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Acquired BCL2 variants associated with venetoclax resistance in acute myeloid leukemia.

作者信息

Brown Fiona C, Wang Xin, Birkinshaw Richard, Chua Chong Chyn, Morley Thomas, Kasapgil Sila, Pomilio Giovanna, Blombery Piers, Huang David C S, Czabotar Peter, Priore Salvatore F, Yang Guang, Carroll Martin, Wei Andrew H, Perl Alexander E

机构信息

Division of Blood Cells and Blood Cancer, Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia.

Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia.

出版信息

Blood Adv. 2025 Jan 14;9(1):127-131. doi: 10.1182/bloodadvances.2024014446.

DOI:10.1182/bloodadvances.2024014446
PMID:39374584
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11742564/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/1eef3ad1663f/BLOODA_ADV-2024-014446-gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/b72e08a6941d/BLOODA_ADV-2024-014446-ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/a01b479a130c/BLOODA_ADV-2024-014446-gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/1eef3ad1663f/BLOODA_ADV-2024-014446-gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/b72e08a6941d/BLOODA_ADV-2024-014446-ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/a01b479a130c/BLOODA_ADV-2024-014446-gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/093c/11742564/1eef3ad1663f/BLOODA_ADV-2024-014446-gr2.jpg

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1
Acquired BCL2 variants associated with venetoclax resistance in acute myeloid leukemia.与急性髓系白血病中维奈克拉耐药相关的获得性BCL2变异体。
Blood Adv. 2025 Jan 14;9(1):127-131. doi: 10.1182/bloodadvances.2024014446.
2
Not BCL2 mutation but dominant mutation conversation contributed to acquired venetoclax resistance in acute myeloid leukemia.并非BCL2突变而是显性突变转换导致急性髓系白血病中获得性维奈托克耐药。
Biomark Res. 2021 May 1;9(1):30. doi: 10.1186/s40364-021-00288-7.
3
Rationale for Combining the BCL2 Inhibitor Venetoclax with the PI3K Inhibitor Bimiralisib in the Treatment of IDH2- and FLT3-Mutated Acute Myeloid Leukemia.将 BCL2 抑制剂 Venetoclax 与 PI3K 抑制剂 Bimiralisib 联合用于治疗 IDH2 和 FLT3 突变的急性髓系白血病的理由。
Int J Mol Sci. 2022 Oct 20;23(20):12587. doi: 10.3390/ijms232012587.
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Venetoclax Overcomes Sorafenib Resistance in Acute Myeloid Leukemia by Targeting BCL2.维奈托克通过靶向BCL2克服急性髓系白血病中的索拉非尼耐药性。
Biology (Basel). 2023 Oct 16;12(10):1337. doi: 10.3390/biology12101337.
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Landscape of Resistance Mutations in a Real-World Cohort of Patients with Relapsed/Refractory Chronic Lymphocytic Leukemia Treated with Venetoclax.维奈托克治疗复发/难治性慢性淋巴细胞白血病患者的真实世界队列中耐药突变的全景。
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Targeting NF-κB-dependent alkaliptosis for the treatment of venetoclax-resistant acute myeloid leukemia cells.靶向 NF-κB 依赖的碱细胞凋亡治疗 Venetoclax 耐药的急性髓系白血病细胞。
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Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia.对患者样本进行综合分析，确定 venetoclax 疗效的生物标志物和急性髓系白血病的联合治疗策略。
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Concomitant targeting of BCL2 with venetoclax and MAPK signaling with cobimetinib in acute myeloid leukemia models.维奈托克联合 cobimetinib 靶向治疗急性髓系白血病模型中的 BCL2 和 MAPK 信号通路。
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Targeting METTL3 mitigates venetoclax resistance via proteasome-mediated modulation of MCL1 in acute myeloid leukemia.靶向METTL3通过蛋白酶体介导的急性髓系白血病中MCL1的调节减轻维奈托克耐药性。
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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。
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Acute Myeloid Leukemia in Older Patients: From New Biological Insights to Targeted Therapies.老年急性髓系白血病：从新的生物学见解到靶向治疗。
Curr Oncol. 2024 Oct 24;31(11):6632-6658. doi: 10.3390/curroncol31110490.

本文引用的文献

1
TP53 mutations predict for poor outcomes in patients with newly diagnosed aggressive B-cell lymphomas in the current era.TP53 突变可预测当代新诊断侵袭性 B 细胞淋巴瘤患者的不良预后。
Blood Adv. 2023 Dec 12;7(23):7243-7253. doi: 10.1182/bloodadvances.2023011384.
2
Acquired mutations in BAX confer resistance to BH3-mimetic therapy in acute myeloid leukemia.BAX 获得性突变赋予急性髓系白血病对 BH3 模拟物治疗的耐药性。
Blood. 2023 Feb 9;141(6):634-644. doi: 10.1182/blood.2022016090.
3
Activation of RAS/MAPK pathway confers MCL-1 mediated acquired resistance to BCL-2 inhibitor venetoclax in acute myeloid leukemia.
RAS/MAPK 通路的激活赋予急性髓系白血病对 BCL-2 抑制剂 venetoclax 的 MCL-1 介导的获得性耐药。
Signal Transduct Target Ther. 2022 Feb 21;7(1):51. doi: 10.1038/s41392-021-00870-3.
4
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.
5
Reduced Mitochondrial Apoptotic Priming Drives Resistance to BH3 Mimetics in Acute Myeloid Leukemia.线粒体凋亡起始减少导致急性髓系白血病对 BH3 模拟物耐药。
Cancer Cell. 2020 Dec 14;38(6):872-890.e6. doi: 10.1016/j.ccell.2020.10.010. Epub 2020 Nov 19.
6
Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia.单核细胞亚克隆赋予急性髓系白血病患者对 Venetoclax 为基础治疗的耐药性。
Cancer Discov. 2020 Apr;10(4):536-551. doi: 10.1158/2159-8290.CD-19-0710. Epub 2020 Jan 23.
7
Multiple BCL2 mutations cooccurring with Gly101Val emerge in chronic lymphocytic leukemia progression on venetoclax.在 Venetoclax 治疗慢性淋巴细胞白血病的进展中，出现了 BCL2 多个突变与 Gly101Val 共存的情况。
Blood. 2020 Mar 5;135(10):773-777. doi: 10.1182/blood.2019004205.
8
Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML.一线 venetoclax 联合治疗老年 AML 患者后的反应和治疗失败的分子模式。
Blood. 2020 Mar 12;135(11):791-803. doi: 10.1182/blood.2019003988.
9
Characterization of a novel venetoclax resistance mutation (BCL2 Phe104Ile) observed in follicular lymphoma.在滤泡性淋巴瘤中观察到的一种新型维奈克拉耐药突变（BCL2 Phe104Ile）的特征描述。
Br J Haematol. 2019 Sep;186(6):e188-e191. doi: 10.1111/bjh.16069. Epub 2019 Jun 24.
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Structures of BCL-2 in complex with venetoclax reveal the molecular basis of resistance mutations.BCL-2 与 venetoclax 复合物的结构揭示了耐药突变的分子基础。
Nat Commun. 2019 Jun 3;10(1):2385. doi: 10.1038/s41467-019-10363-1.