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April 23, 2026Annals of Hematology0 citationsOpen Access

Distinct immunophenotypic and clinical features of TP53-mutated acute myeloid leukemia: high CD34/CD41 expression and lower leukocyte counts

SPSongyi ParkSKSang-A KimSKSheehyun Kim

Key Points

  • The aim is to investigate the unique clinical and molecular characteristics of TP53-mutated acute myeloid leukemia (AML).
  • Conducted a retrospective analysis of 336 AML patients
  • Compared TP53-mutated and non-mutated cases regarding immunophenotypic and clinical features
  • Analyzed the association of TP53 mutations with leukocyte counts and response rates.
  • TP53-mutated AML showed 12.5% dual positivity for CD34/CD41 versus 1.3% in non-mutated AML (p < 0.001)
  • Lower white blood cell counts in TP53-mutated cases (p = 0.016)
  • Significantly lower complete response rates and shorter overall/progression-free survival for TP53-mutated AML.

Abstract

This study investigates the clinical and molecular characteristics of TP53-mutated acute myeloid leukemia (AML), associated with a poor prognosis. A retrospective analysis was conducted on 336 AML patients, focusing on the distinctions between TP53-mutated and non-mutated cases. Our findings reveal that TP53 mutations are linked to a higher proportion of leukemic blasts positive for the primitive stem cell markers CD34 and CD41 (with dual positive: 12.5% vs. 1.3%, p < 0.001), suggesting a more stem/progenitor cell-like nature. Patients with TP53-mutated AML exhibited lower white blood cell counts in peripheral blood (p = 0.016) and reduced blast proportion in bone marrow (with a median of 39.6% in TP53-mutated AML and 56.9% in TP53 wild-type AML, p = 0.01) at diagnosis. TP53-mutated AML was frequently found in therapy-related AML cases and occurred with fewer concurrent genetic mutations compared to non-mutated AML. In terms of outcomes, TP53 mutations corresponded with significantly lower composite complete response rates and shorter overall and progression-free survival. This study highlights the distinct clinical, molecular, and immunophenotypic features of TP53-mutated AML and emphasizes the need for improved therapeutic strategies for this high-risk subtype.

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Cite This Study

Park et al. (2026) studied this question.

synapsesocial.com/papers/69e9b6aa85696592c86eb11bhttps://doi.org/10.1007/s00277-026-07001-4
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