title: Genomics in acute myeloid leukemia: from identification to personalization.
abstract: Acute Myeloid Leukemia (AML) is an aggressive bone marrow malignancy that is fatal if left untreated. Previous classification was strictly based on morphology, which gave little information in terms of prognosis or guide to treatment. Recent research has provided vital information into the chromosomal and molecular pathogenesis of leukemia development. The discovery of these abnormalities via proteomics and genomics have provided two key insights. First, these novel discoveries provide prognostic significance into the predictive result of chemotherapy. Second, these chromosomal and protein abnormalities have provided potential drug targets for new treatment modalities. This article will elaborate on many of these new molecular findings and discuss their implications on the treatment of AML.
authors.affiliation: Department of Medicine, Rhode Island Hospital, Providence, RI.
authors.forename: James M
authors.initials: JM
authors.lastname: Martin
authors.affiliation: Division of Hematology and Oncology, The Warren Alpert Medical School of Brown University, Rhode Island/The Miriam Hospital, Providence, RI.
authors.forename: Eric S
authors.initials: ES
authors.lastname: Winer
mesh_terms: D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D050676:Core Binding Factor Alpha 2 Subunit / Q000235:genetics; D004248:DNA (Cytosine-5-)-Methyltransferases / Q000235:genetics; D019175:DNA Methylation; D000090205:DNA Methyltransferase 3A; D004268:DNA-Binding Proteins / Q000235:genetics; D049308:Dioxygenases; D023281:Genomics; D006801:Humans; D007521:Isocitrate Dehydrogenase / Q000235:genetics; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000628:therapy*; D009687:Nuclear Proteins / Q000235:genetics; D000090243:Nucleophosmin; D011379:Prognosis; D040901:Proteomics; D011518:Proto-Oncogene Proteins / Q000235:genetics; D012097:Repressor Proteins / Q000235:genetics; D051941:fms-Like Tyrosine Kinase 3 / Q000235:genetics
chemical_list: C473949:ASXL1 protein, human; D022762:CCAAT-Enhancer-Binding Proteins; C515848:CEBPA protein, human; D050676:Core Binding Factor Alpha 2 Subunit; D004268:DNA-Binding Proteins; C000717967:DNMT3A protein, human; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; C493728:RUNX1 protein, human; D012097:Repressor Proteins; D000090243:Nucleophosmin; C538784:IDH2 protein, human; D007521:Isocitrate Dehydrogenase; C543588:IDH1 protein, human; D049308:Dioxygenases; C541081:TET2 protein, human; D004248:DNA (Cytosine-5-)-Methyltransferases; D000090205:DNA Methyltransferase 3A; C497970:FLT3 protein, human; D051941:fms-Like Tyrosine Kinase 3
keywords: AML treatment; Acute Myeloid Leukemia