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Article

ATM inhibition exploits checkpoint defects and ATM-dependent double strand break repair in TP53-mutant glioblastoma.

Nature communications - 21 Jun 2024

Laverty Daniel J, Gupta Shiv K, Bradshaw Gary A, Hunter Alexander S, Carlson Brett L, Calmo Nery Matias, Chen Jiajia, Tian Shulan, Sarkaria Jann N, Nagel Zachary D

Abstract excerpt

Determining the balance between DNA double strand break repair (DSBR) pathways is essential for understanding treatment response in cancer. We report a method for simultaneously measuring non-homologous end joining (NHEJ), homologous recombination (HR), and microhomology-mediated end joining (MMEJ). Using this method, we show that patient-derived glioblastoma (GBM) samples with acquired temozolomide (TMZ)...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 38906885
DOI: 10.1038/s41467-024-49316-8
PMCID: PMC11192742

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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