Follicular lymphoma evolves with a surmountable dependency on acquired glycosylation motifs in the B-cell receptor

生物 体细胞突变 滤泡性淋巴瘤 断点群集区域 序列母题 RGD基序 糖基化 癌症研究 基因 淋巴瘤 B细胞 分子生物学 受体 遗传学 整合素 免疫学 抗体
作者
Sarah Haebe,Grady Day,Debra K. Czerwinski,Anuja Sathe,Susan M. Grimes,Tianqi Chen,Steven Long,Brock A. Martin,Michael G. Ozawa,Hanlee P. Ji,Tanaya Shree,Ronald Levy
出处
期刊:Blood [Elsevier BV]
卷期号:142 (26): 2296-2304 被引量:3
标识
DOI:10.1182/blood.2023020360
摘要

Abstract An early event in the genesis of follicular lymphoma (FL) is the acquisition of new glycosylation motifs in the B-cell receptor (BCR) due to gene rearrangement and/or somatic hypermutation. These N-linked glycosylation motifs (N-motifs) contain mannose-terminated glycans and can interact with lectins in the tumor microenvironment, activating the tumor BCR pathway. N-motifs are stable during FL evolution, suggesting that FL tumor cells are dependent on them for their survival. Here, we investigated the dynamics and potential impact of N-motif prevalence in FL at the single-cell level across distinct tumor sites and over time in 17 patients. Although most patients had acquired at least 1 N-motif as an early event, we also found (1) cases without N-motifs in the heavy or light chains at any tumor site or time point and (2) cases with discordant N-motif patterns across different tumor sites. Inferring phylogenetic trees of the patients with discordant patterns, we observed that both N-motif–positive and N-motif–negative tumor subclones could be selected and expanded during tumor evolution. Comparing N-motif–positive with N-motif–negative tumor cells within a patient revealed higher expression of genes involved in the BCR pathway and inflammatory response, whereas tumor cells without N-motifs had higher activity of pathways involved in energy metabolism. In conclusion, although acquired N-motifs likely support FL pathogenesis through antigen-independent BCR signaling in most patients with FL, N-motif–negative tumor cells can also be selected and expanded and may depend more heavily on altered metabolism for competitive survival.
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