The American Cancer Society estimates that there will be 93,800 new cases of colon cancer diagnosed in the United States in 2000 with 47,700 deaths resulting. All types of cancer occur when cell division, normally a very highly regulated process, is out of control. Although environmental factors can certainly contribute to a person’s risk of cancer (smoking, diet and exercise), most cancers have a genetic basis as well. Hundreds of genes and proteins are involved in monitoring the process of cell division and DNA replication, a mutation in one or more of these genes or proteins can sometimes lead to uncontrolled cancerous growth.
Colon cancer is one of the best known hereditary syndromes of cancer. Among the genes to be involved in colorectal cancer are: MSH2 and MSH6 both on chromosome 2 and MLH1 on chromosome 3. Normally, the protein products of these genes help to repair mistakes made in DNA replication. If the MSH2, MSH6, and MLH1 proteins are mutated and therefore do not function properly, the replication errors are not repaired, leading to damaged DNA, and in this case, cancer of the colon.
It is not clear why mutations in genes that are essential in all tissues preferably cause colon cancer. However, studies on the equivalent gene in mice and brewer’s yeast to help deepen our understanding of the mechanisms of DNA repair and the role of environmental factors in colon cancer incidence.
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