| First Author | Escudero B | Year | 2017 |
| Journal | DNA Repair (Amst) | Volume | 54 |
| Pages | 40-45 | PubMed ID | 28460268 |
| Mgi Jnum | J:320763 | Mgi Id | MGI:6878646 |
| Doi | 10.1016/j.dnarep.2017.04.001 | Citation | Escudero B, et al. (2017) Polmu deficiency induces moderate shortening of P53(-/-) mouse lifespan and modifies tumor spectrum. DNA Repair (Amst) 54:40-45 |
| abstractText | Non-homologous end joining (NHEJ) is the main mechanism for double strand break (DSB) DNA repair. The error-prone DNA polymerase mu (Polmu) is involved in immunoglobulin variable region rearrangement and in general, NHEJ in non-lymphoid cells. Deletion of NHEJ factors in P53(-/-) mice, which are highly prone to development of T cell lymphoma, generally increases cancer incidence and shifts the tumor spectrum towards aggressive pro-B lymphoma. In contrast, Polmu deletion increased sarcoma incidence, proportionally reducing pro-B lymphoma development on the P53-deficient background. Array comparative genomic hybridization (aCGH) analyses showed DNA copy number alterations in both P53(-/-) and Polmu(-/-)P53(-/-) lymphomas. Our results also indicate that the increase in sarcoma incidence in Polmu(-/-)P53(-/-) mice could be associated with Cdk4 and Kub3 amplification and overexpression. These results identify a role for Polmu in the prevention of sarcomagenesis on a murine P53-deficient background, in contrast to most other NHEJ factors. |
