title: [EVI1 expression, clinical and cytogenetical characteristics in 447 patients with acute myeloid leukemia].
abstract: Objective:To investigate EVI1 expression and its associated clinical and cytogenetic characteristics in 447 acute myeloid leukemia (AML) patients.Methods:EVI1 expressions were measured in 447 AML cases from Jan. 2007 to Apr. 2015 to couple with clinical, cytogenetic and mutations' characteristics to summarize the features of AMLs with high EVI1 expression.Results:17.9% of AML were high EVI1 expression (EVI1+), and the remainder low EVI1 expression (EVI1-). No significant differences between the two groups in terms of age, sex, hemoglobin level, white blood cell count and platelet count were observed. More M0, M5and M6subtypes were observed in EVI1+group (P= 0.027, 0.004 and 0.011, respectively). Cytogenetic abnormalities of 11q15, 11q23/MLL, 3q26, -7/7q- and t (9;11) were observed more frequently in EVI1+group (P<0.001, <0.001, <0.001, <0.001, =0.014, respectively). Normal karyotype, inv (16), t (8;21) were observed more frequent in EVI1-group (P=0.001, 0.009, 0.002, respectively). EVI1+was more observed in high risk cytogenetics. Mutation of NPM1 was more observed in EVI1-group (P<0.001). Remission rate in EVI1+group was significantly lower than EVI1-group (P<0.001). Leukemia-free survival was improved in EVI1+AML patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT).Conclusions:High EVI1 expression was more observed in FAB subgroup M5, harbored more cytogenetic abnormalities of 11p15, 11q23/MLL, 3q26 rearrangement, -7/7q- and t (9;11). Remission rate of high EVI1 expression AML was lower, which could be improved by allo-HSCT.
authors.affiliation: Jiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, Collaborative Innovation Center of Hematology, Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, Suzhou 215006, China.
authors.forename: X F
authors.initials: XF
authors.lastname: He
authors.forename: Q R
authors.initials: QR
authors.lastname: Wang
authors.forename: J N
authors.initials: JN
authors.lastname: Cen
authors.forename: H Y
authors.initials: HY
authors.lastname: Qiu
authors.forename: A N
authors.initials: AN
authors.lastname: Sun
authors.forename: S N
authors.initials: SN
authors.lastname: Chen
authors.forename: D P
authors.initials: DP
authors.lastname: Wu
mesh_terms: D000293:Adolescent; D000328:Adult; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D003582:Cytogenetics; D004268:DNA-Binding Proteins; D005260:Female; D006801:Humans; D007948:Leukemia, Monocytic, Acute; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology; D000074008:MDS1 and EVI1 Complex Locus Protein / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D000090243:Nucleophosmin; D011379:Prognosis; D011519:Proto-Oncogenes; D012333:RNA, Messenger; D014157:Transcription Factors
chemical_list: D004268:DNA-Binding Proteins; D000074008:MDS1 and EVI1 Complex Locus Protein; C000716967:NPM1 protein, human; D012333:RNA, Messenger; D014157:Transcription Factors; D000090243:Nucleophosmin