Expressions of TGF-β1 and VEGF in patients with acute myeloid leukemia and associations with prognosis

Author:

Xu Yan1,Yu Xianqiu2,Zhang Xinlong1

Affiliation:

1. Hematology, The People’s Hospital of Danyang , Affiliated Danyang Hospital of Nantong University , China

2. Hematology, Affiliated Hospital of Jiangsu University , China

Abstract

Abstract Background: To study the expressions of transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor (VEGF) in patients with acute myeloid leukemia (AML) and their values for prognosis. Methods: A total of 120 AML patients treated from January 2015 to December 2018 were selected. Bone marrow mononuclear cells were isolated. The expressions of TGF-β1 and VEGF were detected by RT-PCR, and their associations with clinical characteristics were analyzed. The overall survival (OS) and disease-free survival (DFS) were assessed using the Kaplan-Meier method. The risk factors for prognosis were analyzed through the Cox proportional hazards model. Results: The AML group had significantly lower relative expression of TGF-β1 and higher relative expression of VEGF than those of the control group (P<0.05). TGF-β1 and VEGF levels were significantly correlated with white blood cell count, hemoglobin, platelets, and peripheral blood juvenile cells (P<0.05). TGF-β1 level was higher and VEGF level was lower in the patients with complete response than those in the patients with partial response and no response (P<0.05). Both OS and DFS of the patients with high TGF-β1 expression were better than those of the patients with low TGF-β1 expression, while they were also superior among the patients with low VEGF expression (P<0.05). Platelets, TGF-β1 and VEGF were independent influencing factors for OS, and white blood cells, TGF-β1 and VEGF were independent influencing factors for DFS (P<0.05). Conclusions: AML patients have decreased expression of TGF-β1 and increased expression of VEGF, and such changes are closely associated with the prognosis of AML.

Publisher

Walter de Gruyter GmbH

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