Decitabine: An effective and safe treatment for myelodysplastic syndrome and acute myeloid leukemia

被引:8
作者
Feng, Xianqi [1 ]
Chen, Xiangyun [3 ]
Nie, Shumin [2 ]
Chang, Yanyan [1 ]
Meng, Fanjun [1 ]
Zhou, Jingjing [1 ]
Mao, Chunxia [1 ]
Li, Tianlan [1 ]
Yan, Xueshen [1 ]
Huang, Junxia [1 ]
Liu, Shanshan [1 ]
Gao, Yan [1 ]
Xiao, Shuxin [1 ]
机构
[1] Qingdao Univ, Affiliated Hosp, Dept Hematol, Qingdao 266555, Peoples R China
[2] Qingdao Univ, Affiliated Hosp, Dept Neurol, Qingdao, Peoples R China
[3] Shandong Jining 1 Peoples Hosp, Dept Hematol, Jining, Peoples R China
关键词
Acute myeloid leukemia; chemotherapy; clinical efficacy; decitabine; myelodysplastic syndromes; safety; DNA METHYLATION; CANCER; 5-AZA-2'-DEOXYCYTIDINE; MULTICENTER; GENE; CHEMOTHERAPY; AZACITIDINE; EXPERIENCE; THERAPY; AGENT;
D O I
10.4103/0973-1482.204849
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: Decitabine is reported to be valuable in treating multiple malignant blood diseases. However, the application of decitabine in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML) has not been fully examined. Thus, our study aimed to investigate the clinical efficacy and safety of decitabine in treating such patients. Materials and Methods: Clinical data of MDS or AML patients treated with decitabine were retrospectively analyzed. All the patients were regularly followed up, and the risk factors affecting clinical efficacy were also detected. Results: A total of 36 patients (MDS, n = 27; AML, n = 9) were included in the study. The response rate of MDS patients was 55%, and there were three cases (15%) of complete remission (CR), three cases (15%) of marrow CR, and five cases (15%) of hematologic improvement. It was about three cycles to achieve the best efficiencies. Gender, age, percentage of blasts in bone marrow, International Prognostic Scoring System risk group, and cytogenetic factors were not associated with response rate. The median overall survival of MDS patients was 8 (1-44) months. Agranulocytosis (P = 0.037) and severe anemia (P = 0.044) were the independent factors for prognosis. The complete response rate of AML was 33.3%. From the investigation, infection was the most common complication in our cohort, especially lung infection with the incidence of 27.8%. Conclusions: Our data demonstrated that decitabine was effective and relatively safe in treating MDS and AML. Patients with agranulocytosis and severe anemia were prone to have poor survival, which should be monitored in clinical practice.
引用
收藏
页码:1471 / 1476
页数:6
相关论文
共 26 条
  • [1] Methylation status of the p15INK4B gene in hematopoietic progenitors and peripheral blood cells in myelodysplastic syndromes
    Aoki, E
    Uchida, T
    Ohashi, H
    Nagai, H
    Murase, T
    Ichikawa, A
    Yamao, K
    Hotta, T
    Kinoshita, T
    Saito, H
    Murate, T
    [J]. LEUKEMIA, 2000, 14 (04) : 586 - 593
  • [3] Epigenetic and chromatin modifiers as targeted therapy of hematologic malignancies
    Bhalla, KN
    [J]. JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (17) : 3971 - 3993
  • [4] Hypermethylation of the suppressor of cytokine signalling-1 (SOCS-1) in myelodysplastic syndrome
    Brakensiek, K
    Länger, F
    Schlegelberger, B
    Kreipe, H
    Lehmann, U
    [J]. BRITISH JOURNAL OF HAEMATOLOGY, 2005, 130 (02) : 209 - 217
  • [5] Clinical application and proposal for modification of the International Working Group (IWG) response criteria in myelodysplasia
    Cheson, Bruce D.
    Greenberg, Peter L.
    Bennett, John M.
    Lowenberg, Bob
    Wijermans, Pierre W.
    Nimer, Stephen D.
    Pinto, Antonio
    Beran, Miloslav
    de Witte, Theo M.
    Stone, Richard M.
    Mittelman, Moshe
    Sanz, Guillermo F.
    Gore, Steven D.
    Schiffer, Charles A.
    Kantarjian, Hagop
    [J]. BLOOD, 2006, 108 (02) : 419 - 425
  • [6] 5-Azacytidine and 5-aza-2′-deoxycytidine as inhibitors of DNA methylation:: mechanistic studies and their implications for cancer therapy
    Christman, JK
    [J]. ONCOGENE, 2002, 21 (35) : 5483 - 5495
  • [7] DNA methylation and gene silencing in cancer: which is the guilty party?
    Clark, SJ
    Melki, J
    [J]. ONCOGENE, 2002, 21 (35) : 5380 - 5387
  • [8] DNA methyltransferases as targets for cancer therapy
    Ghoshal, Kalpana
    Bai, Shoumei
    [J]. DRUGS OF TODAY, 2007, 43 (06) : 395 - 422
  • [9] Mechanisms of disease: Gene silencing in cancer in association with promoter hypermethylation
    Herman, JG
    Baylin, SB
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (21) : 2042 - 2054
  • [10] Jain N, 2007, 49 AM SOC HEM ANN M, P2858