Abstract

Background: Acute myeloid leukemia is a type of hematological malignancy. Chemotherapy is the first-line treatment for AML. The main aim of treatment is to achieve complete remission in patients. Although complete remission is achieved in most patients, still the rate of relapse remains high. Recent studies revealed that drug resistance is an important cause of treatment failure in AML patients. Autophagy as a conserved catabolic process has a significant role in drug resistance of AML. Autophagy can act as a chemo-resistance mechanism in response to chemotherapy in AML patients. However, the role of this pathway in response to treatment of AML patients is not yet fully clarified. Objectives: The aim of this study was to investigate the effect of the BECN1 gene, as a key regulator of autophagy on remission and response to chemotherapy in AML patients. Methods: The BECN1 gene expression was evaluated in 30 AML patients at diagnosis stage, on 18 patients with complete remission and 15 controls using qRT-PCR. Results: The results showed that BECN1 gene expression level was significantly higher in AML patients than controls at the rate of 5/3 fold, P < 0.0001. We found that expression level of BECN1 was significantly reduced in patients with complete remission in comparison with newly diagnosed AML patients at the rate of 0.73 fold, P = 0.004. Conclusions: Low expression of BECN1 gene might be associated to complete remission. Therefore, perhaps BECN1 gene can be used as a biomarker to assess remission status. Moreover, targeting BECN1 can be used as a potential strategy to improve treatment in AML patients.

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