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<p>The co-expression of myeloid and B-cell antigens is characteristic of mixed-phenotype acute leukemia (MPAL)-B/myeloid. This finding can also be observed in AML with t(8;21)(q22;q22)/<i>RUNX1</i>::<i>RUNX1T1</i>, as well as in cases of AML with other <i>RUNX1</i> rearrangements, copy number gains, or mutations. AML with plasmacytoid dendritic cell (pDC) differentiation (pDC-AML) containing clonally-related myeloblasts and neoplastic pDCs, are enriched for <i>RUNX1</i> mutations and have been shown to exhibit B-cell marker expression. Here, we present two cases of pDC-AML with B-cell marker expression in which <i>RUNX1</i> aberrations were not identified. Although previously we speculated on the role of <i>RUNX1</i> in the aberrant expression of B-cell markers such in cases, the absence of <i>RUNX1</i> lesions in the current cases supports the potential inherent ability of pDCs to express B-cell markers during maturation.</p>

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B-cell marker expression in acute myeloid leukemia with plasmacytoid dendritic cell differentiation (pDC-AML) without RUNX1 lesions: An underrecognized diagnostic pitfall

  • 期刊论文

  • 发表日期：

    2026年1月26日

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  • Giby V. George,
  • Neel V. Hegde,
  • Hong Fang,
  • Fatima Zahra Jelloul,
  • L. Jeffrey Medeiros,
  • Wei Wang,
  • Siba El Hussein

摘要

The co-expression of myeloid and B-cell antigens is characteristic of mixed-phenotype acute leukemia (MPAL)-B/myeloid. This finding can also be observed in AML with t(8;21)(q22;q22)/RUNX1::RUNX1T1, as well as in cases of AML with other RUNX1 rearrangements, copy number gains, or mutations. AML with plasmacytoid dendritic cell (pDC) differentiation (pDC-AML) containing clonally-related myeloblasts and neoplastic pDCs, are enriched for RUNX1 mutations and have been shown to exhibit B-cell marker expression. Here, we present two cases of pDC-AML with B-cell marker expression in which RUNX1 aberrations were not identified. Although previously we speculated on the role of RUNX1 in the aberrant expression of B-cell markers such in cases, the absence of RUNX1 lesions in the current cases supports the potential inherent ability of pDCs to express B-cell markers during maturation.