Genetic instability in colorectal cancers

Research output: Contribution to journalArticlepeer-review

Abstract

It has long been considered that genetic instability is an integral component of human neoplasia. In a small fraction of tumours, mismatch repair deficiency leads to a microsatellite instability at the nucleotide sequence level. In other tumours, an abnormal chromosome number (aneuploidy) has suggested an instability, but the nature and magnitude of the postulated instability is a matter of conjecture. We show here that colorectal tumours without microsatellite instability exhibit a striking defect in chromosome segregation, resulting in gains or losses in excess of 10-2 per chromosome per generation. This form of chromo somal instability reflected a continuing cellular defect that per sisted throughout the lifetime of the tumour cell and was not simply related to chromosome number. While microsatellite instability is a recessive trait chromosomal instability appeared to be dominant. These data indicate that persistent genetic instability may be critical for the development of all colorectal cancers, and that such instability can arise through two distinct pathways.

Original languageEnglish (US)
Pages (from-to)623-627
Number of pages5
JournalNature
Volume386
Issue number6625
DOIs
StatePublished - Apr 10 1997

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Genetic instability in colorectal cancers'. Together they form a unique fingerprint.

Cite this