The Clinical Significance of CD371 Expression Detected by Flow Cytometry in Primary Myelofibrosis

Objective This study aims to analyze the expression patterns of CD371 in CD34 + CD117 + bone marrow (BM) cells from patients with primary myelofibrosis (PMF) using flow cytometry (FCM), with a comparative evaluation against conventional antigens to assess its potential clinical utility for identifying aberrant immunophenotypes in PMF. Methods A retrospective analysis was conducted on BM samples from 26 PMF patients and 20 control individuals. We evaluated the proportions of CD34 + CD117 + cells and basophils, as well as the expression profiles—including positive cell percentages, mean fluorescence intensity (MFI), and coefficient of variation (CV) of MFI—of CD371, CD34, CD117, CD13, CD33, CD123, CD38, HLA‐DR, and CD7 within the CD34 + CD117 + population. Results Control group exhibited consistent bimodal CD371 expression, while PMF samples showed three distinct patterns. PMF demonstrated significant differences vs. controls in CD371 MFI ( p < 0.01), MFI CV ( p < 0.01), and CD371 + cell proportion ( p < 0.05). Within CD371 + cells, MFI and MFI CV also differed significantly (both p < 0.01). Significant differences ( p < 0.01) were observed in: CD34 + CD117 + proportion, CD34 MFI/MFI CV, basophil proportion, CD38 dim+ proportion/CD38 MFI/MFI CV. No significant differences were observed for CD13 + cell proportion ( p = 0.154) or CD13 MFI ( p = 0.835), though the MFI CV was significantly different ( p < 0.01). CD33 + cell proportion ( p < 0.05) and CD33 MFI ( p < 0.05) showed significant differences, while the MFI CV did not ( p = 0.276). Conclusion This study provides the first characterization of CD371 expression patterns in PMF, showing significantly different expression profiles compared to controls. While CD371 demonstrated comparable performance to standard markers (CD34/CD38/CD13/CD33) and showed better discrimination than CD123/HLA‐DR, these preliminary findings suggest its potential utility for: (1) identifying abnormal CD34 + CD117 + populations in PMF, and (2) possible integration into routine clinical workflows, pending further validation in larger cohorts.