1. ¹Department of Laboratory Medicine, Ewha Women's University College of Medicine, Seoul, Korea
2. ²Department of Laboratory Medicine, Seoul National University Boramae Hospital, Seoul, Korea
3. ³Molecular Imaging Laboratory, National Research Laboratory for Molecular Imaging, Seoul, Korea
4. ⁴Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea
5. ⁵Department of Laboratory Medicine, Cheju National University College of Medicine, Jeju, Korea
6. ⁶Department of Laboratory Medicine, Seoul National University College of Medicine, Seoul, Korea
7. ⁷Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
8. ⁸Department of Biomedical Engineering, Seoul National University College of Medicine, Seoul, Korea
9. ⁹Department of Laboratory Medicine, Asan University College of Medicine, Seoul, Korea
10. ¹⁰Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

Correspondence: Dr DS Lee, Department of Laboratory Medicine, Seoul National University College of Medicine, 28 Yongun-dong, Chongro-gu, Seoul 110-744, Korea. E-mail: soonlee@plaza.snu.ac.kr, leukemia@plaza.snu.ac.kr

¹¹Co-primary authors

Received 6 October 2005; Revised 5 April 2006; Accepted 13 April 2006; Published online 22 June 2006.

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.