Colorectal cancer genes

Article Abstract:

Cancers of the colon and rectum are very common malignancies. One model of this disease accepted by many researchers is that tumors arise from benign polyps, which then progress to their cancerous stage, the adenocarcinoma. Researchers also believe that this progression requires not one but several separate gene mutations to proceed. Although determining the exact sequence of events in such a complicated process is a daunting task, clues have been provided in the form of colorectal tumors which are clearly inherited. The two primary categories of inherited tumors are adenomatous polyposis coli (APC) and hereditary non-polyposis colon cancer (HNPCC); these account for roughly eight percent of colorectal cancer. By studying families, scientists have located the APC gene on the long arm of chromosome 5 (5q15-q22). However, in many cases, the occurrence of the tumor is sporadic, so little information may be obtained from studying family pedigrees. In these cases, the alternative strategy, called analysis of allele loss, has been to look for genes that have disappeared, so as to identify genes that are capable of suppressing tumors in normal tissues. Although this technique may be used for any tumor, it has been particularly successful in the analysis of colon cancer genetics. Allele loss has been reported on a number of different chromosomes, including 1, 5, 6, 8, 9, 17, 18, and 22. Although all these locations may not be involved in each case, it seems that at least eight mutations are necessary to produce colon cancer. Although similar success has not been achieved for HNPCC, one HNPCC cancer syndrome, Lynch syndrome II, has been linked to the Kidd blood group on chromosome 18. In general, the study of the genetics of APC and HNPCC is likely to yield insights into some previously mysterious aspects of cancer such as the increased risk of relatives of some cancer patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Telomere reduction in human colorectal carcinoma and with ageing

Article Abstract:

The ends of chromosomes, called telomeres, were known to be important even before DNA was demonstrated to be the genetic substance. More recent research has found that special DNA sequences exist in the telomeres, which apparently serve to prevent the inappropriate sticking of the ends of two distinct chromosomes. In many organisms, the breakdown and buildup of these telomeric sequences is in delicate balance. Research has now shown that human somatic cells may have a tendency for telomere breakdown. The observation that end-to-end fusion of chromosomes occurs in some tumor cells lead to the investigation of telomeric sequences in colorectal carcinoma, a very common human cancer. In humans, the telomere consists of a repetition of the sequence TTAGGG. When probes for this sequence are applied to human DNA, more probe will be bound by samples with long telomeres, and less will be bound by probes with sort telomeres. The results showed that the telomeres of colorectal cancer cells are shorter than those in normal cells from the same patient. In addition, it was shown that the telomeres from older normal cells are shorter than those of younger cells. This suggests that the loss of length of the telomeres may be a consequence of the normal replication of cells, and the short telomeres of the cancer cells may reflect the fact that these cells have replicated more often than their normal counterparts. It is worth noting that the reduction of telomere length in the colorectal cancers has already taken place by the time the tissue becomes an adenoma, representing a premalignant early stage of a colorectal cancer. Researchers speculate that these changes may initiate other genetic alterations which control the transition to malignancy. (Consumer Summary produced by Reliance Medical Information, Inc.)

Aging, Chromosome abnormalities, Age, Age (Biology)

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Genetic instability in colorectal cancers

Article Abstract:

Genetic research shows colorectal tumours without microsatellite instability are deficient in chromosome segregation. Cancerous cells lose or gain chromosomes as tissue continues to grow. Chromosomal instability, unlike microsatellite instability, seems to be a dominant genotype. Genetic instability, which appears to arise through two routes, is vital to colorectal cancer progression.

Chromosome replication

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