title: Evi-1 and MDS1-Evi-1 genes in pathogenesis of myelodysplastic syndromes and post-MDS acute myeloid leukemia.
abstract: OBJECTIVE
  To investigate expression of Evi-1 and MDS1-Evi-1 genes in myelodysplastic syndromes (MDS) and post-MDS acute myeloid leukemia (post-MDS AML), and its role in pathogenesis or progression of MDS and post-MDS AML.
  
  
  METHODS
  Expression of Evi-1 and MDS1-Evi-1 genes was examined in 31 MDS, 11 post-MDS AML, and 34 de novo AML patients by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Evi-1 expression was not detected in bone marrow samples of 8 normal controls, but low MDS1-Evi-1 expression levels (MDS1-Evi-1/GAPDH < 0.1) were detected in 3 of the 8 controls. Evi-1 RNA was expressed in 1 of 8 RA, 8 of 13 RAEB and 6 of 9 RAEB-T patients, and the percentage of Evi-1 expression in RAEB(T) patients was higher than that in RA (P < 0.05). MDS1-Evi-1 expression was detected in 5 of 8 RA, 9 of 13 RAEB and 5 of 9 RAEB-T patients, and MDS1-Evi-1 expression levels (MDS1-Evi-1/GAPDH > 0.1) were markedly higher than those in the controls. Evi-1 expression was gradually increased in 4 of 5 RAEB-T patients with transformation from MDS to AML. The percentages of Evi-1 and MDS1-Evi-1 expression in post-MDS AML patients were significantly (P < 0.01 and P < 0.05 respectively) higher than those in de novo AML. The colonies of hematopoietic progenitor cells were decreased in Evi-1 and MDS1-Evi-1-positive MDS patients as compared with those in Evi-1 and MDS1-Evi-1-negative patients.
  
  
  CONCLUSIONS
  Abnormal expression of the Evi-1 gene and overexpression of MDS1-Evi-1 gene may play a role in the pathogenesis or progression of MDS and post-MDS AML.
authors.affiliation: Institute of Hematology, Chinese Academy Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
authors.forename: K
authors.initials: K
authors.lastname: Xu
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Hao
authors.forename: Z
authors.initials: Z
authors.lastname: Shao
authors.forename: Q
authors.initials: Q
authors.lastname: Meng
authors.forename: K
authors.initials: K
authors.lastname: Li
authors.forename: H
authors.initials: H
authors.lastname: Chao
authors.forename: K
authors.initials: K
authors.lastname: Tang
authors.forename: L
authors.initials: L
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics*; D005260:Female; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000209:etiology / Q000235:genetics*; D000074008:MDS1 and EVI1 Complex Locus Protein; D008297:Male; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000209:etiology / Q000235:genetics*; D009363:Neoplasm Proteins; D015514:Oncogene Proteins, Fusion; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics; D011519:Proto-Oncogenes; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis / Q000235:genetics*; D014157:Transcription Factors; D016335:Zinc Fingers
chemical_list: D004268:DNA-Binding Proteins; D000074008:MDS1 and EVI1 Complex Locus Protein; C098704:MDS1-EVI1 fusion protein, human; C063575:MECOM protein, human; D009363:Neoplasm Proteins; D015514:Oncogene Proteins, Fusion; D011506:Proteins; D011993:Recombinant Fusion Proteins; D014157:Transcription Factors