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组蛋白 HIST1 基因与 TIL(肿瘤浸润淋巴细胞)在一名γδ T 细胞急性淋巴细胞白血病患儿中的单细胞测序研究

英文原题:Histone HIST1 genes and tumor-infiltrating lymphocytes in a child with γδ T cell acute lymphoblastic leukemia by single-cell sequencing.

查看英文原题

Histone HIST1 genes and tumor-infiltrating lymphocytes in a child with γδ T cell acute lymphoblastic leukemia by single-cell sequencing.

PubMed 2025/04/23(内容时间) J Leukoc Biol Q2 · IF 3.4(JCR 2025)

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中文摘要

γδ T细胞急性淋巴细胞白血病(γδ T-ALL)是T-ALL的一种罕见亚型,与高诱导失败率、复发率和死亡率增加相关。γδ T-ALL缺乏一个基于生物学信息的框架来指导其分类和治疗策略。在本报告中,我们详细描述了一例儿童γδ T-ALL患者,该患者接受了诱导化疗和强化治疗,随后进行了单倍体相合造血干细胞移植。患者达到了临床完全缓解,并且在移植后接受西达本胺维持治疗,持续保持微小残留病阴性。单细胞RNA测序揭示了组蛋白HIST1基因与γδ T-ALL之间的联系,并确定了γδ T细胞在对抗该白血病中的潜在效应功能。该病例对γδ T-ALL的管理具有重要意义,突出了组蛋白修饰模式与γδ T-ALL细胞中γδTIL(肿瘤浸润淋巴细胞)之间的关系,有助于开发新的治疗策略。

展开英文摘要原文

γδ T cell acute lymphoblastic leukemia (γδ T-ALL) represents a rare subset of T-ALL and is correlated with high rates of induction failure, relapse, and increased mortality. γδ T-ALL lacks a biologically informed framework for guiding its classification and treatment strategies. In this report, we detail a case of child with γδ T-ALL who underwent induction chemotherapy and intensification treatment, followed by haploidentical hematopoietic stem cell transplantation.

The patient achieved a clinical complete remission and remains minimal residual disease negative with chidamide maintenance post-transplantation. Single-cell RNA sequencing revealed a connection between histone HIST1 genes and γδ T-ALL and identified potential effector functions of γδ T cells in combating this leukemia. This case carries significant implications for managing γδ T-ALL, highlighting the relationship between histone modification patterns and γδ tumor-infiltrating lymphocytes in γδ T-ALL cells for developing novel therapeutic approaches.

论文信息

作者
Luo XH、Zhu Y、Duan XQ、Peng W、Pei CX、Yang L、Li Q、Zhao M
单位
Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing 400016, China.China
文献类型
病例报告
期刊
Journal of leukocyte biology2025 Apr 23
原文标识
PubMed 39973604 · DOI 10.1093/jleuko/qiaf022