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Articles by Koki Ueda
MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism
Main text (Cancer Cell 39, 529–547.e1–e7; April 12, 2021) We, the authors of this article, investigated how MDMX overexpression drives the transition from preleukemia to acute myeloid leukemia across multiple mouse models. Following publication, we were alerted to duplications in the flow cytometry plots in Figure 3E.
Ohtani's latest MVP award sparks celebrations in Japan
TOKYO — It's become an annual ritual: Shohei Ohtani wins a Most Valuable Player award and Japan celebrates with newspaper extra editions handed out at a major train station. The two-way Japanese star claimed his fourth career MVP award on Thursday night, and on Friday morning in Tokyo — the Japanese capital is 14 hours ahead of the American east coast — the extras hit the streets. A congratulatory message came in immediately from the top of the government and from down on the sidewalk.
Ohtani's latest MVP award sparks celebrations in Japan
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Prospects and Potential for Chimerism Analysis after Allogeneic Hematopoietic Stem Cell Transplantation
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Prenatal vitamin D deficiency alters immune cell proportions of young adult offspring through alteration of long-term stem cell fates
Abstract Vitamin D deficiency is a common deficiency worldwide, particularly among women of reproductive age. During pregnancy, it increases the risk of immune-related diseases in offspring later in life. However, exactly how the body remembers exposure to an adverse environment during development is poorly understood. Herein, we explore the effects of prenatal vitamin D deficiency on immune cell proportions in offspring using vitamin D deficient mice established by dietary manipulation.
Impaired Repopulating Ability of Uhrf2−/− Hematopoietic Progenitor Cells in Mice
Open AccessArticle by Takahiro Sano 1, Koki Ueda 2, Keiji Minakawa 2, Tsutomu Mori 3, Yuko Hashimoto 4, Haruhiko Koseki 5, Yasuchika Takeishi 6, Kazuhiko Ikeda 2,* and Takayuki Ikezoe 1 1 Department of Hematology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan 2 Department of Blood Transfusion and Transplantation Immunology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan 3 Department of Human Life Sciences; Fukushima Medical University...
Extreme Medialized Repair for Challenging Large and Massive Rotator Cuff Tears Reveals Healing and Significant Functional Improvement
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Gaining MOMENTUM against anaemic myelofibrosis
Treatment with momelotinib, compared with danazol, resulted in clinically significant improvements in myelofibrosis-associated symptoms, anaemia measures, and spleen response, with favourable safety. These findings support the future use of momelotinib as an effective treatment in patients with myelofibrosis, especially in those with anaemia.
Epigenetic Achilles’ heel of AML
Mutations in genes encoding epigenetic modifiers are frequent in acute myelogenous leukemia (AML) and have been proposed to cause AML via activation of oncogenes and repression of tumor suppressors. Two studies now identify unexpected oncogenic mechanisms and therapeutic vulnerabilities in AML arising from mutations in genes encoding the epigenetic regulators DNMT3A and ASXL1. Epigenetic dysregulation is a common feature found across cancer types.
MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism
Bacher U. Haferlach T. Schoch C. Kern W. Schnittger S. Implications of NRAS mutations in AML: a study of 2502 patients. Blood. 2006; 107: 3847-3853 Bereshchenko O. Mancini E. Moore S. Bilbao D. Mansson R. Luc S. Grover A. Jacobsen S.E. Bryder D. Nerlov C. Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML. Cancer Cell. 2009; 16: 390-400 Bhagat T.D. Chen S. Bartenstein M. Barlowe A.T. Von Ahrens D. Choudhary G.S. Tivnan P. Amin E.
Fueling clonal dominance through TRAFficking of NF-κB signaling
Activation of TLR–TRAF6 signaling by chronic inflammation in myelodysplastic syndromes increases the competitive advantage of HSPCs harboring MDS mutations through the upregulation of the ubiquitin-modifying enzyme A20 and a switch from canonical to non-canonical NF-κB signaling. Fig. 1: Overexpression of TRAF6 and systemic inflammation support clonal dominance in MDS. References 1. Muto, T. et al. Nat. Immunol. https://doi.org/10.1038/s41590-020-0663-z (2020). 2. Barreyro, L., Chlon, T. M.
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