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2
Loss of ATRX, genome instability, and an altered DNA damage response are hallmarks of the alternative lengthening of telomeres pathway.ATRX 缺失、基因组不稳定和 DNA 损伤反应改变是端粒的替代延长途径的特征。
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Life and cancer without telomerase: ALT and other strategies for making sure ends (don't) meet.没有端粒酶的生命与癌症：替代延长端粒途径（ALT）及确保染色体末端（不）融合的其他策略
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Alternative Lengthening of Telomeres: DNA Repair Pathways Converge.端粒的替代性延长：DNA 修复途径汇聚。
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The macroH2A1.2 histone variant links ATRX loss to alternative telomere lengthening.组蛋白变体 macroH2A1.2 将 ATRX 缺失与替代性端粒延长联系起来。
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ATRX loss induces telomere dysfunction and necessitates induction of alternative lengthening of telomeres during human cell immortalization.ATR 缺失会导致端粒功能障碍，并在人类细胞永生化过程中需要诱导端粒的替代延长。
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Alternative mechanisms of telomere lengthening: permissive mutations, DNA repair proteins and tumorigenic progression.端粒延长的替代机制：许可性突变、DNA 修复蛋白和致瘤进展。
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The single-stranded DNA-binding factor SUB1/PC4 alleviates replication stress at telomeres and is a vulnerability of ALT cancer cells.单链DNA结合因子SUB1/PC4可缓解端粒处的复制应激，是替代延长途径（ALT）癌细胞的一个脆弱点。
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本文引用的文献

1
Nuclear receptors regulate alternative lengthening of telomeres through a novel noncanonical FANCD2 pathway.核受体通过一种新的非典型 FANCD2 途径调节端粒的非经典延长。
Sci Adv. 2019 Oct 9;5(10):eaax6366. doi: 10.1126/sciadv.aax6366. eCollection 2019 Oct.
2
Rad52 Restrains Resection at DNA Double-Strand Break Ends in Yeast.Rad52 抑制酵母中 DNA 双链断裂末端的切除。
Mol Cell. 2019 Dec 5;76(5):699-711.e6. doi: 10.1016/j.molcel.2019.08.017. Epub 2019 Sep 18.
3
BRCA2 Deletion Induces Alternative Lengthening of Telomeres in Telomerase Positive Colon Cancer Cells.BRCA2 缺失诱导端粒酶阳性结肠癌细胞端粒的非经典延长。
Genes (Basel). 2019 Sep 10;10(9):697. doi: 10.3390/genes10090697.
4
SLX4IP Antagonizes Promiscuous BLM Activity during ALT Maintenance.SLX4IP 拮抗 BLM 广泛活性以维持 ALT。
Mol Cell. 2019 Oct 3;76(1):27-43.e11. doi: 10.1016/j.molcel.2019.07.010. Epub 2019 Aug 22.
5
RAD51AP1 Is an Essential Mediator of Alternative Lengthening of Telomeres.RAD51AP1 是端粒替代延长的必需介质。
Mol Cell. 2019 Oct 3;76(1):11-26.e7. doi: 10.1016/j.molcel.2019.06.043. Epub 2019 Aug 7.
6
TSPYL5 Depletion Induces Specific Death of ALT Cells through USP7-Dependent Proteasomal Degradation of POT1.TSPYL5 通过 USP7 依赖的 POT1 蛋白酶体降解诱导 ALT 细胞特异性死亡。
Mol Cell. 2019 Aug 8;75(3):469-482.e6. doi: 10.1016/j.molcel.2019.05.027. Epub 2019 Jul 2.
7
Clustered telomeres in phase-separated nuclear condensates engage mitotic DNA synthesis through BLM and RAD52.相分离核凝聚物中的聚集端粒通过 BLM 和 RAD52 参与有丝分裂 DNA 合成。
Genes Dev. 2019 Jul 1;33(13-14):814-827. doi: 10.1101/gad.324905.119. Epub 2019 Jun 6.
8
The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT).FANCM-BLM-TOP3A-RMI 复合物抑制端粒的 ALT 延长。
Nat Commun. 2019 May 28;10(1):2252. doi: 10.1038/s41467-019-10180-6.
9
FANCM limits ALT activity by restricting telomeric replication stress induced by deregulated BLM and R-loops.FANCM 通过限制 BLM 和 R 环引起的端粒复制应激来限制 ALT 活性。
Nat Commun. 2019 May 28;10(1):2253. doi: 10.1038/s41467-019-10179-z.
10
Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation.Rad52 可防止复制叉过度反转，并防止新生链降解。
Nat Commun. 2019 Mar 29;10(1):1412. doi: 10.1038/s41467-019-09196-9.

端粒的替代性延长：连接染色体末端的桥梁。

Alternative Lengthening of Telomeres: Building Bridges To Connect Chromosome Ends.

机构信息

Department of Pharmacology and Chemical Biology, Hillman Cancer Center, University of Pittsburgh School of Medicine (UPMC), Pittsburgh, PA, USA.

Department of Pharmacology and Chemical Biology, Hillman Cancer Center, University of Pittsburgh School of Medicine (UPMC), Pittsburgh, PA, USA.

出版信息

Trends Cancer. 2020 Mar;6(3):247-260. doi: 10.1016/j.trecan.2019.12.009. Epub 2020 Jan 23.

DOI:10.1016/j.trecan.2019.12.009
PMID:32101727
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7199893/
Abstract

Alternative lengthening of telomeres (ALT) is a mechanism of telomere maintenance that is observed in many of the most recalcitrant cancer subtypes. Telomeres in ALT cancer cells exhibit a distinctive nucleoprotein architecture shaped by the mismanagement of chromatin that fosters cycles of DNA damage and replicative stress that activate homology-directed repair (HDR). Mutations in specific chromatin-remodeling factors appear to be key determinants of the emergence and survival of ALT cancer cells. However, these may represent vulnerabilities for the targeted elimination of ALT cancer cells that infiltrate tissues and organs to become devastating tumors. In this review we examine recent findings that provide new insights into the factors and mechanisms that mediate telomere length maintenance and survival of ALT cancer cells.

摘要

端粒的非经典延长（ALT）是端粒维持的一种机制，在许多最顽固的癌症亚型中都有观察到。ALT 癌细胞中的端粒表现出独特的核蛋白结构，这种结构是由染色质的错误管理形成的，促进了 DNA 损伤和复制应激的循环，从而激活同源重组修复（HDR）。特定染色质重塑因子的突变似乎是 ALT 癌细胞出现和存活的关键决定因素。然而，这些可能代表着靶向消除浸润组织和器官并成为致命肿瘤的 ALT 癌细胞的脆弱性。在这篇综述中，我们研究了最近的发现，这些发现为介导端粒长度维持和 ALT 癌细胞存活的因素和机制提供了新的见解。