Effectiveness and Mechanism of Decitabine Maintenance Therapy in Patients with Medium and Low-risk Acute Myeloid Leukemia

Abstract

To investigate the efficacy and mechanism of decitabine maintenance therapy in patients with medium and low-risk acute myeloid leukemia(AML). The newly diagnosed medium- and low-risk AML patients in the Second Affiliated Hospital of Anhui Medical University from December 2016 to December 2020 were retrospectively analyzed. Seventy-eight AML patients who were still in remission after consolidation treatment were divided into maintenance treatment group (31 cases) and control group (47 cases). The maintenance treatment patients received decitabine at 20 mg/m2 IV daily for 5 days, every three months for 6 cycles, the control group was only observed and tested regularly. Follow-up was completed by telephone or by viewing outpatient or inpatient medical records. Primary indicators were overall survival (OS), and secondary indicators include relapse-free survival (RFS), tolerance, cellular immune function and analysis of risk factors related to survival. Median RFS in maintenance theatment and control groups was 30.1(26.2-33.8) months and 24.3(21.7-30.3) months (P=0.011), median OS 34.7(29.8-39.7) months and 27.7(24.1-31.3) months respectively（P=0.024）, with a statistically significant difference. For the univariate and multivariate Cox regression analysis, only the minimal residual disease (HR=25.185, P<0.001) and the treatment methods (HR=0.124, P<0.001) affected the PFS and OS of patients. In the maintenance treatment group, CD3+T cells, CD8+T cells and NK cells increased significantly after decitabine maintenance treatment, and the regulatory T cells decreased significantly (P<0.05). Patients had a low incidence of grade 3-4 adverse events, hematological adverse events were mainly neutropenia and thrombocytopenia, non-hematological adverse events were mainly digestive tract symptoms, and the patient was well tolerated. Maintenance treatment with decitabine provided benefit survival in patients with medium- and low-risk AML and is well tolerated. The mechanism may be inhibition the proliferation of regulatory T cells, induce and enhance the cytotoxic effect of CD8+ T cells on tumor antigens.