The hereditary colorectal cancer syndrome is commonly known as familial adenomatous polyposis coli (FAP), where hundreds of polyps are found. This is associated with APC mutation.
There is another kind of hereditary predisposition of colon cancer where there is any increase in the number of polyps. The patient with this condition is called hereditary nonplyposis colorectal cancer or HNPCC. In these cases the tumor cells exhibit a normal number and karyotypes of the chromosomes.
The DNA repairing mechanism is one of the important events in the cellular function. Because of the absence of proof reading proteins, spontaneous mutation of the remaining functional gene produces a clone of somatic cells that accumulate mutations unusually rapidly. Thus most cancers arise from cells deficient in mismatch proof reading, therefore, have a greatly enhanced chance of becoming cancerous. We are fortunate that most of us inherit two good copies of each gene that encodes a mismatch proof reading protein. Mutations in any one of this gene inevitable DNA replication error and immediately elevate the spontaneous mutation rate by a hundred fold or more. These genetically unstable cells allow a clone of cells to progress malignancy. This genetic instability produces changes in the chromosomes; because the changes occur in short mono or dinucleotide repeat. This type of mutation in mismatch repair genes are found in about 15% of colorectal cancer, with no inheritable mutation and the chromosome karyotype is also normal.