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激活诱导的胞嘧啶脱氨酶在双打击淋巴瘤中的过表达:新型抗癌治疗的潜在靶点。

Activation-induced cytidine deaminase overexpression in double-hit lymphoma: potential target for novel anticancer therapy.

机构信息

Bone Marrow Transplantation Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, Zhejian, People's Republic of China.

Department of Hematology, Jinhua Hospital of Zhejiang University (Jinhua Municipal Central Hospital), Jinhua, 321100, Zhejiang, People's Republic of China.

出版信息

Sci Rep. 2020 Aug 25;10(1):14164. doi: 10.1038/s41598-020-71058-y.

DOI:10.1038/s41598-020-71058-y
PMID:32843697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7447639/
Abstract

Activation-induced cytidine deaminase (AID) is one kind of the mutant enzymes, which target regulating the immunoglobulin (Ig) gene in Burkitt's lymphoma to initiate class switch recombination (CSR), resulting in c-Myc chromosomal translocation. However, it is not clear that whether AID induces c-Myc/IgH translocation in double-hit lymphoma (DHL) with c-Myc gene translocation. In this study, the AID in DHL tissues and classical diffuse large b-cell lymphoma (DLBCL) tissues were compared. The results suggested that AID is of important value in predicting DHL, stronger CSR of AID was observed in DHL patients, which exhibited AID overexpression and c-Myc gene translocation of DHL after CSR induction. It is concluded that AID directly induces CSR in DHL and may result in c-Myc gene translocation. Targeting AID may be a good treatment regimen for DHL.

摘要

激活诱导胞嘧啶脱氨酶(AID)是一种突变酶,其靶向调节Burkitt 淋巴瘤中的免疫球蛋白(Ig)基因以启动类别转换重组(CSR),导致 c-Myc 染色体易位。然而,目前尚不清楚 AID 是否会在具有 c-Myc 基因易位的双打击淋巴瘤(DHL)中诱导 c-Myc/IgH 易位。在这项研究中,比较了 DHL 组织和经典弥漫性大 B 细胞淋巴瘤(DLBCL)组织中的 AID。结果表明,AID 在预测 DHL 方面具有重要价值,DHL 患者的 CSR 更强,DHL 患者在 CSR 诱导后表现出 AID 过表达和 c-Myc 基因易位。结论是,AID 直接诱导 DHL 中的 CSR,并可能导致 c-Myc 基因易位。靶向 AID 可能是 DHL 的一种良好治疗方案。

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