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

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

doi:10.1038/ncomms14013

Nature Communications (Jan 2017)

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

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

Affiliations

Youn-Jung Kang: Department of Pathology, Beth Israel Deaconess Medical Center
Barbara Balter: Department of Pathology, Beth Israel Deaconess Medical Center
Eva Csizmadia: Department of Surgery, Beth Israel Deaconess Medical Center
Brian Haas: The Broad Institute of MIT and Harvard
Himanshu Sharma: Department of Pathology, Beth Israel Deaconess Medical Center
Roderick Bronson: Dana-Farber/Harvard Cancer Center Rodent Histopathology Core, Harvard Medical School
Catherine T. Yan: Department of Pathology, Beth Israel Deaconess Medical Center

DOI: https://doi.org/10.1038/ncomms14013
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 15

Abstract

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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.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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