| First Author | González-Suárez E | Year | 2003 |
| Journal | Cancer Res | Volume | 63 |
| Issue | 21 | Pages | 7047-50 |
| PubMed ID | 14612493 | Mgi Jnum | J:87029 |
| Mgi Id | MGI:2682986 | Citation | Gonzalez-Suarez E, et al. (2003) Telomere dysfunction results in enhanced organismal sensitivity to the alkylating agent N-methyl-N-nitrosourea. Cancer Res 63(21):7047-50 |
| abstractText | Here, we use telomerase-deficient mice, Terc(-/-), to study the impact of telomerase abrogation in response to treatment with the alkylating agent N-Methyl-N-Nitrosourea (MNU), a potent carcinogen in the mouse. Wild-type mice treated with MNU developed lymphomas and carcinomas. In contrast, similarly treated G5 Terc(-/-) mice with critically short telomeres did not develop tumors and died of acute toxicity to the small intestine. G2 Terc(-/-) mice, which have long telomeres, were less susceptible to MNU-induced tumors than wild-type mice, as well as less sensitive to MNU toxicity than G5 Terc(-/-) mice. The results indicate that short telomeres suppress tumor growth and that lack of telomerase retards tumor progression, even in the presence of long telomeres. Finally, G5 Terc(-/-) hypersensitivity to MNU supports the notion that short telomeres interfere with proper DNA damage repair. |
