title: Acute myeloid leukemia with t(8;21)/AML1/ETO: a distinct biological and clinical entity.
abstract: OBJECTIVE
  Recent investigations in acute myeloid leukemia (AML) have clearly demonstrated that specific karyotypic abnormalities result in distinct biological and clinical entities. We focus on recent advances on biology and treatment of AML with t(8;21).
  
  
  METHODS
  The information presented here derives from literature data and experience of the authors. The most relevant studies are critically analyzed and discussed.
  
  
  BACKGROUND
  Peculiar molecular, morphologic, immunophenotypic and epidemiologic findings of AML with t(8;21) as well as current methods for the evaluation of minimal residual disease are presented. Results from current therapeutic options including consolidation chemotherapy or transplantation procedures are critically reviewed.
  
  
  CONCLUSIONS
  Innovative therapeutic approaches based on risk-adapted, patient-oriented approaches would be possible in this AML subtype, provided that answers to many unresolved questions are given.
authors.affiliation: Divisione di Ematologia, Ospedale A. Cardarelli, Naples, Italy. ferrara@itb.it
authors.forename: Felicetto
authors.initials: F
authors.lastname: Ferrara
authors.forename: Luigi
authors.initials: L
authors.lastname: Del Vecchio
mesh_terms: D000208:Acute Disease; D002891:Chromosomes, Human, Pair 21; D002898:Chromosomes, Human, Pair 8; D050676:Core Binding Factor Alpha 2 Subunit; D006801:Humans; D007951:Leukemia, Myeloid / Q000175:diagnosis* / Q000235:genetics* / Q000628:therapy; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D000075142:RUNX1 Translocation Partner 1 Protein; D014157:Transcription Factors / Q000235:genetics; D014178:Translocation, Genetic / Q000235:genetics*
chemical_list: C107844:AML1-ETO fusion protein, human; D050676:Core Binding Factor Alpha 2 Subunit; D015514:Oncogene Proteins, Fusion; D000075142:RUNX1 Translocation Partner 1 Protein; D014157:Transcription Factors