Recurrent genomic alterations characterize medulloblastoma arising from DNA double-strand break repair deficiency

Inactivation of homologous recombination (HR) or nonhomologous end-joining (NHEJ) predisposes to a spectrum of tumor types. Here, we inactivated DNA double-strand break repair (DSBR) proteins, DNA Ligase IV (Lig4), Xrcc2, and Brca2, or combined Lig4/Xrcc2 during neural development using Nestin-cre....

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2009-02, Vol.106 (6), p.1880-1885
Hauptverfasser:	Frappart, Pierre-Olivier, Lee, Youngsoo, Russell, Helen R, Chalhoub, Nader, Wang, Yong-Dong, Orii, Kenji E, Zhao, Jingfeng, Kondo, Naomi, Baker, Suzanne J, McKinnon, Peter J
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological Sciences BRCA2 Protein - genetics Breast cancer Cancer Chromosome Aberrations Chromosomes Cyclins Deoxyribonucleic acid DNA DNA Breaks, Double-Stranded DNA Ligase ATP DNA Ligases - genetics DNA Repair DNA Repair-Deficiency Disorders - etiology DNA-Binding Proteins - genetics Genetic mutation Genomic Instability Genomics Inactivation Medulloblastoma Medulloblastoma - etiology Medulloblastoma - genetics Medulloblastoma - pathology Mice Mice, Knockout Mutation Neurons Patched Receptors Patched-1 Receptor Proteins Receptors, Cell Surface - physiology Tumor Suppressor Protein p53 - deficiency Tumor Suppressor Proteins Tumors
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