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Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells
Susumu Goyama,1 Janet Schibler,1 Lea Cunningham,2 Yue Zhang,1 Yalan Rao,1 Nahoko Nishimoto,3 Masahiro Nakagawa,3 Andre Olsson,4 Mark Wunderlich,1 Kevin A. Link,1 Benjamin Mizukawa,1 H. Leighton Grimes,1,4 Mineo Kurokawa,3 P. Paul Liu,2 Gang Huang,1 and James C. Mulloy1
1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. 2Oncogenesis and Development Section, National Human Genome Research Institute (NHGRI), NIH, Bethesda, Maryland, USA. 3Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 4Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA.
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Published November 1, 2013 - More info
J Clin Invest. 2013;123(11):4979–4979. https://doi.org/10.1172/JCI73313.
© 2013 The American Society for Clinical Investigation
Related article:
Abstract
RUNX1 is generally considered a tumor suppressor in myeloid neoplasms. Inactivating RUNX1 mutations have frequently been found in patients with myelodysplastic syndrome (MDS) and cytogenetically normal acute myeloid leukemia (AML). However, no somatic RUNX1 alteration was found in AMLs with leukemogenic fusion proteins, such as core-binding factor (CBF) leukemia and MLL fusion leukemia, raising the possibility that RUNX1 could actually promote the growth of these leukemia cells. Using normal human cord blood cells and those expressing leukemogenic fusion proteins, we discovered a dual role of RUNX1 in myeloid leukemogenesis. RUNX1 overexpression inhibited the growth of normal cord blood cells by inducing myeloid differentiation, whereas a certain level of RUNX1 activity was required for the growth of AML1-ETO and MLL-AF9 cells. Using a mouse genetic model, we also showed that the combined loss of
Authors
Susumu Goyama, Janet Schibler, Lea Cunningham, Yue Zhang, Yalan Rao, Nahoko Nishimoto, Masahiro Nakagawa, Andre Olsson, Mark Wunderlich, Kevin A. Link, Benjamin Mizukawa, H. Leighton Grimes, Mineo Kurokawa, P. Paul Liu, Gang Huang, James C. Mulloy
Original citation: J. Clin. Invest. 2013;123(9):3876–3888. doi:10.1172/JCI68557.
Citation for this corrigendum: J. Clin. Invest. 2013;123(11):4979. doi:10.1172/JCI73313.
The institutional affiliation for Lea Cunningham and P. Paul Liu was incorrect. The correct author and affiliation list is above.
The authors regret the error.
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ISSN: 0021-9738 (print), 1558-8238 (online)