title: Clinical significance of BCR-ABL fusion gene subtypes in chronic myelogenous and acute lymphoblastic leukemias.
abstract: BACKGROUND
  Some reports have suggested that chronic myeloid leukemia (CML) patients have a higher prevalence of M-bcr than acute lymphoblastic leukemia (ALL) patients, which show a higher prevalence of m-bcr. However, the relationship between BCR-ABL subtypes and progression of CML and ALL remains unclear.
  
  
  METHODS
  354 CML chronic phase (CML-CP) patients, 26 CML blastic phase (CML-BP) patients and 72 ALL patients before treatment with BCR-ABL positive were recruited for blood routine examination and bone marrow smear cytology. Some 80 CML-CP and 32 ALL patients after imatinib (IM) treatment were followed-up for BCR-ABL relative concentrations detected after treatment for 3, 6 and 9 months and 1 year.
  
  
  RESULTS
  Before treatment, CML-CP patients showed lower BCR-ABL relative concentrations with a higher proportion of M-bcr (42.7%) compared to CML-BP and ALL patients while ALL patients had a higher BCR-ABL relative concentration with high expression of m-bcr (51.4%). Patients with M-bcr demonstrated higher WBC counts than those with m-bcr and the mixed group and higher PLT counts were noted in the CML-CP and ALL groups. After imatinib (IM) treatment, patients with m-bcr showed higher BCR-ABL relative concentrations in both CML-CP and ALL groups.
  
  
  CONCLUSIONS
  This study identified the BCR-ABL gene as an important factor in CML and ALL cases. The M-bcr subtype was associated more with CML while the m-bcr subtype was associated more with ALL. Patients with m-bcr seem to have a poorer response to IM in either CML or ALL patients compared to M-bcr patients.
authors.affiliation: Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, China E-mail : docbwy@126.com; luxiaojun1972@163.com.
authors.forename: Yuan-Xin
authors.initials: YX
authors.lastname: Ye
authors.forename: Juan
authors.initials: J
authors.lastname: Zhou
authors.forename: Yan-Hong
authors.initials: YH
authors.lastname: Zhou
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhou
authors.forename: Xing-Bo
authors.initials: XB
authors.lastname: Song
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Lin
authors.forename: Bin-Wu
authors.initials: BW
authors.lastname: Ying
authors.forename: Xiao-Jun
authors.initials: XJ
authors.lastname: Lu
mesh_terms: D000293:Adolescent; D000328:Adult; D001549:Benzamides / Q000627:therapeutic use; D001752:Blast Crisis / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D016022:Case-Control Studies; D056905:Chromosome Breakpoints; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D010879:Piperazines / Q000627:therapeutic use; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055815:Young Adult
chemical_list: D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D012333:RNA, Messenger; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl