生物
造血
髓样
淋巴瘤
祖细胞
癌症的体细胞进化
骨髓
套细胞淋巴瘤
癌症研究
等位基因
免疫学
起源细胞
脾边缘带淋巴瘤
表型
基因分型
遗传学
突变
种系突变
免疫分型
连锁不平衡
克隆(Java方法)
分子生物学
造血干细胞
基因型
细胞分化
干细胞
血细胞
体细胞
白血病
作者
Laura Wiegand,PATRÍCIA ROCHA SILVA,Daniel Noerenberg,Friederike Christen,Klara Kopp,Benjamin N. Locher,Pelle Löwe,Marlon Tilgner,Robert Altwasser,Vanessa Storzer,Catarina M. Stein,Franziska Briest,Christopher Maximilian Arends,Mareike Frick,Jana Ihlow,Anna Dolnik,Naveed Ishaque,Ulrich Keller,Il‐Kang Na,Livius Penter
出处
期刊:Blood
[Elsevier BV]
日期:2026-01-05
卷期号:147 (15): 1723-1734
被引量:6
标识
DOI:10.1182/blood.2025030489
摘要
ABSTRACT: The contribution of clonal hematopoiesis (CH) and disease-initiating precursors in B-cell non-Hodgkin lymphomas (B-NHLs) remains underexplored. Such precursors may drive clonal evolution, contributing to disease progression and relapse. Here, we systematically profiled genetic precursor lesions in 43 patients with B-NHL using complementary whole-exome, targeted, and single-cell sequencing approaches. CH-associated mutations with a variant allele frequency of ≥1% were detected in the peripheral blood of 55% of patients, with significantly higher frequencies in indolent compared with aggressive B-NHL (P = .03). Quantification of allele burden in flow-sorted cell populations revealed a B-cell-skewed expansion of CH clones, contrasting the myeloid differentiation bias reported in individuals without hematologic malignancies. Gene-specific expansion patterns were evident among the most frequent CH lesions, with DNMT3A-mutant clones exhibiting impaired hematopoietic differentiation and TET2-mutant clones having multilineage propagation. Notably, identical CH clones were detected in 41% of corresponding lymphomas, displaying distinct clonal dynamics: tumor-promoting CH (expansion in B-NHL; 10/16 clones; mainly TP53) and tumor-infiltrating CH (no expansion; mainly DNMT3A). Moreover, we identified lymphoma-associated mutations in flow-sorted hematopoietic progenitors from patients with indolent but not aggressive B-NHL and observed a stepwise accumulation of mutations along the lymphoid differentiation path. Single-cell genotyping confirmed the presence of mutated progenitors in 3 follicular, 2 mantle cell, and 2 marginal zone lymphoma patients, providing direct evidence of a preneoplastic state in disease pathogenesis. Our findings offer novel insight into the cellular origin of nodal B-NHLs and highlight a previously underappreciated role for early clonal events involving the stem/progenitor cell compartment.
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