Abstract
Acute myeloid leukemia (AML) is a heterogeneous group of disorders with distinct characteristics and prognoses. Although cytogenetic changes and gene mutations are associated with AML prognosis, there is a need to identify further factors. CD56 is considered a prognostic factor for AML, which is abnormally expressed in leukemia cells. However, a clear consensus for this surface molecule is lacking, which has prompted us to investigate its prognostic significance. Bone marrow samples of de novo non-M3 AML were collected to detect CD56 expression using multiparameter flow cytometry (FCM). As a result, the CD56 expression in de novo non-M3 AML was found to be significantly higher than that in acute lymphoma leukemia (ALL, P = 0.017) and healthy controls (P = 0.02). The X-Tile program produced a CD56 cutoff point at a relative expression level of 24.62%. Based on this cutoff point, high CD56 expression was observed in 29.21% of de novo non-M3 AML patients. CD56-high patients had a poor overall survival (OS, P = 0.015) compared to CD56-low patients. Bone marrow transplantation (BMT) improved OS (P = 0.004), but a poor genetic risk was associated with an inferior OS (P = 0.002). Compared with CD56-low patients, CD56-high patients had lower peripheral blood platelet (PLT) counts (P = 0.010). Our research confirmed that high CD56 expression is associated with adverse clinical outcomes in de novo non-M3 AML patients, indicating that CD56 could be used as a prognostic marker for a more precise stratification of de novo non-M3 AML patients.
Highlights
Acute myeloid leukemia (AML) is a heterogeneous hematopoietic malignancy caused by the malignant proliferation of immature myeloid cells
Patients diagnosed with therapy-related myeloid neoplasms (t-AML), AML derived from myelodysplastic syndrome (MDS), or secondary to other malignancies (AHD AML) were excluded because of the complexity of these clinical conditions
And 1(b), the independent-sample t-test indicated that de novo non-M3 AML patients showed a higher intensity of the CD56 expression compared with acute lymphoma leukemia (ALL) (P = 0:017) or the healthy controls (P = 0:02). This indicates that the CD56 antigen is more likely to be highly expressed in AML cells
Summary
Acute myeloid leukemia (AML) is a heterogeneous hematopoietic malignancy caused by the malignant proliferation of immature myeloid cells. AML can be divided into eight subtypes, from M0 to M7, according to the French-AmericanBritish (FAB) classification of AML. It can be classified into four major types, according to the 2016 WHO classification [2]. Patients with AML respond variably to treatment as a result of clinical and genetic heterogeneity [3,4,5]. Recent advances in genetic markers have stratified patients with AML into favorable, intermediate, and adverse ELN risk categories. This stratification cannot fulfill all clinical situations, and patients with refractory AML are found across all risk groups [6]. This suggests that certain nongenetic factors play an important role in the prognosis of AML, indicating that AML patients require a more precise prognostic stratification
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