Journal Article

Tumors arising in DNA mismatch repair-deficient mice show a wide variation in mutation frequency as assessed by a transgenic reporter gene

Agnes Baross-Francis, M.Kate Milhausen, Susan E. Andrew, Gareth Jevon and Frank R. Jirik

in Carcinogenesis

Volume 21, issue 6, pages 1259-1262
Published in print June 2000 | ISSN: 0143-3334
Published online June 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.6.1259
Tumors arising in DNA mismatch repair-deficient mice show a wide variation in mutation frequency as assessed by a transgenic reporter gene

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We reported previously that thymic lymphomas arising in mice lacking the DNA mismatch repair (MMR) gene, Msh2−/−, exhibited striking elevations in the mutation frequency of a transgenic lacI reporter gene when compared with normal Msh2−/− tissues. To investigate whether hypermutation was a feature of all tumors arising in MMR-deficient mice, lacI transgene mutation frequencies were obtained from several different mouse tumors deficient for PMS2 and/or MSH2. While lacI gene hypermutation was again clearly evident in Msh2+/−Pms2−/− and Msh2−/−Pms2−/− thymic lymphomas, three non-thymic MSH2-deficient tumors failed to show lacI gene mutation frequency elevations when compared with a normal tissue of MMR-deficient mice. The elevated mutation frequencies in the lymphoid tumors, and the finding of multiple clustered mutations in lacI genes rescued from these tumors, suggest that they are possibly generated by a lymphoma-specific hypermutational mechanism.

Keywords: MMR, mismatch repair.

Journal Article.  3282 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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