| First Author | Baross-Francis A | Year | 1998 |
| Journal | Proc Natl Acad Sci U S A | Volume | 95 |
| Issue | 15 | Pages | 8739-43 |
| PubMed ID | 9671748 | Mgi Jnum | J:49341 |
| Mgi Id | MGI:1277346 | Doi | 10.1073/pnas.95.15.8739 |
| Citation | Baross-Francis A, et al. (1998) Tumors of DNA mismatch repair-deficient hosts exhibit dramatic increases in genomic instability. Proc Natl Acad Sci U S A 95(15):8739-43 |
| abstractText | DNA mismatch repair (MMR) deficiency is associated with an increased mutational burden and predisposition to certain malignancies. Relatively little is known, however, about gene-specific mutation frequencies within MMR-deficient primary tumors. Thymic lymphomas from Msh2(-/-) mice were thus analyzed by using a lacI-based transgenic shuttle- phage mutation detection system. All tumors exhibited greatly elevated lad gene mutation frequencies, ranging from 3.2- to 17.4-fold above the approximate to 15-fold elevations present within normal Msh2(-/-) thymi, In addition, lad genes hal boring multiple changes, including clusters of mutations, were found in thymic tumor DNA, The results suggest that an additional mutator activity, such as an error-prone DNA polymerase, leads to increased genomic instability in these MMR-deficient tumors. |
