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[Cancer Research 61, 6046-6049, August 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Instabilotyping

Comprehensive Identification of Frameshift Mutations Caused by Coding Region Microsatellite Instability1

Yuriko Mori, Jing Yin, Asma Rashid, Barbara A. Leggett, Joanne Young, Lisa Simms, Peter M. Kuehl, Patricia Langenberg, Stephen J. Meltzer2 and O. Colin Stine

Department of Medicine, Division of Gastroenterology and Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore V. A. Hospital, Baltimore, Maryland 21201 [Y. M., J. Y., S. J. M.]; Human Genetics Program, University of Maryland School of Medicine, Baltimore, Maryland 21201 [A. R., P. M. K., O. C. S.]; Conjoint Gastroenterology Lab, Royal Brisbane Hospital Foundation, Clinical Research Centre, Bancroft Centre, Herston, Queensland 4029, Australia [B. A. L., J. Y., L. S.]; and Department of Epidemiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 [P. L., O. C. S.]

Coding region frameshift mutation caused by microsatellite instability (MSI) is one mechanism contributing to tumorigenesis in cancers with MSI in high frequency. Mutation of TGFBR2 is one example of this process. To identify additional examples, a large-scale genomic screen of coding region microsatellites was conducted. 1115 coding homopolymeric loci with six or more nucleotides were identified in an online genetic database. Mutational screening was performed at 152 of these loci in 46 colorectal tumors with MSI in high frequency. Nine loci were mutated in >=20% of tumors, 10 loci in 10–20%, 24 loci in 5–10%, 43 loci in <5%, and 66 loci were not mutated in any tumors. The most frequently mutated novel loci were the activin type II receptor gene (58.1%), SEC63 (48.8%), AIM 2 (47.6%), a gene encoding a subunit of the NADH-ubiquinone oxidoreductase complex (27.9%), a homologue of mouse cordon-bleu (23.8%), and EBP1/PA2G4 (20.9%). This genome-wide approach identifies coding region MSI in genes or pathways not implicated previously in colorectal tumorigenesis, which may merit functional study or other additional analysis.




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Copyright © 2001 by the American Association for Cancer Research.