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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'.对《基因组不稳定和非同源末端连接压力通过三阴性乳腺癌中的DNA修复危机开关驱动化疗耐药性》的更正
NAR Cancer. 2021 Sep 22;3(3):zcab041. doi: 10.1093/narcan/zcab041. eCollection 2021 Sep.
2
Genome instability and pressure on non-homologous end joining drives chemotherapy resistance via a DNA repair crisis switch in triple negative breast cancer.基因组不稳定和非同源末端连接上的压力通过三阴性乳腺癌中的DNA修复危机开关驱动化疗耐药性。
NAR Cancer. 2021 Jun 15;3(2):zcab022. doi: 10.1093/narcan/zcab022. eCollection 2021 Jun.
3
The absence of Ku but not defects in classical non-homologous end-joining is required to trigger PARP1-dependent end-joining.Ku 的缺失而非经典非同源末端连接的缺陷是触发 PARP1 依赖性末端连接所必需的。
DNA Repair (Amst). 2013 Dec;12(12):1134-42. doi: 10.1016/j.dnarep.2013.10.005. Epub 2013 Nov 7.
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Rb family-independent activating E2F increases genome stability, promotes homologous recombination, and decreases non-homologous end joining.Rb 家族非依赖性激活 E2F 增加基因组稳定性，促进同源重组，减少非同源末端连接。
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Prevention of DNA Replication Stress by CHK1 Leads to Chemoresistance Despite a DNA Repair Defect in Homologous Recombination in Breast Cancer.尽管乳腺癌同源重组中的 DNA 修复缺陷，但 CHK1 可预防 DNA 复制应激，从而导致化疗耐药性。
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Prevalence of Germline Mutations in Genes Engaged in DNA Damage Repair by Homologous Recombination in Patients with Triple-Negative and Hereditary Non-Triple-Negative Breast Cancers.三阴性乳腺癌和遗传性非三阴性乳腺癌患者中参与同源重组DNA损伤修复的基因的种系突变患病率
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Pathological complete response after cisplatin neoadjuvant therapy is associated with the downregulation of DNA repair genes in BRCA1-associated triple-negative breast cancers.顺铂新辅助治疗后的病理完全缓解与BRCA1相关三阴性乳腺癌中DNA修复基因的下调有关。
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Analysis of chromatid-break-repair detects a homologous recombination to non-homologous end-joining switch with increasing load of DNA double-strand breaks.分析着丝粒断裂修复检测到同源重组向非同源末端连接的转换，这种转换随着 DNA 双链断裂负荷的增加而增加。
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KU70 Inhibition Impairs Both Non-Homologous End Joining and Homologous Recombination DNA Damage Repair Through SHP-1 Induced Dephosphorylation of SIRT1 in T-Cell Acute Lymphoblastic Leukemia (T-ALL) [corrected].KU70抑制通过SHP-1诱导的T细胞急性淋巴细胞白血病（T-ALL）中SIRT1去磷酸化损害非同源末端连接和同源重组DNA损伤修复[已校正]
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本文引用的文献

1
Genome instability and pressure on non-homologous end joining drives chemotherapy resistance via a DNA repair crisis switch in triple negative breast cancer.基因组不稳定和非同源末端连接上的压力通过三阴性乳腺癌中的DNA修复危机开关驱动化疗耐药性。
NAR Cancer. 2021 Jun 15;3(2):zcab022. doi: 10.1093/narcan/zcab022. eCollection 2021 Jun.

对《基因组不稳定和非同源末端连接压力通过三阴性乳腺癌中的DNA修复危机开关驱动化疗耐药性》的更正

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'.

作者信息

Wiegmans Adrian P, Ward Ambber, Ivanova Ekaterina, Duijf Pascal H G, Adams Mark N, Najib Idris Mohd, Van Oosterhout Romy, Sadowski Martin C, Kelly Greg, Morrical Scott W, O'Byrne Ken, Lee Jason S, Richard Derek J

机构信息

Queensland University of Technology (QUT), Cancer and Ageing Research Program, Centre for Genomics and Personalised Health, School of Biomedical Sciences, Translational Research Institute, Woolloongabba QLD 4121, Australia.

School of Medicine, University of Queensland, Herston, QLD, 4006, Australia.

出版信息

NAR Cancer. 2021 Sep 22;3(3):zcab041. doi: 10.1093/narcan/zcab041. eCollection 2021 Sep.

DOI:10.1093/narcan/zcab041
PMID:34570837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8457359/
Abstract

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

摘要

[本文纠正了文章的数字对象标识符：10.1093/nar/zcab022。]