CMML and Plasmacytoid Dendritic Cells: A Flow Cytometry Diagnostic Trap

A case where the classification changed after the timeline was recovered

Chen, Liu and Ren published a peer-reviewed case report on 22 October 2026 in Frontiers in Oncology (DOI 10.3389/fonc.2026.1961676). An 88-year-old man with a marrow plasmacytoid dendritic cell (pDC) expansion was initially classified as myelodysplastic neoplasm with increased blasts 2 (MDS-IB2). A later reconstruction of persistent monocytosis and the integrated morphology supported chronic myelomonocytic leukemia (CMML-2). This is a diagnostic observation involving one patient, not a prospective performance study of a flow cytometry panel.

The case illustrates how apparently precise numbers can describe different compartments. The reported blood absolute monocyte count was approximately 4.12 x 10^9/L, representing 35.3% of leukocytes. Marrow morphology recorded 13.5% blasts in its own assessment, while multiparameter flow cytometry reported 3.54% aberrant immature myeloid cells and a distinct 8.60% pDC-like population. The numbers should not be placed in one denominator or treated as interchangeable measures of blasts. Flow enumeration, aspirate morphology and final classification follow different methods and definitions.

Recognise a pDC-associated phenotype without overcalling it

The reported pDC-like population was positive for CD4, brightly CD123-positive and CD303-positive, with partial CD304 and negative CD34, CD117 and CD56. Those findings supported a mature pDC interpretation in context. They did not alone prove that every pDC-like event was neoplastic, nor did they establish blastic plasmacytoid dendritic cell neoplasm (BPDCN). An atypical cluster on a CD123 plot is a prompt for a differential, not a diagnosis by itself.

When pDC expansion accompanies a myeloid neoplasm, panel selection should distinguish immature myeloid blasts, mature pDC, other dendritic-lineage cells and background populations. The investigation may need markers beyond those in a screening tube. In this case the authors acknowledge incomplete BPDCN-related marker characterization, including absence of TCF4/TCL1 assessment. No isolated pDC population was tested genomically. Therefore the case does not demonstrate that the expanded pDC cells share the patient's myeloid mutations.

Why the longitudinal full blood count mattered

Persistent peripheral monocytosis documented before the final diagnostic assessment altered how the marrow and ancillary studies were interpreted. The WHO fifth-edition CMML framework requires both absolute and relative monocytosis, with additional lineage, blast and exclusion criteria. In a transferred chart, missing previous differential counts can lead the interpreting team to anchor on the present aspirate morphology alone. A useful laboratory workflow therefore makes historical monocyte trends visible alongside current flow findings.

Reported monosomy 7 and a TP53 variant were relevant genomic context, but they do not settle pDC lineage clonality without a suitable cellular linkage. That inference would require isolated-cell or other appropriately designed evidence. Equally, aberrant marrow precursors and mature pDC must not be combined just because both are visually unusual; doing so may distort the apparent blast burden and risk category. The paper also describes several incomplete exclusion tests and the absence of a repeat marrow evaluation at one phase.

CFCM diagnostic checklist for similar questions

Before suggesting a change of diagnostic category, compare current and historical complete blood counts with differential, slide morphology, relevant immunophenotypes and the classification criteria applicable to the work-up. Preserve acquisition plots and marker definitions for both blast and pDC gates. Ask whether apparent monocytosis could be reactive and whether competing myeloid or tyrosine-kinase-associated entities have been appropriately excluded. Be explicit about which cellular populations were actually tested for variants.

This does not authorize CFCM to assign a patient diagnosis from a panel or to recommend treatment. Morphology, clinical history, molecular tests and integrated hematopathology remain necessary. The appropriate take-away is a diagnostic reasoning pathway to verify locally, not a stand-alone pDC flow algorithm or an estimate of CMML prevalence.

Daily Learning Pill — an unusual population is not an extra blast count

Flow cytometry is most valuable when a small population is identified and interpreted within a disease framework. Separate the flow pDC fraction from morphological blast estimates and from longitudinal blood monocytosis. The compartments, methods and diagnostic meanings differ even when each number is technically correct.

Evidence boundary, rights and further CFCM learning

This article critically interprets a single peer-reviewed case report. Sections read: Case presentation, immunophenotypic and genetic findings, diagnostic reasoning and Discussion. No original FCS files, histology image data, or independently stained samples were available. A previous request to the authors for Figure 2 has SENT status only, not reuse clearance; CFCM uses an independently produced conceptual diagram instead. This is not independent clinical validation or a recommendation for patient management.

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