相似文献
1
Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies.线粒体重编程是淋巴恶性肿瘤对 BCL-2 抑制产生耐药的基础。
Cancer Cell. 2019 Oct 14;36(4):369-384.e13. doi: 10.1016/j.ccell.2019.08.005. Epub 2019 Sep 19.
2
Splicing modulation sensitizes chronic lymphocytic leukemia cells to venetoclax by remodeling mitochondrial apoptotic dependencies.剪接调控通过重塑线粒体凋亡依赖性使慢性淋巴细胞白血病细胞对 venetoclax 敏感。
JCI Insight. 2018 Oct 4;3(19):121438. doi: 10.1172/jci.insight.121438.
3
Pathways and mechanisms of venetoclax resistance.维奈克拉耐药的途径和机制。
Leuk Lymphoma. 2017 Sep;58(9):1-17. doi: 10.1080/10428194.2017.1283032. Epub 2017 Jan 31.
4
Hyperphosphorylation of BCL-2 family proteins underlies functional resistance to venetoclax in lymphoid malignancies.BCL-2 家族蛋白的过度磷酸化是淋巴瘤对 venetoclax 产生功能性耐药的基础。
J Clin Invest. 2023 Nov 15;133(22):e170169. doi: 10.1172/JCI170169.
5
Potential mechanisms of resistance to venetoclax and strategies to circumvent it.对维奈克拉耐药的潜在机制及克服耐药的策略。
BMC Cancer. 2017 Jun 2;17(1):399. doi: 10.1186/s12885-017-3383-5.
6
Bruton's tyrosine kinase inhibition increases BCL-2 dependence and enhances sensitivity to venetoclax in chronic lymphocytic leukemia.布鲁顿酪氨酸激酶抑制增加慢性淋巴细胞白血病对BCL-2的依赖性并增强对维奈托克的敏感性。
Leukemia. 2017 Oct;31(10):2075-2084. doi: 10.1038/leu.2017.32. Epub 2017 Jan 23.
7
High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.BCL-2抑制剂ABT199（维奈托克）在高表达BCL-2的神经母细胞瘤细胞系和异种移植模型中疗效显著，以及与MCL-1抑制联合使用的合理性。
Oncotarget. 2016 May 10;7(19):27946-58. doi: 10.18632/oncotarget.8547.
8
Venetoclax resistance in acute lymphoblastic leukemia is characterized by increased mitochondrial activity and can be overcome by co-targeting oxidative phosphorylation.急性淋巴细胞白血病中的威托克耐药性的特征是线粒体活性增加，并可通过靶向氧化磷酸化来克服。
Cell Death Dis. 2024 Jul 3;15(7):475. doi: 10.1038/s41419-024-06864-7.
9
Targeting Mitochondrial Structure Sensitizes Acute Myeloid Leukemia to Venetoclax Treatment.靶向线粒体结构可增强急性髓系白血病对 venetoclax 的治疗敏感性。
Cancer Discov. 2019 Jul;9(7):890-909. doi: 10.1158/2159-8290.CD-19-0117. Epub 2019 May 2.
10
Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias.完整的 TP-53 功能对于维持白血病患者对 BH3 模拟药物的持久反应至关重要。
Blood. 2021 May 20;137(20):2721-2735. doi: 10.1182/blood.2020010167.
引用本文的文献
1
Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.细胞沉降、迁移和随机癌症基因表达表明钾离子膜通量可能引发pH值逆转。
Biomolecules. 2025 Aug 16;15(8):1177. doi: 10.3390/biom15081177.
2
The oral CDK9 inhibitor voruciclib combined with venetoclax for patients with relapsed/refractory acute myeloid leukemia.口服CDK9抑制剂沃鲁西利与维奈克拉联合用于复发/难治性急性髓系白血病患者。
Blood Neoplasia. 2025 Apr 25;2(3):100108. doi: 10.1016/j.bneo.2025.100108. eCollection 2025 Aug.
3
Cathepsin D promotes acute myeloid leukemia progression through stabilization of the anti-apoptotic proteins.组织蛋白酶D通过稳定抗凋亡蛋白促进急性髓系白血病进展。
Cell Death Dis. 2025 Aug 12;16(1):611. doi: 10.1038/s41419-025-07949-7.
4
ZBTB11 depletion targets metabolic vulnerabilities in KRAS inhibitor-resistant PDAC.锌指和BTB结构域蛋白11缺失靶向KRAS抑制剂耐药性胰腺癌中的代谢脆弱性。
Nat Chem Biol. 2025 Aug 11. doi: 10.1038/s41589-025-01978-1.
5
Superoxide-mediated phosphorylation and stabilization of Mcl-1 by AKT underlie venetoclax resistance in hematologic malignancies.超氧化物介导的AKT对Mcl-1的磷酸化和稳定作用是血液系统恶性肿瘤中维奈克拉耐药的基础。
Leukemia. 2025 Jul 24. doi: 10.1038/s41375-025-02694-4.
6
Multi-selective RAS(ON) Inhibition Targets Oncogenic RAS Mutations and Overcomes RAS/MAPK-Mediated Resistance to FLT3 and BCL2 Inhibitors in Acute Myeloid Leukemia.多选择性RAS（激活状态）抑制靶向致癌性RAS突变并克服急性髓系白血病中RAS/丝裂原活化蛋白激酶介导的对FLT3和BCL2抑制剂的耐药性。
bioRxiv. 2025 Jun 14:2025.06.10.658786. doi: 10.1101/2025.06.10.658786.
7
High mtDNA content identifies oxidative phosphorylation-driven acute myeloid leukemias and represents a therapeutic vulnerability.高线粒体DNA含量可识别氧化磷酸化驱动的急性髓系白血病，并代表一种治疗弱点。
Signal Transduct Target Ther. 2025 Jul 14;10(1):222. doi: 10.1038/s41392-025-02303-x.
8
Resistance to targeted therapies in chronic lymphocytic leukemia: Current status and perspectives for clinical and diagnostic practice.慢性淋巴细胞白血病中靶向治疗的耐药性：临床与诊断实践的现状及展望
Leukemia. 2025 Jun 24. doi: 10.1038/s41375-025-02662-y.
9
Enitociclib, a selective CDK9 inhibitor: in vitro and in vivo preclinical studies in multiple myeloma.艾尼托西利布，一种选择性CDK9抑制剂：多发性骨髓瘤的体外和体内临床前研究
Blood Neoplasia. 2024 Oct 24;2(1):100050. doi: 10.1016/j.bneo.2024.100050. eCollection 2025 Feb.
10
upregulation via aurora kinase inhibition overcomes primary failure to venetoclax in rearranged lymphomas.通过极光激酶抑制实现的上调克服了重排淋巴瘤中对维奈托克的原发性耐药。
iScience. 2025 May 2;28(6):112584. doi: 10.1016/j.isci.2025.112584. eCollection 2025 Jun 20.
本文引用的文献
1
Acquisition of the Recurrent Gly101Val Mutation in BCL2 Confers Resistance to Venetoclax in Patients with Progressive Chronic Lymphocytic Leukemia.复发性 Gly101Val 突变的获得使慢性淋巴细胞白血病患者对 Venetoclax 产生耐药性。
Cancer Discov. 2019 Mar;9(3):342-353. doi: 10.1158/2159-8290.CD-18-1119. Epub 2018 Dec 4.
2
Inhibition of Amino Acid Metabolism Selectively Targets Human Leukemia Stem Cells.抑制氨基酸代谢可选择性靶向杀伤人类白血病干细胞。
Cancer Cell. 2018 Nov 12;34(5):724-740.e4. doi: 10.1016/j.ccell.2018.10.005.
3
Venetoclax with azacitidine disrupts energy metabolism and targets leukemia stem cells in patients with acute myeloid leukemia.维奈克拉联合阿扎胞苷可破坏急性髓系白血病患者的能量代谢并靶向白血病干细胞。
Nat Med. 2018 Dec;24(12):1859-1866. doi: 10.1038/s41591-018-0233-1. Epub 2018 Nov 12.
4
Reproducible workflow for multiplexed deep-scale proteome and phosphoproteome analysis of tumor tissues by liquid chromatography-mass spectrometry.通过液相色谱-质谱联用技术对肿瘤组织进行多重深度蛋白质组和磷酸化蛋白质组分析的可重现工作流程。
Nat Protoc. 2018 Jul;13(7):1632-1661. doi: 10.1038/s41596-018-0006-9.
5
DeTiN: overcoming tumor-in-normal contamination.DeTiN：克服肿瘤-正常组织污染。
Nat Methods. 2018 Jul;15(7):531-534. doi: 10.1038/s41592-018-0036-9. Epub 2018 Jun 25.
6
Real-world outcomes and management strategies for venetoclax-treated chronic lymphocytic leukemia patients in the United States.美国接受维奈托克治疗的慢性淋巴细胞白血病患者的真实世界结局和管理策略。
Haematologica. 2018 Sep;103(9):1511-1517. doi: 10.3324/haematol.2018.193615. Epub 2018 Jun 7.
7
Metabolic changes associated with metformin potentiates Bcl-2 inhibitor, Venetoclax, and CDK9 inhibitor, BAY1143572 and reduces viability of lymphoma cells.与二甲双胍相关的代谢变化增强了Bcl-2抑制剂维奈托克和CDK9抑制剂BAY1143572的作用，并降低了淋巴瘤细胞的活力。
Oncotarget. 2018 Apr 20;9(30):21166-21181. doi: 10.18632/oncotarget.24989.
8
Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes.弥漫性大 B 细胞淋巴瘤的分子亚型与不同的发病机制和预后相关。
Nat Med. 2018 May;24(5):679-690. doi: 10.1038/s41591-018-0016-8. Epub 2018 Apr 30.
9
Clonal dynamics towards the development of venetoclax resistance in chronic lymphocytic leukemia.慢性淋巴细胞白血病中对维奈托克耐药性发展的克隆动力学
Nat Commun. 2018 Feb 20;9(1):727. doi: 10.1038/s41467-018-03170-7.
10
Antagonism of PPAR-γ signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis.PPAR-γ 信号拮抗作用通过增强糖酵解来扩增人类造血干/祖细胞。
Nat Med. 2018 Mar;24(3):360-367. doi: 10.1038/nm.4477. Epub 2018 Jan 29.
Zotero 插件