Abstract This paper examines how colorectal cancer is the third most frequent cause of cancer death behind lung and prostate cancer in men and the third behind lung and breast in women in the U.S and the U.K.. It reviews the current statistics of colorectal cancer and the basics for its development as well as the current status of a very significant factor of carcinogenesis a protein called MBD4. Tables and diagrams aer included.
From the Paper "Cancer is a malignant growth which results from uncontrolled cell proliferation and loss of cell differentiation and programmed apoptosis. The word "cancer" describes a group of diseases that can affect any part of the human body. Cancer is a problem of great importance, affecting millions of people around the world and owes its success partly to the ability to spread-metastasize to other areas of the body through the lymphatic system and blood stream. According to McDonald (1997), cancer begins when a single cell undergoes mutation. This mutation promotes cell growth and permits this cell to bypass normal controls of proliferation. Additional mutations will occur, producing tumours."
Tags:carcinogenesis, malignant, growth, tumour, protein
Abstract This paper is an examination of the mechanisms of colon tumorigenesis involving the mutation cluster region of the APC gene. There is an explanation of colon carcinogenesis including an analysis of the Wnt signaling pathway, the roles of the APC gene's different domains, "Knudon's two- hit hypothesis and the "just right" level of signaling theory. The paper also includes a critical discussion about the scientific arguments and research evidence that exists to challenge current understanding of the underlying mechanisms of colon tumorigenesis. One illustration is included which depicts the varying domains of the APC gene.
From the Paper "Colorectal cancer is the third most common form of cancer and the second leading cause of death in the western world. Nearly 34,900 people are diagnosed with it in the U.K each year and about 16,000 of these die. About 15% of colorectal cancers are hereditary. Hereditary conditions are divided into two categories: the polyposis and the non polyposis types. Two hereditary conditions that have been identified are Familial Adenomatous Polyposis Coli (FAP) and Hereditary Non Polyposis Colorectal Cancer (HNPCC). The adenomatous polyposis coli (APC) gene is known to be mutated in all cases of FAP but this condition only accounts for less than 1% of colorectal cancer cases. The condition HNPCC results when mutation occurs in the DNA mismatch repair genes MSH2 and MLH-1 leading to microsatellite instability and defective DNA repair. Non inherited mutations of the APC gene have been detected in over 85% of the remaining sporadic colorectal cancers. "
Abstract This paper discusses the role of soybean consumption in cancer prevention. A review of the relevant literature on the anti carcinogenic activity of soybeans is presented. A proposal for a research study to determine the effects on cancer prevention of providing a soy-rich diet for cattle used for human consumption is offered.
From the Paper "Soybeans are used for human consumption as well as animal consumption. It is put through a heat process so that the nutritional value is enhanced. ?The so-called protease inhibitors have received the most attention in this regard and have been shown to exert their antinutritional effect in the short term by causing pancreatic hypertrophy and hyperplasia in the rat, the underlying cause for an inhibition of growth in these animals(Liener, 2000). The prolonged feeding of raw soy flour or an enriched trypsin inhibitor fraction from soybeans to rats results in the development of hyperplastic and neoplastic nodules of the pancreas, including carcinomas(Liener, 2000). It should be emphasized that all of these adverse effects are seen when protease inhibitors are present in relatively high concentrations in the diet and may be completely unrelated to the anticarcinogenic effects seen at low concentrations of the Bowman-Birk inhibitor(Liener, 2000).?"
Abstract This paper explains that it is next to impossible to avoid sources of natural radiation in our everyday life, but precautions can be taken to maintain distance from local sources of radiation and to use distance, time, and radiation-shielding as protection. The author points out that radiation is not responsible for the assumed mechanism of carcinogenesis caused by the exposure to magnetic fields. The paper relates that the nuclear industry and many other sources of radioactivity are used in an enormous range of industrial processes, such as industrial radiography, thickness gauges, smoke alarms, and medical diagnosis and treatment.
Table of Contents
Types and Sources of Ionising Radiation
The Effect of Radiation on the Body
Detecting Radiation
Regulating Body Standards and the Workplace
Ionizing Radiation
Contamination
Stochastic Effects
Deterministic Effects
Monitoring Radiation Exposure
Radiation Accidents
Types of Radiation Accident
The Food Industry Uses Radiation
From the Paper "Ionising radiation does not accumulate in our body, but science proves that the radiation effects are evident from exposure to large amounts of radiation, as in sunburns from too much exposure to strong sunlight. Radiation carries energy that has a damaging effect on the living cells of living things and can either kill them or change their structure and function to inhibit correct functioning but this would take large doses to kill a good number of cells to cause death. Radiation dose would have to be several thousand times bigger than the dose received annually from the environment to cause death. Death would occur if the person were exposed more over a year. For example, exposure to sunlight over a year gives one a suntan, but one-day exposure of sunbaking could cause death by sunstroke."
Abstract The paper examines the adenoma to carcinoma sequence proposed by B. Volgenstein and E.R. Fearon. The paper explains how this model acts as a basis for understanding the mechanisms which are thought to cause eighty per cent of sporadic colon cancers and cases of familial adenematous polyposis. The paper also describes an alternative pathway resulting in microsatellite instability and thought to underlie cases of hereditary non polyposis colon cancer. In addition, the paper looks at the molecular events involving mutated mismatch repair enzymes.
From the Paper "Colorectal cancer causes approximately 15,000 deaths per year in the U.K and about 30,000 individuals are diagnosed with it each year making it the second most common cause of death from cancer. Of these, about 70% are colon cancers which affect men and women and are much more prevalent in the Western World than India or Asia. About 25% of colon cancers occur where there's a family history of it but only 5% are due to known familial syndromes. These include Familial adenomatous polyposis (FAP); a mendelian dominant disorder which sees a germline mutation of APC and hereditary non polyposis colon cancer (HNPCC); a disorder in which germline mutations in mismatch repair enzymes are caused. The other 20% of clusters of colon cancer in families are unexplained but postulated risks are "mild" APC and mismatch repair gene mutations or polymorphisms of genes involved in nutrient or carcinogen metabolism and also non genetic factors. The main proportion of colon cancer though arises from sporadic adenomatous polyps (75%)."
