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Instabilotyping Reveals Unique Mutational Spectra in Microsatellite-Unstable Gastric Cancers¹

Departments of Medicine [Y. M., F. S., F. M. S., A. O., M. C. K., S. W., Y. X., J. Y., T-T. Z., J. M. A., S. J. M.] and Surgery [K. P., D. S.], Division of Gastroenterology and Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore Veterans Affairs Hospital, Baltimore, Maryland 21201; Department of Epidemiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 [O. C. S.]; Department of Pathology, Yamagata University School of Medicine, Yamagata 990-9585, Japan [G. T.]; Department of Gastroenterological Surgery, School of Medicine, Okayama University, Okayama 700-8558, Japan [N. M.]; Conjoint Gastroenterology Lab, Royal Brisbane Hospital Foundation, Clinical Research Centre, Bancroft Centre, Herston, Queensland 4029, Australia [B. L., J. Y.]; and Respiratory Oncology and Molecular Medicine, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan [T. N.]

Microsatellite instability (MSI) within coding regions causes frameshift mutations (FSMs). This type of mutation may inactivate tumor suppressor genes in cancers with frequent MSI (MSI-H cancers). To identify novel FSMs in gastric carcinogenesis in an unbiased and comprehensive manner, we screened for this type of mutation at 154 coding region repeat loci in 18 MSI-H gastric cancers. We also compared FSM rates and spectra in MSI-H gastric versus colorectal cancers. Thirteen novel loci showed FSMs in >20% of gastric tumors. Novel loci with the highest mutation frequencies included the activin type 2 receptor gene (44.4%), DKFZp564K112 (a homologue of the Drosophila tumor suppressor gene multi-sex-combs; 41.2%), and an endoplasmic reticulum chaperone protein gene SEC63 (37.5%). The mutational spectra for genes with high mutation frequencies were also significantly different between MSI-H gastric and colorectal cancers.

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