Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
We know that defects in DNA repair genes are associated with cancer development. Here the authors eliminate XRCC4, a non-homologous end-joining protein, and p53 in the developing brain and find that this causes glioblastoma development as a consequence of reduced PTEN function.
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| Autores principales: | , , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2017
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/f33589217b7d48c4b64850b9eada2abb |
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| Sumario: | We know that defects in DNA repair genes are associated with cancer development. Here the authors eliminate XRCC4, a non-homologous end-joining protein, and p53 in the developing brain and find that this causes glioblastoma development as a consequence of reduced PTEN function. |
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