ABSTRACT
Objective:To investigate the effect of chidamide combined with arsenic acid on the proliferation inhibitory of T cell lymphoma Hut-78 cells and its mechanism.Methods:Low concentration group included 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide + 4.0 μmol/L arsenic trioxide). High concentration group included 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide + 6.0 μmol/L arsenic trioxide). Both groups were used to treat Hut-78 cells for 24 h and 48 h, respectively. Cell proliferation of Hut-78 cells in all drug treatment groups was tested by using methyl thiazolyl tetrazolium (MTT) method, and the proliferation inhibitory rate was also calculated. The expressions of vascular endothelial growth factor (VEGR) and bcl-2 protein of Hut-78 cells in different drug treatment groups by using Western blotting.Results:The cell proliferation inhibitory rate of Hut-78 cells treated for 24 h of 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) was (8.8±0.1)%, (9.2±0.5)% and (11.0±0.1)%, respectively ( F = 12.45, P < 0.05); The cell proliferation inhibitory rate of Hut-78 cells treated for 48 h was (19.1±0.5)%, (18.3±0.9)%, (23.1±1.3)%, respectively ( F = 9.86, P < 0.05). The cell proliferation inhibitory rate of Hut-78 cells treated for 24 h of 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) was (15.4±0.9)%, (13.2±0.9)% and (18.2±1.1)%, respectively ( F = 7.06, P < 0.05); The cell proliferation inhibitory rate of Hut-78 cells treated for 48 h was (28.5±1.2)%, (31.3±0.8)%, (45.2±2.1)%, respectively ( F = 14.32, P < 0.05). When Hut-78 cells were treated with 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) for 24 h, the relative expression level of bcl-2 protein was (58.4±2.9)%, (55.9±3.8)%, (53.2±2.1)%, respectively ( F = 17.52, P < 0.05); the relative expression level of VEGF protein was (60.5±4.2)%, (57.5±2.8)%, (50.9±3.5)%, respectively ( F = 7.36, P < 0.05). When Hut-78 cells were treated with 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) for 48 h, the relative expression level of bcl-2 protein was (48.2±1.8)%, (40.1±2.2)%, (32.3±3.1)%, respectively ( F = 10.38, P < 0.05); the relative expression level of VEGF protein was (51.4±4.1)%, (48.9±2.9)%, (40.8±3.8)%, respectively ( F = 8.96, P < 0.05). When Hut-78 cells were treated with 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) for 24 h, the relative expression level of bcl-2 protein was (55.4±3.1)%, (42.5±2.8)%, (37.8±4.2)%, respectively ( F= 10.35, P < 0.05); the relative expression level of VEGF protein was (49.2±3.4)%, (42.1±4.9)%, (34.3±5.1)%, respectively ( F= 17.82, P <0.05). When Hut-78 cells were treated with 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) for 48 h, the relative expression level of bcl-2 protein was (40.1±0.9)%, (35.3±1.6)%, (27.8±2.4)%, respectively ( F = 15.36, P < 0.05); the relative expression level of VEGF protein was (40.3±3.8)%, (35.9±4.6)%, (20.1±2.9)%, respectively ( F = 9.78, P < 0.05). Conclusion:Chidamide and arsenic trioxide have synergistic inhibitory effects on T cell lymphoma Hut-78 cells, which may be related to the down-regulated expressions of bcl-2 and VEGR.
ABSTRACT
Objective:To explore the clinical effect of azacitidine combined with CAG regimen on the treatment of relapsed/refractory acute myeloid leukemia (AML).Methods:The data of 50 patients with relapsed/refractory AML (non-acute promyelocytic leukemia) in Jining No. 1 People's Hospital from September 2018 to September 2019 was retrospectively analyzed, and the patients were divided into the control group and the test group according to the different treatment drugs. The control group (28 cases) was treated with CAG regimen alone, and the test group (22 cases) was treated with azacitidine combined with CAG regimen. The total effective rate and adverse reactions of the two groups were observed after 1 course of treatment.Results:After one course of treatment, the total clinical effective rate in the test group was 86% (19/22), and the rate in the control group was 71% (20/28), there was a statistically significant difference between the two groups (χ 2 = 5.273, P < 0.05). There were no significant differences in the incidence of adverse reactions such as fever, pulmonary infection, vomiting, and thrombocytopenia between the two groups (all P > 0.05). Conclusion:Azacitidine combined with CAG regimen in the treatment of relapsed/refractory AML can improve the clinical efficacy without increasing the adverse reactions.
ABSTRACT
Inrecentyearsmanytargetedagentstreatinggastriccancerhavebeenevaluatedinclinical studies.Trastuzumab,an anti-HER-2 monoclonal antibody,has shown activity against HER-2-positive gastric cancer and become the first targeted agent approved in gastric cancer.Drugs targeting epidermal growth factor receptor,including monoclonal antibody and tyrosine kinase inhibitor,bring survival benefit to patients with gastric cancer.Addi tionally,vascular endothelial growth factor inhibitors are also under investigation.Other targeted agents are in preclinical or early clinical development,such as m-TOR inhibitors and c-MET inhibi-tors.