Abstract:

Objective To investigate the role of transform growth factor β₁ (TGF-β₁) in pathogenesis of hyperleukocytic acute myeloid leukemia (AML).Methods The mRNA transcription levels of TGF-β₁ from bone marrow mononuclear cells (BMMNC) in 38 AML patients, protein expression levels of intracellular TGF-β₁ from BMMNC in 48 AML patients, and serum levels of TGF-β₁ from 40 AML patients were measured by real-time fluorescence quantitative polymerase chain reaction (RQ-PCR), flow cytometry, and double-antibody sandwich enzyme-linked immunosorbent assay (ELISA), respectively. Results The relative levels of the TGF-β₁ gene expression among hyperleukocytic AML patients, non-hyperleukocytic AML patients, and NC has no significant difference (P>0.05). The protein expression levels of TGF-β₁ in both hyperleukocytic AML and non-hyperleukocytic AML patients were significantly higher than that in NC (P<0.05), the plasma levels were significantly lower than that in NC (P<0.05). There was no significant difference in intracellular protein expression levels and plasma levels of TGF-β₁ between hyperleukocytic AML and non-hyperleukocytic AML patients (P>0.05). There was no significant difference in intracellular protein expression levels and plasma levels of TGF-β₁ between the FAB subtypes in hyperleukocytic and non-hyperleukocytic AML (P>0.05). Conclusion Decreased serum levels of TGF-β₁ may be involved in the pathogenesis of AML. However, decreased TGF-β₁ serum levels may not reflect reduced TGF-β₁ production by BMMNC. Our study showed that TGF-β₁ had no important impact on the pathogenesis of hyperleukocytic AML.

Key words: transform growth factor β₁, acute myeloid leukemia, hyperleukocytic