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[Cancer Research 60, 803-807, February 15, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

The DNA Mismatch Repair Genes Msh3 and Msh6 Cooperate in Intestinal Tumor Suppression1

Winfried Edelmann, Asad Umar, Kan Yang, Joerg Heyer, Melanie Kucherlapati, Marie Lia, Burkhard Kneitz, Elena Avdievich, Kunhua Fan, Edmund Wong, Gray Crouse, Thomas Kunkel, Martin Lipkin, Richard D. Kolodner and Raju Kucherlapati2

Departments of Cell Biology [W. E., B. K., E. A., E. W.] and Molecular Genetics [W. E., J. H., M. K., M. Lia, E. W., R. K.], Albert Einstein College of Medicine, Bronx, New York 10461; Laboratory of Molecular Genetics, National Institute of Environmental Health Services, Research Triangle Park, North Carolina 27700 [A. U., T. K.]; Strang Cancer Prevention Center, New York, New York 10021 [K. Y., K. F., M. Lip.]; Emory University, Atlanta, Georgia 30322 [G. C.]; Ludwig Institute for Cancer Research, La Jolla, California 92093 [R. D. K.]

Repair of mismatches in DNA in mammalian cells is mediated by a complex of proteins that are members of two highly conserved families of genes referred to as MutS and MutL homologues. Germline mutations in several members of these families, MSH2, MSH6, MLH1, and PMS2, but not MSH3, are responsible for hereditary non-polyposis colorectal cancer. To examine the role of MSH3, we generated a mouse with a null mutation in this gene. Cells from Msh3-/- mice are defective in repair of insertion/deletion mismatches but can repair base-base mismatches. Msh3-/- mice develop tumors at a late age. When the Msh3-/- and Msh6-/- mutations are combined, the tumor predisposition phenotype is indistinguishable from Msh2-/- or Mlh1-/- mice. These results suggest that MSH3 cooperates with MSH6 in tumor suppression.




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