Correction to 'Genome instability and pressure on non-homologous end joining drives chemotherapy resistance via a DNA repair crisis switch in triple negative breast cancer'.

NAR Cancer Pub Date : 2021-09-22 eCollection Date: 2021-09-01 DOI:10.1093/narcan/zcab041
Adrian P Wiegmans, Ambber Ward, Ekaterina Ivanova, Pascal H G Duijf, Mark N Adams, Idris Mohd Najib, Romy Van Oosterhout, Martin C Sadowski, Greg Kelly, Scott W Morrical, Ken O'Byrne, Jason S Lee, Derek J Richard
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Abstract

[This corrects the article DOI: 10.1093/nar/zcab022.].

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更正“基因组不稳定和非同源末端连接的压力通过三阴性乳腺癌的DNA修复危机开关驱动化疗耐药性”。
[这更正了文章DOI: 10.1093/nar/zcab022.]。
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Pan-cancer analysis of promoter activity quantitative trait loci Large-scale phenogenomic analysis of human cancers uncovers frequent alterations affecting SMC5/6 complex components in breast cancer. Inhibition of nonsense-mediated mRNA decay reduces the tumorigenicity of human fibrosarcoma cells. CDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombination. Editorial: DNA repair and nucleic acid therapeutics in cancer.
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