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• W2894744183 abstract "Abstract 1,2:5,6-Dianhydrogalactitol (DAG) is a bifunctional DNA-targeting agent causing N 7 -guanine alkylation and inter-strand DNA crosslinks currently in clinical trial for treatment of glioblastoma. While preclinical studies and clinical trials have demonstrated antitumor activity of DAG in a variety of malignancies, understanding the molecular mechanisms underlying DAG-induced cytotoxicity is essential for proper clinical qualification. Using non-small cell lung cancer (NSCLC) as a model system, we show that DAG-induced cytotoxicity materializes when cells enter S phase with unrepaired N 7 -guanine DNA crosslinks. In S phase, DAG-mediated DNA crosslink lesions translated into replication-dependent DNA double-strand breaks (DSBs) that subsequently triggered irreversible cell cycle arrest and loss of viability. DAG-treated NSCLC cells attempt to repair the DSBs by homologous recombination (HR) and inhibition of the HR repair pathway sensitized NSCLC cells to DAG-induced DNA damage. Accordingly, our work describes a molecular mechanism behind N 7 -guanine crosslink-induced cytotoxicity in cancer cells and provides a rationale for using DAG analogs to treat HR-deficient tumors." @default.
• W2894744183 created "2018-10-12" @default.
• W2894744183 creator A5009807263 @default.
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• W2894744183 date "2018-10-03" @default.
• W2894744183 modified "2023-10-13" @default.
• W2894744183 title "Dianhydrogalactitol induces replication-dependent DNA damage in tumor cells preferentially resolved by homologous recombination" @default.
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• W2894744183 doi "https://doi.org/10.1038/s41419-018-1069-9" @default.
• W2894744183 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6170372" @default.
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• W2894744183 hasPublicationYear "2018" @default.
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