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[Cancer Research 61, 4545-4549, June 1, 2001]
© 2001 American Association for Cancer Research

Regular Articles

Microsatellite Marker Analysis in Screening for Hereditary Nonpolyposis Colorectal Cancer (HNPCC)1

Anu Loukola2, Katja Eklin2, Päivi Laiho2, Reijo Salovaara, Paula Kristo, Heikki Järvinen, Jukka-Pekka Mecklin, Virpi Launonen and Lauri A. Aaltonen3

Departments of Medical Genetics [A. L., K. E., P. L., R. S., P. K., V. L., L. A. A.] and Pathology [R. S.], Biomedicum Helsinki, FIN-00014 University of Helsinki, Finland; Second Department of Surgery, Helsinki University Central Hospital, FIN-00029 Helsinki, Finland [H. J.]; Department of Surgery, Jyväskylä Central Hospital, FIN-40620 Jyväskylä, Finland [J-P. M.]; and Department of Oncology, Helsinki University Central Hospital, FIN-00029 Helsinki, Finland [L. A. A.]

Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant cancer predisposition syndrome caused by germ-line mutations in DNA mismatch repair genes. It is relevant to identify HNPCC patients because colonoscopic screening of individuals with HNPCC mutations reduces cancer morbidity and mortality. Microsatellite instability (MSI) is characteristic of HNPCC tumors. A panel of five markers (BAT25, BAT26, D2S123, D5S346, and D17S250, the so-called Bethesda markers) has been proposed for screening for MSI. To test a hypothesis that the use of BAT26 alone is feasible in screening for MLH1/MSH2 mutation-positive HNPCC patients, we compared the MSI results of 494 colorectal cancer patients obtained using BAT26 with results obtained using the Bethesda markers. BAT26 was able to identify all 27 mutation-positive individuals in this series. The marker failed to identify 2 high MSI tumors and 20 low MSI tumors, all of which expressed MLH1, MSH2, and MSH6 when scrutinized by immunohistochemistry.




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Copyright © 2001 by the American Association for Cancer Research.