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Pulp cell-like protrusion cells (pDC) are the protrusion cells that produce the main natural type I interferon.
tumor amplification of
pDC and pDC premeditations leads to maternal cell-like degenerative cell tumors (BPDCN), which has been described in chronic granulocyte monocytoblast leukemia (CMML).
but the role of pDC amplification in acute myeloid leukemia (AML) is unclear.
study, the researchers outlined the characteristics of patients with PDC amplification-positive AML (pDC-AML).
pDC-AML accounts for about 5% of AML.
pDC-AML typically has cross-spectrum antigen expression and has a poor risk stratation associated with prognostic differences.
runX1 mutation is the most common somogenal cell mutation in pDC-AML, and is more common than AML without pDC amplification and BPDCN.
that pDC originated in pDC-AML in leukemia mother cells, and its cloning is closely related.
leukemia mother cells, which are the source of RUNX-mutant AML, can be adjusted for pDC transcription, allowing cells to differentiate and amplification to pDC.
, tagraxofusp, a targeted drug that directly targets CD123, reduces the leukemia burden of patient-sourced transplant tumor models and eliminates pDC.
, pDC-AML is characterized by runX1 high-frequency mutations and an increase in the expression of pDC transcription programs.
target CD123 may be a potential treatment for pDC-AML.
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