Aberrant expression of HOXA9, DEK, CBL and CSF1R in acute myeloid leukemia.
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.
Casas
Sílvia
S
Department of Pathology, Haartman Institute, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
Nagy
Bálint
B
Elonen
Erkki
E
Aventín
Anna
A
Larramendy
Marcelo L
ML
Sierra
Jorge
J
Ruutu
Tapani
T
Knuutila
Sakari
S
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
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