title: Aberrant expression of HOXA9, DEK, CBL and CSF1R in acute myeloid leukemia.
abstract: Previous gene function analyses have indicated that HOXA9, DEK, CBL and CSF1R are aberrantly expressed in acute myeloid leukemia (AML). We analyzed the expression of these genes in a series of 41 adult patients with AML using quantitative real-time RT-PCR, and tested the association of the expression with the following hematologic and clinical parameters: age, FAB, immunophenotype and karyotype aberrations. A high proportion of the patients showed over- or underexpression of the analyzed genes. DEK was overexpressed in 98% of the cases, whereas CBL, CSF1R and HOXA9 were either overexpressed in 20%, 17% and 78% or underexpressed in 20%, 42% and 15% of the cases, respectively. Patients whose karyotype contained t(8;21)(q22;q22), showed lower relative expression of HOXA9 at a statistically significant level (p < 0.05). Bone marrow samples without expression of CD34 antigen were associated with either overexpression of DEK or HOXA9. Furthermore, an association was found between the AML-M2 subtype and lower expression of CBL, CSF1R or HOXA9, and between the AML-M5 subtype and CBL or CSF1R overexpression.
authors.affiliation: Department of Pathology, Haartman Institute, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
authors.forename: Sílvia
authors.initials: S
authors.lastname: Casas
authors.forename: Bálint
authors.initials: B
authors.lastname: Nagy
authors.forename: Erkki
authors.initials: E
authors.lastname: Elonen
authors.forename: Anna
authors.initials: A
authors.lastname: Aventín
authors.forename: Marcelo L
authors.initials: ML
authors.lastname: Larramendy
authors.forename: Jorge
authors.initials: J
authors.lastname: Sierra
authors.forename: Tapani
authors.initials: T
authors.lastname: Ruutu
authors.forename: Sakari
authors.initials: S
authors.lastname: Knuutila
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D002868:Chromosomal Proteins, Non-Histone; D002891:Chromosomes, Human, Pair 21 / Q000235:genetics; D002898:Chromosomes, Human, Pair 8 / Q000235:genetics; D005260:Female; D015973:Gene Expression Regulation, Leukemic; D018398:Homeodomain Proteins / Q000032:analysis / Q000235:genetics*; D006801:Humans; D016130:Immunophenotyping; D007621:Karyotyping; D007951:Leukemia, Myeloid / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis / Q000235:genetics; D050722:Oncogene Protein v-cbl; D015513:Oncogene Proteins / Q000032:analysis / Q000235:genetics*; D000075223:Poly-ADP-Ribose Binding Proteins; D011505:Protein-Tyrosine Kinases / Q000032:analysis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000032:analysis / Q000235:genetics*; D015682:Retroviridae Proteins, Oncogenic / Q000032:analysis / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014178:Translocation, Genetic
chemical_list: D015703:Antigens, CD; D002868:Chromosomal Proteins, Non-Histone; C084738:DEK protein, human; D018398:Homeodomain Proteins; D009363:Neoplasm Proteins; D050722:Oncogene Protein v-cbl; D015513:Oncogene Proteins; D000075223:Poly-ADP-Ribose Binding Proteins; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D015682:Retroviridae Proteins, Oncogenic; C097899:homeobox protein HOXA9; D011505:Protein-Tyrosine Kinases; D016186:Receptor, Macrophage Colony-Stimulating Factor