title: Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.
abstract: OBJECTIVE
  Karyotype is an independent indicator of prognosis in acute myeloid leukemia (AML) that is widely applied to risk-adapted therapy. Because AML is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
  
  
  METHODS
  This cytogenetic study of 729 childhood patients classified them into 22 subgroups and evaluated their incidence and risk.
  
  
  RESULTS
  Rearrangements of 11q23 were the most frequent abnormality found in approximately 16% of patients, with 50% of these in infants. The outcome for all patients with 11q23 abnormalities was intermediate; no difference was observed for those with t(9;11)(p21-22;q23). The core binding factor leukemias with the translocations t(8;21)(q22;q22) and inv(16)(p13q22) occurred at incidences of 14% and 7%, respectively, predominantly in older children, and their prognosis was favorable. An adverse outcome was observed in patients with monosomy 7, abnormalities of 5q, and t(6;9)(p23;q34). Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this childhood series. However, the presence of 12p abnormalities predicted a poor outcome.
  
  
  CONCLUSIONS
  Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with AML, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
authors.affiliation: Leukaemia Research Cytogenetics Group, Northern Institute for Cancer Research, Newcastle University, Queen Victoria Road, Newcastle-upon-Tyne, UK. christine.harrison@newcastle.ac.uk
authors.forename: Christine J
authors.initials: CJ
authors.lastname: Harrison
authors.forename: Robert K
authors.initials: RK
authors.lastname: Hills
authors.forename: Anthony V
authors.initials: AV
authors.lastname: Moorman
authors.forename: David J
authors.initials: DJ
authors.lastname: Grimwade
authors.forename: Ian
authors.initials: I
authors.lastname: Hann
authors.forename: David K H
authors.initials: DK
authors.lastname: Webb
authors.forename: Keith
authors.initials: K
authors.lastname: Wheatley
authors.forename: Siebold S N
authors.initials: SS
authors.lastname: de Graaf
authors.forename: Eva
authors.initials: E
authors.lastname: van den Berg
authors.forename: Alan K
authors.initials: AK
authors.lastname: Burnett
authors.forename: Brenda E S
authors.initials: BE
authors.lastname: Gibson
mesh_terms: D000293:Adolescent; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D016026:Bone Marrow Transplantation; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations; D002879:Chromosomes, Human, Pair 10; D002881:Chromosomes, Human, Pair 12; D016001:Confidence Intervals; D020732:Cytogenetic Analysis; D018572:Disease-Free Survival; D005260:Female; D005453:Fluorescence; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D006801:Humans; D017403:In Situ Hybridization; D007223:Infant; D053208:Kaplan-Meier Estimate; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000401:mortality* / Q000473:pathology / Q000628:therapy; D016015:Logistic Models; D008297:Male; D015999:Multivariate Analysis; D016017:Odds Ratio; D011336:Probability; D011379:Prognosis; D016016:Proportional Hazards Models; D012042:Registries; D012189:Retrospective Studies; D018570:Risk Assessment; D016019:Survival Analysis; D016896:Treatment Outcome; D006113:United Kingdom