Evidence map›Paper›PMID 39299959›Full record

ArticleJournal of cancer research and clinical oncology2024

Imatinib mesylate reduces c-MYC expression in double-hit lymphoma cells by suppressing inducible cytidine deaminase.

JingCheng Zhang, Sheng Zhou, SiSi Jiang, Fang He, Yan Tu, HuiXian Hu

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Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

JingCheng Zhang *Department of Hematology, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, China.
Sheng Zhou *Department of Hematology, Lanxi People's Hospital, Lanxi, 321100, China.
SiSi Jiang *Department of Internal Medicine, Yongkang Traditional Chinese Medicine Hospital, Yongkang, 321000, China.
Fang HeDepartment of Hematology, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, China.
Yan TuDepartment of Hematology, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, China.
HuiXian HuDepartment of Hematology, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, China. huhuixian@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDouble-hit lymphoma (DHL) with c-MYC gene translocation is highly aggressive and has a poor prognosis. In DHL cells, activation-induced cytidine deaminase (AID) promotes antibody class switch recombination (CSR), ultimately leading to c-MYC gene translocation caused by Myc/IgH DNA double-strand breaks. However, currently there is still no method to suppress the expression of AID.

methodsIn this study, we compared the clinical significance of AID expression in DHL, Additionally, two human double-hit lymphoma cell lines were used to analyze the effect of imatinib mesylate on c-MYC in vitro, and the therapeutic effect was also evaluated in xenograft mouse models.

resultsImatinib mesylate downregulated the AID and c-MYC proteins in patients with chronic myelogenous leukemia associated with DHL. In addition, imatinib mesylate reduced AID and c-MYC expression in SU-DHL-4 and OCI-Ly18 DHL cells. Imatinib mesylate exerted significant inhibitory effects on the proliferation and metastasis of SU-DHL-4 and OCI-Ly18 cells. Finally, imatinib mesylate reduced not only tumor burden in DHL mouse models, but also AID and c-MYC expression in vivo.

conclusionThese findings reveal that imatinib mesylate effectively reduces the carcinogenic function of c-MYC in DHL, providing novel strategies for developing therapies targeting c-MYC-driven DHL.

Indexed as

Cytidine DeaminaseImatinib MesylateProto-Oncogene Proteins c-mycXenograft Model Antitumor AssaysAICDA (Activation-Induced Cytidine Deaminase)AnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLymphomaMaleMiceAICDA (Activation-Induced Cytidine Deaminase)Antineoplastic AgentsCytidine DeaminaseImatinib MesylateMYC protein, humanProto-Oncogene Proteins c-mycActivation-induced cytidine deaminaseC-MycDiffuse large B-cell lymphomaDouble-hit lymphomaImatinib mesylate

Identifiers

PMID39299959
PMCPMC11413099

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