Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival

oleh: Youn-Jung Kang, Barbara Balter, Eva Csizmadia, Brian Haas, Himanshu Sharma, Roderick Bronson, Catherine T. Yan

Format: Article
Diterbitkan: Nature Portfolio 2017-01-01

Deskripsi

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.