| ObjectiveWe elvaluated the clinical safety and efficacy of decitabine in patients with acutemyeloid leukemia or myelodysplastic syndromes accompanied with complex karyotype.MethodsFrom2009.04to2013.09, A total of16patients with MDS/AML accompanied withcomplex karyotype in First Affiliated Hospital of Soochow University were included forretrospective analysis. Decitabine was administered alone by20mg/m2for5days in allpatients.ResultsAmong16patients,9CR,2PR, overall response rate (CR and PR) was68.75%（11of16）.9patients with MDS, the CR rate was55.6%（5of9）;7patients with AML,overall response rate was85.7%(6of7).6patients with chromosome7aberration, overallresponse rate was66.7%（4of6）.7patients with3to5kinds of chromosomalabnormalities, and there are85.7%patients responsive;55.6%(5of9) patients with morethan5kinds of chromosomal abnormalities were responsive to treatment. A total of16patients, one course (5patients),≥two courses（11patients）, the overall response rate was40%and81.8%（P>0.05）. Grade3to4hematological toxicity was observed in8cases.Grade3to4infections were clinically documented in5patients, Grade1to2non-hematological toxicity contain infections (3patients), hematuria (1patients), bleeding (1patients). The last follow-up at2013.09,4patients were survival,7deaths,5were lost tofollow-up.4cases underwent allo-HSCT and they were still of relapse-free survival now.The median survival of16.1months (range,3~31months).ConclusionsThere are high efficacy, less treatment related side effects and better tolerance ofdecitabine treating MDS/AML with complex karyotype, especially for AML. If allogeneichematopoietic stem cell transplantation was given after complete response, It will improverecurrence-free survival rate. ObjectiveTo observe the clinical safety and efficacy of decitabine in patients of acute myeloidleukemia and myelodysplastic syndromes.MethodsTotally79patients with MDS/AML were divided into three groups:1) treated withdecitabine alone (20mg/m2for5days).2）combination with half dose AAG chemotherapy(Acla20mg qod×3d, Ara-C10mg/m2q12h×7d, G-CSF300ug qd, the dose of G-CSFadjust to the amount of blood routine).3) combination with AAG chemotherapy(Acla20mg qod×4d, Ara-C10mg/m2q12h×14d, G-CSF300ug qd, the dose of G-CSFadjust to the amount of blood routine). We observed the complete remission (CR) rate, theoverall response rate (ORR) and overall survival (OS rate) of the three groups, meanwhile,we analyzed the factors relevant to decitabine efficacy and the prognosis.ResultsThe overall response rate in the three groups were respectively53.3%,56.5%and 69.2%. There were no statistically significant between the three groups (P>0.05).underwent follow-up at2014.04,20patients were survival,45deaths,14were lost tofollow-up. The5-year cumulative survival rate of79patients was25.3%, the overallsurvival were of the three groups were respectively20.0%,21.7and34.6%. There were nostatistically significant between the three groups (P>0.05). COX analysis revealed thatwhether hematopoietic stem cell transplantation was given after treated with decitabine is aindependent prognostic factor. Adverse event mainly caused by decitabine was infectionand bleeding. Grade3to4hematological toxicity was observed in72cases, and theaverage time for the lack of granulocytes was14.8days.59patients accompanied withinfectious, including grade3or4infections in14cases, grade1or2infection in45cases.Rates of infection in the three groups were respectively60.0%,73.9%and61.5%, rates ofbleeding were6.7%.8.7%and3.8%, duration of neutrophenia were15.07,16.74and12.88days, mean MAP transfusion were9.3u,8.8u and8.9u, and mean platelet transfusion were58.4u,66.1u and84.6u. There were no statistically significant (P>0.05).79patients weresafely through bone marrow suppression by anti-infective and supportive treatment, notreatment-related deaths.ConclusionsTreating MDS/AML with decitabine alone, in combination with half course or onecourse CAG regimen have high efficacy. Comparely, the overall response rate of decitabinein combination with one course CAG regimen was higher. There were no statisticallysignificant in the side effects of three groups, such as duration of neutrophenia, rates ofinfection and rates of bleeding. ObjectiveTo detect the level of MDS/AML patients treated with decitabine and study therelationship between the level of DNA methylation in the tumor cells of MDS/AML anddecitabine. To discuss the mechanism of decitabine treating MDS/AML.MethodsTotally20patients of MDS/AML, including9AML (3MDS-AML),4MDS-RAEB-I,3MDS-RAEB-II,2MDS-RCMD. They were treated with decitabine20mg/m2×5d or combined with other chemotherapy regimens such as AAG. Collect thebone marrow samples of20patients before and after the treatment and then extract DNA.To design the methylation-specific and unmethylation-specific primers for PAX6, GDNFand TJP1gene. We employed methyladon-specific PCR(MSP) to examine the methylationstatus of PAX6, GDNF and TJP1gene in20MDS/AML patients. the gray value ofmethylated bands and unmethylated bands were detected and the change of methylationlevel before and after treatment with decitabine were analyzed.Results(1) Positive rates of PAX6, GDNF and TJP1genes were respectively85%,95%,100%before treatment. the methylation rate of PAX6decreased by10%after treatment,but there are no significant change in GDNF and TJP1gene.(2) We use the method ofcomparing the gray before and after the treatment to analyze experimental results. Theresults show that the gray value of PAX6, GDNF and TJP1gene decreased respectively26.8%,20.7%and5.2%after treatment with decitabine. For patients obtaining completeremission, the gray declined respectively32.3%,26.6%and14.1%. But in patients notobtaining complete remission, the gray of PAX6and GDNF were reduced by20.6%and14.7%. By contrast, the gray of TJP1gene rosed12.2%. ConclusionsDecitabine can partially reversed the methylation state of PAX6, GDNF and TJP1gene in the vivo of patients with MDS/AML, which provides a theoretical basis for clinicaltreatment. |
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