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吉瑞替尼克服了一名FLT3野生型难治性/复发性急性髓系白血病患者对维奈托克的原发性耐药：病例报告及可能机制探索

Gilteritinib overcomes primary resistance to venetoclax in a patient with FLT3 wild-type refractory/relapsed AML: Case report and exploration of possible mechanisms.

作者信息

Li Man, Yang Xiawan, Hong Yaonan, Liu Qi, Shen Yingying, Hu Tonglin, Shen Yiping, Kai Guoyin, Wu Dijiong

机构信息

Zhejiang Key TCM Laboratory for Chinese Resource Innovation and Transformation, Jinhua Academy, School of Pharmaceutical Sciences, The Third Affiliated Hospital, Academy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.

Department of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.

出版信息

Heliyon. 2024 Aug 10;10(16):e35847. doi: 10.1016/j.heliyon.2024.e35847. eCollection 2024 Aug 30.

DOI:10.1016/j.heliyon.2024.e35847
PMID:39211920
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11357765/
Abstract

Venetoclax, a selective BCL-2 inhibitor, has shown superior efficacy in the treatment of AML. Nevertheless, some AML patients with respond poorly to venetoclax treatment. In this report, a relapsed/refractory (R/R) venetoclax resistant positive AML patient showed rapid tumor regression after combination therapy with gilteritinib and venetoclax. Additional laboratory findings indicated that the combined impact of the two drugs may be associated with the induction of the integrated stress response. This case presents a novel therapeutic approach for the treatment of FLT3 wild-type RR, AML patients who have primary resistance to venetoclax.

摘要

维奈托克是一种选择性BCL-2抑制剂，已在急性髓系白血病（AML）治疗中显示出卓越疗效。然而，部分AML患者对维奈托克治疗反应不佳。在本报告中，一名复发/难治性（R/R）维奈托克耐药的FLT3阳性AML患者在接受吉瑞替尼与维奈托克联合治疗后肿瘤迅速消退。其他实验室检查结果表明，两种药物的联合作用可能与整合应激反应的诱导有关。该病例为治疗对维奈托克具有原发性耐药的FLT3野生型RR AML患者提供了一种新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/ce1824b98e1c/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/7105415cd644/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/3f4e9032b56e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/c35111d8d8a7/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/ce1824b98e1c/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/7105415cd644/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/3f4e9032b56e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/c35111d8d8a7/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e655/11357765/ce1824b98e1c/mmcfigs2.jpg

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Gilteritinib overcomes primary resistance to venetoclax in a patient with FLT3 wild-type refractory/relapsed AML: Case report and exploration of possible mechanisms.吉瑞替尼克服了一名FLT3野生型难治性/复发性急性髓系白血病患者对维奈托克的原发性耐药：病例报告及可能机制探索
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本文引用的文献

1
Prognostic value of European LeukemiaNet 2022 criteria and genomic clusters using machine learning in older adults with acute myeloid leukemia.基于机器学习的欧洲白血病网 2022 标准和基因组聚类在老年急性髓系白血病中的预后价值。
Haematologica. 2024 Apr 1;109(4):1095-1106. doi: 10.3324/haematol.2023.283606.
2
Development of a scoring system for predicting primary resistance to venetoclax plus hypomethylating agents (HMAs) in acute myeloid leukemia patients.开发一种评分系统，用于预测急性髓系白血病患者对 venetoclax 联合低甲基化药物（HMAs）的原发性耐药。
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Venetoclax synergizes with gilteritinib in FLT3 wild-type high-risk acute myeloid leukemia by suppressing MCL-1.
维奈托克与吉特替尼联合应用通过抑制 MCL-1 在 FLT3 野生型高危急性髓系白血病中发挥协同作用。
Blood. 2022 Dec 15;140(24):2594-2610. doi: 10.1182/blood.2021014241.
4
Gilteritinib or Chemotherapy for Relapsed or Refractory -Mutated AML.吉特替尼与化疗用于治疗复发/难治性 - 突变型 AML。
N Engl J Med. 2019 Oct 31;381(18):1728-1740. doi: 10.1056/NEJMoa1902688.
5
Venetoclax-based therapies for acute myeloid leukemia.基于 Venetoclax 的急性髓系白血病疗法。
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6
Selective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukaemia: a multicentre, first-in-human, open-label, phase 1-2 study.吉瑞替尼对复发或难治性急性髓系白血病中FLT3的选择性抑制作用：一项多中心、首例人体、开放标签的1-2期研究。
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7
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Blood. 2017 Jan 26;129(4):424-447. doi: 10.1182/blood-2016-08-733196. Epub 2016 Nov 28.
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Biochemistry (Mosc). 2010 Dec;75(13):1650-66. doi: 10.1134/s0006297910130092.
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Molecular characterization of AML with ins(21;8)(q22;q22q22) reveals similarity to t(8;21) AML.伴有 ins(21;8)(q22;q22q22)的 AML 的分子特征与 t(8;21) AML 相似。
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