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本文引用的文献

1
The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity.ASCIZ-DYNLL1 轴促进 53BP1 依赖性非同源末端连接和 PARP 抑制剂敏感性。
Nat Commun. 2018 Dec 17;9(1):5406. doi: 10.1038/s41467-018-07855-x.
2
Radiosensitivity Is an Acquired Vulnerability of PARPi-Resistant BRCA1-Deficient Tumors.放射敏感性是 PARPi 耐药 BRCA1 缺陷型肿瘤获得的脆弱性。
Cancer Res. 2019 Feb 1;79(3):452-460. doi: 10.1158/0008-5472.CAN-18-2077. Epub 2018 Dec 10.
3
DYNLL1 binds to MRE11 to limit DNA end resection in BRCA1-deficient cells.DYNLL1 与 MRE11 结合以限制 BRCA1 缺陷细胞中的 DNA 末端切除。
Nature. 2018 Nov;563(7732):522-526. doi: 10.1038/s41586-018-0670-5. Epub 2018 Oct 31.
4
Nuclear cGAS suppresses DNA repair and promotes tumorigenesis.核 cGAS 抑制 DNA 修复并促进肿瘤发生。
Nature. 2018 Nov;563(7729):131-136. doi: 10.1038/s41586-018-0629-6. Epub 2018 Oct 24.
5
53BP1 cooperation with the REV7-shieldin complex underpins DNA structure-specific NHEJ.53BP1 与 REV7-shieldin 复合物的合作是 DNA 结构特异性 NHEJ 的基础。
Nature. 2018 Aug;560(7716):122-127. doi: 10.1038/s41586-018-0362-1. Epub 2018 Jul 25.
6
53BP1-RIF1-shieldin counteracts DSB resection through CST- and Polα-dependent fill-in.53BP1-RIF1-shieldin 通过 CST 和 Polα 依赖性填补来阻止 DSB 切除。
Nature. 2018 Aug;560(7716):112-116. doi: 10.1038/s41586-018-0324-7. Epub 2018 Jul 18.
7
Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells.Shieldin 复合物促进 DNA 末端连接,并在 BRCA1 缺失细胞中对抗同源重组。
Nat Cell Biol. 2018 Aug;20(8):954-965. doi: 10.1038/s41556-018-0140-1. Epub 2018 Jul 18.
8
The Importance of Poly(ADP-Ribose) Polymerase as a Sensor of Unligated Okazaki Fragments during DNA Replication.聚(ADP-核糖)聚合酶作为 DNA 复制过程中未连接的冈崎片段传感器的重要性。
Mol Cell. 2018 Jul 19;71(2):319-331.e3. doi: 10.1016/j.molcel.2018.06.004. Epub 2018 Jul 5.
9
Selective Loss of PARG Restores PARylation and Counteracts PARP Inhibitor-Mediated Synthetic Lethality.选择性缺失 PARG 可恢复 PAR 化并拮抗 PARP 抑制剂介导的合成致死性。
Cancer Cell. 2018 Jun 11;33(6):1078-1093.e12. doi: 10.1016/j.ccell.2018.05.008.
10
The CST Complex Mediates End Protection at Double-Strand Breaks and Promotes PARP Inhibitor Sensitivity in BRCA1-Deficient Cells.CST 复合物介导双链断裂的末端保护并增强 BRCA1 缺陷细胞中 PARP 抑制剂的敏感性。
Cell Rep. 2018 May 15;23(7):2107-2118. doi: 10.1016/j.celrep.2018.04.046.

聚腺苷二磷酸核糖聚合酶抑制剂耐药机制在癌症中的研究进展及其对 DNA 损伤反应的启示

Mechanisms of PARP inhibitor resistance in cancer and insights into the DNA damage response.

机构信息

Institute of Animal Pathology, Vetsuisse Faculty, Länggassstrasse, University of Bern, 3012, Bern, Switzerland.

Division of Molecular Pathology, The Netherlands Cancer Institute, 1006 BE, Amsterdam, The Netherlands.

出版信息

Genome Med. 2018 Dec 28;10(1):101. doi: 10.1186/s13073-018-0612-8.

DOI:10.1186/s13073-018-0612-8
PMID:30593284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6309079/
Abstract

Inhibitors of poly(ADP-ribose) polymerase (PARPi) have entered the clinic for the treatment of patients with cancers that lack homology-directed DNA repair, but drug resistance remains a clinical hurdle. Recent advances in the identification of PARPi resistance mechanisms have yielded a better understanding of DNA end protection and the relevance of endogenous poly(ADP-ribose) glycohydrolase, highlighting new vulnerabilities.

摘要

聚(ADP-核糖)聚合酶(PARPi)抑制剂已进入临床,用于治疗缺乏同源定向 DNA 修复的癌症患者,但耐药性仍然是临床面临的一个难题。最近在鉴定 PARPi 耐药机制方面的进展,使人们更好地理解了 DNA 末端保护和内源性聚(ADP-核糖)糖水解酶的相关性,突出了新的弱点。