title: [Clinical and biological characteristics of childhood acute myeloid leukemia with EVI1 gene positive expression].
abstract: OBJECTIVE
  To study the expression of ecotropic viral integration site (EVI1) gene in childhood acute myeloid leukemia (AML) and the clinical features of EVI1-positive children with AML.
  
  
  METHODS
  The clinical data of EVI1-positive children with AML were collected and analyzed. RT-PCR and real-time quantitative PCR were used for qualitative and quantitative analysis of expression of EVI1. Flow cytometry (FCM) was used for determining the immunophenotypes of bone marrow cells. Multiparameter FCM was used for monitoring minimal residual disease. The karyotypes were determined.
  
  
  RESULTS
  Of 241 children with AML, 33 (13.7%) were positive for EVI1 expression. There were no significant differences in age at first visit as well as the white blood cell count, hemoglobin level, and platelet count in peripheral blood between EVI1-positive and EVI1-negative children with AML (P>0.05), but EVI1-positive children had a significantly increased proportion of females compared with EVI1-negative children (P<0.05). The change in EVI1 expression was not synchronous with clinical remission and the change of MRD: some children had clinical remission or negative conversion of MRD before negative conversion of EVI1, while some had negative conversion of EVI1 before clinical remission or while MRD showed positive. EVI1 gene was usually co-expressed with other fusion genes. CD33 (100%), CD38 (88%), and HLADR (76%) were highly expressed in EVI1-positive children with AML. Abnormal chromosome structure or number was found in 15 patients. Compared with EVI1-negative children, EVI1-positive children had significantly lower complete remission rates after the first course of treatment (P<0.05).
  
  
  CONCLUSIONS
  EVI1-positive children with AML have a poor short-term prognosis. In the development of AML, the activation of EVI1 gene is not isolated, but the result of interactions with other genes or chromosome abnormalities, and the mechanism of activation and its function need further study.
authors.affiliation: Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Scinence and Technology, Wuhan 430022, China. erke_xiehe@aliyun.com.
authors.forename: Min
authors.initials: M
authors.lastname: Jiang
authors.forename: Xiao-Qing
authors.initials: XQ
authors.lastname: Li
authors.forename: Dong
authors.initials: D
authors.lastname: Hu
authors.forename: Yi-Ning
authors.initials: YN
authors.lastname: Qiu
authors.forename: Zhi-Quan
authors.initials: ZQ
authors.lastname: Zhang
authors.forename: Bing-Yu
authors.initials: BY
authors.lastname: Zhang
authors.forename: Juan
authors.initials: J
authors.lastname: Han
authors.forename: Run-Ming
authors.initials: RM
authors.lastname: Jin
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D005434:Flow Cytometry; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D016130:Immunophenotyping; D007223:Infant; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000276:immunology; D000074008:MDS1 and EVI1 Complex Locus Protein; D008297:Male; D018365:Neoplasm, Residual; D011379:Prognosis; D011519:Proto-Oncogenes / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D000074008:MDS1 and EVI1 Complex Locus Protein; C063575:MECOM protein, human; D014157:Transcription Factors