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Updated: Jan 27, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
Published on: September 1, 2019
B-cell marker expression in acute myeloid leukemia with plasmacytoid dendritic cell differentiation (pDC-AML) without
Giby V George1, Neel V Hegde2, Hong Fang3
1Department of Pathology, University of Pennsylvania, Philadelphia, PA, USA.
None:
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.
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