title: Therapeutic use of granulocyte-colony stimulating factor could conceal residual malignant cells in patients with AML1/ETO+ acute myelogenous leukemia.
abstract: We have experienced a number of cases of AML1/ETO+ acute myelogenous leukemia that showed remission based on bone marrow (BM) morphological criteria, but that revealed clonal abnormalities in most cells by fluorescence in situ hybridization (FISH). Interestingly, most of these cases had AML with AML1/ETO rearrangement. The malignant cells were differentiated and considered mature cells after granulocyte-colony stimulating factor (G-CSF) treatment. To clarify the possible mechanisms underlying this phenomenon, we investigated the expression levels of G-CSFR in AML cells with AML1/ETO rearrangement by flow cytometry and real-time polymerase chain reaction (PCR). The number of AML1/ETO+ cells expressing G-CSFR at baseline was significantly higher than that of AML1/ETO- AML cells (2673 vs 522). In addition, the G-CSFR gene was more highly expressed in AML1/ETO+ cells than in AML1/ETO- cells by real-time PCR. This study reveals that cases showing remission after treatment with G-CSF mostly had leukemia with AML1/ETO rearrangement. This finding might be explained by the higher expression of G-CSF receptor in AML1/ETO+ cells than in AML1/ETO- cells. We recommend that remission should be confirmed by FISH, because malignant clones can be differentiated and masked in morphological examination or chromosome test, especially for AML with AML1/ETO rearrangement.
authors.affiliation: Department of Laboratory Medicine, Ewha Womens University College of Medicine, Seoul, Korea.
authors.forename: H W
authors.initials: HW
authors.lastname: Moon
authors.forename: S
authors.initials: S
authors.lastname: Shin
authors.forename: H Y
authors.initials: HY
authors.lastname: Kim
authors.forename: Y R
authors.initials: YR
authors.lastname: Kim
authors.forename: H I
authors.initials: HI
authors.lastname: Cho
authors.forename: S S
authors.initials: SS
authors.lastname: Yoon
authors.forename: S
authors.initials: S
authors.lastname: Park
authors.forename: B K
authors.initials: BK
authors.lastname: Kim
authors.forename: H
authors.initials: H
authors.lastname: Chun
authors.forename: H C
authors.initials: HC
authors.lastname: Kim
authors.forename: C J
authors.initials: CJ
authors.lastname: Park
authors.forename: Y H
authors.initials: YH
authors.lastname: Min
authors.forename: D S
authors.initials: DS
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D000328:Adult; D002648:Child; D050676:Core Binding Factor Alpha 2 Subunit / Q000235:genetics*; D005260:Female; D005434:Flow Cytometry; D015321:Gene Rearrangement; D016179:Granulocyte Colony-Stimulating Factor / Q000627:therapeutic use*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy* / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D018365:Neoplasm, Residual; D016133:Polymerase Chain Reaction; D016188:Receptors, Granulocyte Colony-Stimulating Factor / Q000032:analysis / Q000235:genetics
chemical_list: D050676:Core Binding Factor Alpha 2 Subunit; C493728:RUNX1 protein, human; D016188:Receptors, Granulocyte Colony-Stimulating Factor; D016179:Granulocyte Colony-Stimulating Factor