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[Cancer Research 62, 2447-2454, May 1, 2002]
© 2002 American Association for Cancer Research

Review

Mutations at Coding Repeat Sequences in Mismatch Repair-deficient Human Cancers

Toward a New Concept of Target Genes for Instability1

Alex Duval and Richard Hamelin2

Institut National de la Santé et de la Recherche Médicale U434: CEPH, 75010 Paris, France

Because the discovery of a link between mismatch repair deficiency and sporadic or inherited human cancers characterized by microsatellite instability (MSI-H tumors), genes containing coding repeat sequences have been found to be mutated at these repeats in MSI-H tumors from different primary sites as reported in the present review. Accumulation of such alterations appears to be the main molecular mechanism by which MSI-H cells accumulate functional changes with putative oncogenic effects. These mutations occur in many genes at variable frequencies. They can affect genes with a putative role in human carcinogenesis involved in different or similar pathways and are thus thought to be inactivating or activating events selected for in these cancers in a recessive or dominant manner. However, because of the high level of instability characterizing these cancers, they are also likely to occur in genes without any expected role in MSI-H carcinogenesis. In light of these recent data, the concept of target genes for instability and their possible role in MSI-H cancers is reconsidered here.




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