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Clonal hematopoiesis is clonally unrelated to multiple myeloma and is associated with specific microenvironmental changes

生物 造血 免疫系统 多发性骨髓瘤 免疫学 肿瘤微环境 不确定意义的单克隆抗体病 CD8型 祖细胞 癌症研究 干细胞 抗体 遗传学 单克隆 单克隆抗体
作者
Marta Lionetti,Margherita Scopetti,Antonio Matera,Akihiro Maeda,Alessio Marella,Francesca Lazzaroni,Giancarlo Castellano,Sonia Fabris,Stefania Pioggia,Silvia Lonati,Alfredo Marchetti,Alessandra Cattaneo,Marta Tornese,Antonino Neri,Claudia Leoni,Loredana Pettine,Valentina Traini,Ilaria Silvestris,Marzia Barbieri,G. Fabbiano
出处
期刊:Blood [Elsevier BV]
卷期号:146 (5): 571-584 被引量:2
标识
DOI:10.1182/blood.2024026236
摘要

Abstract Multiple myeloma (MM) initiation is dictated by genomic events. However, its progression from asymptomatic stages to an aggressive disease that ultimately fails to respond to treatments is also dependent on changes of the tumor microenvironment (TME). Clonal hematopoiesis of indeterminate potential (CHIP) is a prevalent clonal condition of the hematopoietic stem cell whose presence is causally linked to a more inflamed microenvironment. Here, we demonstrate in 106 patients with MM that CHIP is frequently coexisting with MM at diagnosis, associates with a more advanced Revised International Staging System stage and higher age, and has a nonsignificant trend toward lower median hemoglobin. In our cohort, the 2 conditions do not share a clonal origin. Single-cell RNA sequencing in 16 patients with MM highlights significant TME changes when CHIP is present: decreased naive T cells, a proinflammatory TME, decreased antigen-presenting function by dendritic cells, and expression of exhaustion markers in CD8 cells. Inferred interactions between cell types in CHIP-positive TME suggested that especially monocytes, T cells, and clonal plasma cells may have a prominent role in mediating inflammation, immune evasion, and pro-survival signals in favor of MM cells. Altogether, our data reveal that, in the presence of CHIP, the TME of MM at diagnosis is significantly disrupted in line with what is usually found in more advanced disease, with potential translational implications. Our data highlight the relevance of this association and prompt for further studies on the modifier role of CHIP in the MM TME.
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