Aspirin and colorectal cancer.

surprising observation was that in 11 of 14 familial tumours there were errors in DNA replication not only in the dinucleotide repeat marker on chromosome 2 but throughout the tumour genome, and replication errors also affected trinucleotide repeats, indicating widespread genetic in- stability.Multiple replication errors have also been found in 13% of sporadic tumours.1 1213 The tumours with errors were found to have some of the characteristics of familial tumours-they were more frequently right sided and diploid and had a lower frequency of loss of heterozygosity despite there being no characteristic family history.These results suggest that up to 15% of apparently sporadic tumours may be associated with genetic instability.Familial colon cancer associated with the gene mapped to chromosome 2 may be one of most common forms of heritable disease in man.It seems to cause errors of DNA replication in tumours.Identification and characterisation of the gene should greatly facilitate surveillance programmes for colon cancer (and associated cancers) in affected individuals and may ultimately permit population screening.Even before the gene is isolated, however, more effort should be made to recognise patients with familial colon cancer so that they and their relatives are managed appropriately.This should probably include screening those at risk from the age of 25 by colonoscopy every three to five years and, in women, by pelvic ultrasonography.Those who develop colorectal cancer should be treated by subtotal colectomy-these patients have a high incidence ofmetachronous colonic tumours.