相似文献
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Alternative Lengthening of Telomeres: Building Bridges To Connect Chromosome Ends.端粒的替代性延长：连接染色体末端的桥梁。
Trends Cancer. 2020 Mar;6(3):247-260. doi: 10.1016/j.trecan.2019.12.009. Epub 2020 Jan 23.
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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。
PLoS Genet. 2012;8(7):e1002772. doi: 10.1371/journal.pgen.1002772. Epub 2012 Jul 19.
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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
Crit Rev Biochem Mol Biol. 2017 Feb;52(1):57-73. doi: 10.1080/10409238.2016.1260090. Epub 2016 Nov 28.
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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。
Trends Genet. 2017 Dec;33(12):921-932. doi: 10.1016/j.tig.2017.09.003. Epub 2017 Sep 29.
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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。
Nat Struct Mol Biol. 2019 Mar;26(3):213-219. doi: 10.1038/s41594-019-0192-3. Epub 2019 Mar 4.
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Anti-recombination function of MutSα restricts telomere extension by ALT-associated homology-directed repair.MutSα 的抗重组功能通过 ALT 相关同源定向修复限制端粒延伸。
Cell Rep. 2021 Dec 7;37(10):110088. doi: 10.1016/j.celrep.2021.110088.
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Telomeric replication stress: the beginning and the end for alternative lengthening of telomeres cancers.端粒复制应激：端粒的替代延长与癌症的开始和结束。
Open Biol. 2022 Mar;12(3):220011. doi: 10.1098/rsob.220011. Epub 2022 Mar 9.
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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。
EMBO J. 2019 Oct 1;38(19):e96659. doi: 10.15252/embj.201796659. Epub 2019 Aug 27.
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ATRX affects the repair of telomeric DSBs by promoting cohesion and a DAXX-dependent activity.ATR-X 蛋白通过促进着丝粒黏合和依赖于 DAXX 的活性来影响端粒 DSB 的修复。
PLoS Biol. 2020 Jan 2;18(1):e3000594. doi: 10.1371/journal.pbio.3000594. eCollection 2020 Jan.
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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。
Mutat Res. 2013 Mar-Apr;743-744:142-150. doi: 10.1016/j.mrfmmm.2012.11.006. Epub 2012 Dec 3.
引用本文的文献
1
Atypical R-loops in cancer: decoding molecular chaos for therapeutic gain.癌症中的非典型R环：破解分子混乱以实现治疗效益。
J Transl Med. 2025 Aug 14;23(1):912. doi: 10.1186/s12967-025-06929-x.
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Cellular adaptations impact the biological activity of naphthalene diimide G-quadruplex ligands in ALT-positive osteosarcoma cells.细胞适应性影响萘二亚胺G-四链体配体在端粒酶替代途径（ALT）阳性骨肉瘤细胞中的生物学活性。
Cell Death Dis. 2025 Aug 1;16(1):581. doi: 10.1038/s41419-025-07908-2.
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Alternative Lengthening of Telomeres: The Need for Mutations Is Lineage-Dependent.端粒的替代延长：对突变的需求因谱系而异。
Int J Mol Sci. 2025 Jul 15;26(14):6765. doi: 10.3390/ijms26146765.
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Combined inhibition of de novo glutathione and nucleotide biosynthesis is synthetically lethal in glioblastoma.在胶质母细胞瘤中，从头合成谷胱甘肽和核苷酸生物合成的联合抑制具有合成致死性。
Cell Rep. 2025 May 27;44(5):115596. doi: 10.1016/j.celrep.2025.115596. Epub 2025 Apr 19.
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Mechanisms and molecular characterization of relapsed/refractory neuroblastomas.复发性/难治性神经母细胞瘤的机制及分子特征
Front Oncol. 2025 Mar 6;15:1555419. doi: 10.3389/fonc.2025.1555419. eCollection 2025.
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- Transcriptional Cascade Suggests Activation Mechanism for -Dependent Alternative Lengthening of Telomeres During Malignant Transformation of Malignant Peripheral Nerve Sheath Tumors: Elongation of Telomeres and Poor Survival.转录级联反应揭示恶性周围神经鞘瘤恶变过程中依赖于端粒酶的端粒替代延长激活机制：端粒延长与不良生存
Biomedicines. 2025 Jan 23;13(2):281. doi: 10.3390/biomedicines13020281.
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Chemotherapeutic 6-thio-2'-deoxyguanosine selectively targets and inhibits telomerase by inducing a non-productive telomere-bound telomerase complex.化疗药物6-硫代-2'-脱氧鸟苷通过诱导一种无活性的端粒结合端粒酶复合物，选择性地靶向并抑制端粒酶。
bioRxiv. 2025 Feb 19:2025.02.05.636339. doi: 10.1101/2025.02.05.636339.
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Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.锁定永生之门：靶向端粒替代延长（ALT）途径。
Med Oncol. 2025 Feb 18;42(3):78. doi: 10.1007/s12032-025-02627-2.
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CHROMOPHOBE HEPATOCELLULAR CARCINOMA: DIAGNOSTIC CHALLENGES.嫌色性肝细胞癌：诊断挑战
Arq Bras Cir Dig. 2025 Jan 20;37:e1863. doi: 10.1590/0102-6720202400069e1863. eCollection 2025.
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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。
Proc Natl Acad Sci U S A. 2025 Jan 14;122(2):e2419712122. doi: 10.1073/pnas.2419712122. Epub 2025 Jan 7.
本文引用的文献
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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