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<p>Primary cardiac lymphoma (PCL), a rare B-cell non-Hodgkin’s lymphoma, has shown a rising incidence, yet the lack of clarity regarding its molecular basis continues to hinder the development of effective targeted therapies. In this study, we utilized single-nucleus RNA sequencing and Visium CytAssist spatial transcriptomics in two patients with PCL to examine the metabolic and immune landscape of PCL. Our data implicate chromosomal instability (CIN) as a potential driver of disease progression, likely by modulating cellular sensitivity to metabolic stress. Single-cell analysis identified five distinct malignant B-cell states, including a B3 subset defined by subclonal diversification and enriched fatty acid metabolism-MAPK signaling. NFYA was also noted as a transcription factor potentially involved in this lipid reprogramming. Spatial observations suggest that B3 cells may contribute to an immunosuppressive microenvironment, with the CD44-LGALS9 axis acting as a possible mediator of endothelial cell remodeling and T-cell suppression. Ultimately, this study provides fresh insights into the clonal evolution and metabolic adaptations of PCL. These findings suggest that fatty acid metabolic reprogramming and CD44-LGALS9-mediated immune evasion play roles in tumor maintenance within the cardiac environment, offering a preliminary basis for future targeted therapeutic intervention.</p><p></p>

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Single-nucleus and spatial transcriptomics analyses reveal interplay between evolutionary dynamics and energy metabolism in primary cardiac lymphoma

  • 期刊论文

  • 发表日期：

    2026年5月22日

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  • Xiaojuan Wei,
  • Qianbing Zhang,
  • Pengjun Liao,
  • Sichu Liu,
  • Xinmiao Jiang,
  • Ling Huang,
  • Su Yao,
  • Hui Yuan,
  • Kezhen Li,
  • Wenyu Li,
  • Liwei Hao,
  • Sipei Wu

摘要

Primary cardiac lymphoma (PCL), a rare B-cell non-Hodgkin’s lymphoma, has shown a rising incidence, yet the lack of clarity regarding its molecular basis continues to hinder the development of effective targeted therapies. In this study, we utilized single-nucleus RNA sequencing and Visium CytAssist spatial transcriptomics in two patients with PCL to examine the metabolic and immune landscape of PCL. Our data implicate chromosomal instability (CIN) as a potential driver of disease progression, likely by modulating cellular sensitivity to metabolic stress. Single-cell analysis identified five distinct malignant B-cell states, including a B3 subset defined by subclonal diversification and enriched fatty acid metabolism-MAPK signaling. NFYA was also noted as a transcription factor potentially involved in this lipid reprogramming. Spatial observations suggest that B3 cells may contribute to an immunosuppressive microenvironment, with the CD44-LGALS9 axis acting as a possible mediator of endothelial cell remodeling and T-cell suppression. Ultimately, this study provides fresh insights into the clonal evolution and metabolic adaptations of PCL. These findings suggest that fatty acid metabolic reprogramming and CD44-LGALS9-mediated immune evasion play roles in tumor maintenance within the cardiac environment, offering a preliminary basis for future targeted therapeutic intervention.