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Background <p>Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare, aggressive blood cancer from plasmacytoid dendritic cell precursors. It’s marked by CD4, CD56, CD123, and CD303/CD304 expression and involves molecular disruptions like chromatin deletions, mutations, and chromosomal translocations.</p> Methods <p>The current study employed a comprehensive method with clinical samples, histology, FACS immunophenotyping, karyotype analysis, transcriptome and protein structure analysis, and single-cell sequencing to explore BPDCN’s molecular basis.</p> Results <p>The study discovered a new MYB-ZFAT gene fusion in a BPDCN patient and showed a diverse cell population, contradicting a single cell type theory. It found four major clusters (Cluster 1,2,3,8 ) and one cluster (clulster 12) with unique profiles and roles in disease progression. The research noted Key pathways include T cell receptor signaling, NK cell cytotoxicity, and hematopoiesis are involved in pathogenesis. The study emphasized MYB activation’s role in BPDCN’s cellular clustering and identity.</p> Conclusion <p>The study indicates BPDCN’s complexity with varied cellular origins and a significant role for MYB activation in its development. This research deepens our comprehension of BPDCN’s pathogenesis and cell populations.</p>

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Single cell sequencing deciphering the heterogeneous landscape of blastic plasmacytoid dendritic cell neoplasm with novel MYB-ZFAT fusion gene

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月21日

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  • Ruijuan Li,
  • Wenyong Kuang,
  • Haixia Yang,
  • Benshan Zhang,
  • Kexin Zhao,
  • Weiyi Fang,
  • Zhao Cheng,
  • Xianming Fu,
  • Hongling Peng

摘要

Background

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare, aggressive blood cancer from plasmacytoid dendritic cell precursors. It’s marked by CD4, CD56, CD123, and CD303/CD304 expression and involves molecular disruptions like chromatin deletions, mutations, and chromosomal translocations.

Methods

The current study employed a comprehensive method with clinical samples, histology, FACS immunophenotyping, karyotype analysis, transcriptome and protein structure analysis, and single-cell sequencing to explore BPDCN’s molecular basis.

Results

The study discovered a new MYB-ZFAT gene fusion in a BPDCN patient and showed a diverse cell population, contradicting a single cell type theory. It found four major clusters (Cluster 1,2,3,8 ) and one cluster (clulster 12) with unique profiles and roles in disease progression. The research noted Key pathways include T cell receptor signaling, NK cell cytotoxicity, and hematopoiesis are involved in pathogenesis. The study emphasized MYB activation’s role in BPDCN’s cellular clustering and identity.

Conclusion

The study indicates BPDCN’s complexity with varied cellular origins and a significant role for MYB activation in its development. This research deepens our comprehension of BPDCN’s pathogenesis and cell populations.