title: [Study on mismatch repair genes of chronic myeloid leukemia].
abstract: OBJECTIVE
  To investigate the expression and regulation mechanism of mismatch repair (MMR) genes in chronic myeloid leukemia (CML).
  
  
  METHODS
  Expression of MMR genes hMSH2, hMSH3, hMSH6, hMLH1 and hPMS2 mRNAs in 62 CML patients and K562 cell line were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of bcr-abl mRNA and MMR genes mRNA were detected by RT-PCR in 26 CML patients with allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and 4 CML patients on imatinib treatment. Expression of bcr-abl mRNA was detected by RT-PCR and tyrosine phosphorylation of BCR-ABL fusion protein by Western blot.
  
  
  RESULTS
  Expression of hMSH2, hMSH3 and hMLH1 mRNA was significantly lower in CML and K562 cells than in normal control (P < 0.05). In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased. In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.
  
  
  CONCLUSIONS
  Expressions of hMSH2, hMSH3 and hMLH1 mRNA were down-regulated by bcr-abl fusion gene.
authors.affiliation: Department of Hematology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Luo
authors.forename: Zhi-gang
authors.initials: ZG
authors.lastname: Peng
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Yong-rong
authors.initials: YR
authors.lastname: Lai
authors.forename: Yu-ying
authors.initials: YY
authors.lastname: Lu
authors.forename: Shan-jun
authors.initials: SJ
authors.lastname: Song
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000494:pharmacology; D001549:Benzamides; D053843:DNA Mismatch Repair; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D000068877:Imatinib Mesylate; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010879:Piperazines / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D012333:RNA, Messenger; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl