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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Telomere dysfunction results in enhanced organismal sensitivity to the alkylating agent N-methyl-N-nitrosourea.

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.[1]

References

  1. Telomere dysfunction results in enhanced organismal sensitivity to the alkylating agent N-methyl-N-nitrosourea. González-Suárez, E., Goytisolo, F.A., Flores, J.M., Blasco, M.A. Cancer Res. (2003) [Pubmed]
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