title: Adverse prognostic impact of abnormal lesions detected by genome-wide single nucleotide polymorphism array-based karyotyping analysis in acute myeloid leukemia with normal karyotype.
abstract: OBJECTIVE
  This study attempted to analyze the prognostic role of single nucleotide polymorphism array (SNP-A) -based karyotying in 133 patients with acute myeloid leukemia with normal karyotype (AML-NK), which presents with diverse clinical outcomes, thus requiring further stratification of patient subgroups according to their prognoses.
  
  
  METHODS
  A total of 133 patients with AML-NK confirmed by metaphase cytogenetics (MC) and fluorescent in situ hybridization analysis were included in this study. Analysis by Genome-Wide Human SNP 6.0 Array was performed by using DNAs derived from marrow samples at diagnosis.
  
  
  RESULTS
  Forty-three patients (32.3%) had at least one abnormal SNP lesion that was not detected by MC. One hundred thirteen abnormal SNP lesions included 55 losses, 23 gains, and 35 copy-neutral losses of heterozygosity. Multivariate analyses showed that detection of abnormal SNP lesions by SNP-A karyotyping results in an unfavorable prognostic value for overall survival (hazard ratio [HR], 2.69; 95% CI, 1.50 to 4.82; P = .001); other significant prognostic factors included secondary AML (HR, 5.55; 95% CI, 1.80 to 17.14; P = .003), presence of the FLT3 mutation (HR, 3.17; 95% CI, 1.71 to 5.87; P < .001), and age (HR, 1.03; 95% CI, 1.01 to 1.05; P = .020).
  
  
  CONCLUSIONS
  Our data demonstrated that abnormal SNP lesions detected by SNP-A karyotyping might indicate an adverse prognosis in patients with AML-NK, thus requiring a more sophisticated treatment strategy for improvement of treatment outcomes.
authors.affiliation: Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul, Korea.
authors.forename: Jun Ho
authors.initials: JH
authors.lastname: Yi
authors.forename: Jungwon
authors.initials: J
authors.lastname: Huh
authors.forename: Hee-Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Sun-Hee
authors.initials: SH
authors.lastname: Kim
authors.forename: Hyeoung-Joon
authors.initials: HJ
authors.lastname: Kim
authors.forename: Yeo-Kyeoung
authors.initials: YK
authors.lastname: Kim
authors.forename: Sang Kyun
authors.initials: SK
authors.lastname: Sohn
authors.forename: Joon Ho
authors.initials: JH
authors.lastname: Moon
authors.forename: Sung Hyun
authors.initials: SH
authors.lastname: Kim
authors.forename: Kyoung Ha
authors.initials: KH
authors.lastname: Kim
authors.forename: Jong Ho
authors.initials: JH
authors.lastname: Won
authors.forename: Yeung Chul
authors.initials: YC
authors.lastname: Mun
authors.forename: Hawk
authors.initials: H
authors.lastname: Kim
authors.forename: Jinny
authors.initials: J
authors.lastname: Park
authors.forename: Chul Won
authors.initials: CW
authors.lastname: Jung
authors.forename: Dong Hwan
authors.initials: DH
authors.lastname: Kim
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015894:Genome, Human; D006801:Humans; D007621:Karyotyping / Q000379:methods*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D016896:Treatment Outcome; D055815:Young Adult