title: [Clinical efficacy of switching to 2nd generation of tyrosine kinase inhibitor on CML patients at poor responses to imatinib].
abstract: OBJECTIVE
  This study was to investigate the timing and clinical efficacy of switching to the 2nd generation of tyrosine kinase inhibitor (TKI) for CML patients at poor response to imatinib (dissatifed efficacy or intolerance).
  
  
  METHODS
  The therapeatic efficacy and side reaction of switched 2nd TKI in patients with newly diagnsed CML-CP who poorly responded to imatinib were observed, anong them 3 cases were intolerant, 6 cases did not acquire satisfied efficacy.
  
  
  RESULTS
  After switching to 2nd generation TKI, 3 patients with intolerance achieved complete cytogenetic remission (CCyR) in 3 months, and major molecular remission (MMR) in 3-6 months. All of them achieved optimal efficacy according to European Leukemia Network (ELN), but the pleural effusion appeared in 1 case after use of 2nd generation of TKI for 3 months, and the dadatinib was stoped temporally, and the curative efficacy still was maintained. Among 6 cases with poor efficacy by treatment with imatinib, 2 cases with BCR/ABL mutation progressed after switching 2nd generation of TKI, out of them 1 case with poor tolerance progeressed to the accelerated phase, but was cured by haploidentical allogeneic hematopoictic stem cell transplantation, 1 case progressed to blastic crisis and died of serious infection; the another 4 cases achieved MMR in 3-12 months after using 2nd generation of TKI, and maintained CMR for 12-36 months.
  
  
  CONCLUSIONS
  CML-CP patients without the optimal response to imatinib should be treated by switching to 2nd generation of TKI as soon as possible, and thereby patients may acquired satisfactory therapentic efficacy.
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China. E-mail: qiaojh@vip.sina.com.
authors: Jian-Hui
authors: JH
authors: Qiao
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Ze-Chuan
authors: ZC
authors: Zhang
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Bo
authors: B
authors: Yao
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Bing-Xia
authors: BX
authors: Li
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Mei
authors: M
authors: Guo
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Qi-Yun
authors: QY
authors: Sun
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Kai-Xun
authors: KX
authors: Hu
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Chang-Lin
authors: CL
authors: Yu
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Zheng
authors: Z
authors: Dong
authors: Department of Hematology, The Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
authors: Hui-Sheng
authors: HS
authors: Ai
mesh_terms: D001549:Benzamides; D001752:Blast Crisis; D003582:Cytogenetics; D016044:Fusion Proteins, bcr-abl; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D000068877:Imatinib Mesylate; D007938:Leukemia; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive; D009154:Mutation; D010879:Piperazines; D010996:Pleural Effusion; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D012074:Remission Induction; D016896:Treatment Outcome
chemical_list: D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl