ABSTRACT
Objective To investigate the safety and efficacy of decitabine combined with CAG regimen in treatment of acute myeloid leukemia (AML) ineligible for conventional chemotherapy. Methods The data of 20 cases with AML ineligible for conventional chemotherapy from January 2013 to May 2015 were retrospectively analyzed. Decitabine combined with CAG regimen was used during induction therapy. The primary induction regimen was used 26 times after remission, the standard 3+7 regimen were used 7 times, and intermediate-dose cytarabine were used 3 times. The total course of treatment included 2-8 cycles. Results All of the 20 patients completed the first cycle of induction therapy, including 11 cases of complete remission (CR), 5 cases of partial remission and no response in 4 cases, and the overall response rate (ORR) was 80 % (16/20). ORR was 69.2 % (9/13) and 100.0 % (7/7) in high-risk group and middle-low risk group respectively. ORR was 60.0%(6/10) in AML evolving from MDS. 8 patients were infected during the induction therapy and the infection rate was 40.0% (8/20). 2 patients were died of pulmonary infection. The median number of suspended red blood cell and platelet infused were (9.1±5.7) U and (57.5±51.9) U respectively. Neutrophil recovery time was (8.7±5.6) days during induction therapy. All patients were followed up for at least 1 year, and 12 cases were dead. Overall survival rate was 85.0%at 3 months, 80.0%at 6 months, and 40.0%at 1 year. While in 12 CR patients relapse-free survival rate was 75.0%at 3 months, 75.0%at 6 months,and 65.6%at 1 year respectively. Conclusion Decitabine combined with CAG regimen with high remission rate and well tolerance, can be used as a first therapy for AML ineligible for conventional chemotherapy.
ABSTRACT
ObjectiveToll-like receptors (TLRs) play important role in the progression and tumor immunity of some types of cancer,some research have demonstrated that agonist of TLR3 can trigger apoptosis of cancers.This study was proposed to investigate if Poly(I:C),the specific agonist of TLR3,could impact proliferation or apoptosis of progressive breast cancer cells MDA-MB-231,and to investigate the primary mechanism of the function.MethodsExpression of TLR1-10 mRNA was detected by quantitative real-time reverse transcription-polymerase chain reaction.Cell Counting Kit-8 was used to determine the inhibitory effect of Poly(I:C) on proliferation of MDA-MB-231 cells.Cell apoptosis was assayed by flow cytometry with V-FITC/PI staining.Results First,the toll-like receptors 1-10 were all expressed on MDA-MB-231 cells,while the expression level of TLR8 was lower than that of others.Second,according to the CCK-8,the proliferation of MDA-MB-231 cells was inhibited,but the apoptosis was not affected on the basis of Apoptosis Kit.At last,the mRNA expression of TNF-α、IFN-β and IFN-γ were elevated approximately 20 times after Poly(I:C) stimulation for 6 hours.ConclusionMDA-MB-231 cells express all toll-like receptors on mRNA level,and TLR8 was expressed lower than others.The stimulation of TLR3 with Poly(I:C) can inhibit the proliferation of MDA-MB-231,but had no effect on apoptosis.TNF-α、IFN-β and IFN-γ maybe participate in this process.