Inside Colon Cancer - Part 1 of Part two

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By Dr. Carlton Fraser

ColonCancer.jpgThe word Cancer has many origins; Middle English from Old English 'cancer', from the Old French 'cancre', both from Latin 'cancer' meaning crab or malignant disease. Cancer essentially defines abnormal cellular regeneration. It results from genetic change or destruction of the chromosomal material of the cell i.e. from mutation.

Every normal cell contains 23 pairs of chromosomes which consist of the double spiral DNA molecule; that dictates the genetic characteristics in the chromosomes inherited. Within the chromosomes are 'millions' of genes that determine our growth, function and behaviour patterns.

Cells influenced by mutation disregard the clinically defined limits of growth or regeneration, exhibiting bizarre cellular behaviour. The hallmarks of (cellular) regeneration, disciplined growth/duplication and spatial limitation, are ignored. The original genetic code is no longer the determining factor for cellular development and cellular 'maturity' is now more influenced by other insidious factors. All human (cellular) elements are susceptible and the familiar tumor is a usual representation of pathological growth.
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In above fashion the development of cancer of the colon will occur and we must be thankful of the North Africans (Egyptians) who developed anatomy, most cogently at the Medical School of Alexandria in Egypt under Macedonian rule (after 334 B.C.) during the time of Erasistrato, as today we know that the colon or large intestines is approximately 1.80 meters long (about 5ft.).

It extends from the termination of the small intestines (the ileum) communicating by the ileocecal valve. The colon is approximately 1/5th the entire length of the large intestines, which commences in the 'right iliac fossa' in a dilation of considerable size, the caecum. It ascends to the undersurface of the liver, passes transversely (transverse colon) across the abdomen to the confines of the naval region to the left area in proximity to the spleen, then descends (descending colon) through the left lumbar region where it becomes convoluted and the forms the sigmoid flexure, finally entering the pelvis as it descends along its posterior surface to the anus. The large intestines reabsorbs water from the liquid mass (chyle) entering from the ileum (small intestines) and excretes waste products by peristalsis (muscular movement). Here fermentation and purification occurs. Within the rectum, absorption of water ends and faeces accumulate.

Bowel cancer usually grows in the large bowel; it is rare in the small bowel. Bowel cancer includes cancer of the proximal colon (large bowel), cancer of the distal colon rectum (the back passage), and cancer of the anus (the exit from the back passage). Colorectal cancers are almost all adenocarcinoma. Carcinoma of the colon takes various forms such as mass that is beginning to fungate in the caecum and ascending colon; a hard infiltrating mass in the transverse, descending and sigmoid colon; flat ulcer in the rectum. It is strongly believed that the majority of colorectal cancers arise from malignant transformation of adenomatous polyps. Familial adenomatous polyposis is an autosomal dominant condition that results in the development of hundreds of thousand of adenomas in the colon which begin to appear between ages 10-35. The defect has been localized to the APC gene chromosome 5Q²1. The chain of events that leads to cancer is very complex and each individual body reacts differently. Colon cancer for example is among the cancers believed to be directly inhibited by cruciferous vegetables.

A number of factors increase the risk of developing colorectal cancer. A few of these factors are:

* Age 50 or older. Colorectal cancers incidence rises sharply after age 40 which corresponds to the reduction in immune (resistance) function. 90% of the cases occur in persons over 50.
* A family history of cancer of the colon or rectum. A family history of colorectal cancer is present in 25% of patients with colon cancer. A person with one family member (1st degree relative) has a two fold or three fold increased risk and if the affected family member was under age 45 years old at the time of diagnosis, the risk is much greater.
* A personal history of cancer of the colon, rectum, ovary, endometrium, or breast. A history of adenomatous polyps especially if multiple or larger than 1cm, will increase an individuals risk of developing colon cancer.
* Familial Polyposis Syndrome; these autosomal dominant conditions dramatically increase the risk of developing cancer but they account for less than 1% of causes of colon cancer.
* Hereditary Non-Polyposis Colorectal Cancer (HNPCC-Lynch Syndrome); two autosomal conditions have been described with increased risk of developing colon cancer. These patients have few or no (adenomatous) polyps. A thorough family history is vital.
* Inflammatory Bowel Disease; the risk of adenocarcinoma of the colon begins to rise approx. 7-10 after disease onset in patients with ulcerative colitis (ulcers in the lining of the large intestine) or Crohn's disease.
* An unhealthy diet. Unhealthy eating patterns, including regular consumption of red meat, will increase ones risk of colon cancer.

 

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