 10 yars of the disease but increases at a rate of about 0.5 to 1% per year. The risk is higher for younger patients with pancolitis. Also, for unknown reasons, patients with a history of Streptococcus bovis Bacteremia and develop endocarditis or septicemia have a higher risk in developing occult colorectal tumors and also gastrointestinal cancers. Ureterosigmoidostomy also has a 5 to 10% incidence of colon cancer 15 to 20 years after correcting congenital extrophy of the bladder. Tumors are characteristically found at the site… [END OF PREVIEW] . . . READ MORE

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How to Cite "Colorectal Cancer" Term Paper in a Bibliography:

APA Style

Colorectal Cancer.  (2008, May 10).  Retrieved April 14, 2021, from

MLA Format

"Colorectal Cancer."  10 May 2008.  Web.  14 April 2021. <>.

Chicago Style

"Colorectal Cancer."  May 10, 2008.  Accessed April 14, 2021.