Clinical implications of molecular genetic aberrations in acute myeloid leukemia.
The role of different cytogenetic changes has been extensively evaluated in patients with acute myeloid leukemia (AML), and cytogenetic analysis of AML blasts is essential to form prognostic subgroups in order to stratify for the extent of therapy. Nevertheless, 40-45% of AML patients lack such cytogenetic markers, i.e., cytogenetically normal AML (CN-AML). In the past decade, different molecular aberrations were identified in AML and especially CN-AML can now be discriminated into certain prognostic subgroups. This review considers the latest advances to define the prognostic impact of molecular aberrations in AML and gives insights how such molecular markers can be applied for analysis of minimal residual disease. Furthermore, therapeutic implications as well as the potential role of new methodological techniques in analyzing expression patterns of AML blasts are discussed.
Scholl
Sebastian
S
Department of Internal Medicine II, Universitätsklinikum, Jena, Germany. sebastian.scholl@med.uni-jena.de
Fricke
Hans-Joerg
HJ
Sayer
Herbert G
HG
Höffken
Klaus
K
D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D002869:Chromosome Aberrations; D020440:Gene Duplication; D005787:Gene Frequency; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000401:mortality / Q000628:therapy*; D008967:Molecular Biology; D009363:Neoplasm Proteins / Q000235:genetics; D011379:Prognosis; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D016019:Survival Analysis; D025721:WT1 Proteins / Q000235:genetics; D051941:fms-Like Tyrosine Kinase 3 / Q000235:genetics
C442828:BAALC protein, human; D022762:CCAAT-Enhancer-Binding Proteins; C515848:CEBPA protein, human; D009363:Neoplasm Proteins; D025721:WT1 Proteins; C497970:FLT3 protein, human; D011505:Protein-Tyrosine Kinases; D051941:fms-Like Tyrosine Kinase 3