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Molecular and Population Genetics Laboratory [S. H., A. R., I. To.] and Mathematics, Statistics and Epidemiology [P. S.], Imperial Cancer Research Fund, London WC2A 3PX, United Kingdom; Cancer and Immunogenetics Laboratory, Imperial Cancer Research Fund, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DZ, United Kingdom [S. H., W. B.]; Department of Medical Oncology, Hammersmith Hospital, London W12 0HS, United Kingdom [H. W.]; Academic Department of Pathology, St Mark’s and Northwick Park Hospitals, Harrow HA1 3UJ, United Kingdom [I. Ta.]; School of Pathology, University of NSW, Sydney, 2052, Australia [N. H.]; Department of Medical Oncology, St Vincent’s Hospital, Victoria St, Darlinghurst, NSW, 2010, Australia [R. W.]
About 10–15% of colorectal cancers show high-level microsatellite instability. The characteristics and very existence of low-level instability (MSI-L) are unclear, although some studies have found associations between MSI-L and molecular characteristics, notably more frequent K-ras mutations and a low level of allele loss near APC. We have attempted to define a MSI-L group of tumors by analyzing 107 sporadic colorectal carcinomas at 44 microsatellites. Ten (9.7%) MSI-H cancers were identified, but there was no evidence for a discrete MSI-L group. However, the 97 non-MSI-H cancers showed greater variation in the frequency of MSI than was expected by chance. Most cancers (68%) in the non-MSI-H group showed some MSI and could therefore be classed as nominally MSI-L. No association was found between MSI-L (or the level of MSI) and any clinicopathological or molecular variable, including K-ras mutation and loss of heterozygosity at APC. The causes of variation in level of the MSI in non-MSI-H colorectal cancers are unknown, but the differences are quantitative and probably reflect the evolutionary histories of the cancers rather than qualitatively different genetic pathways of tumorigenesis.
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