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Faculty of Medicine School of Medicine Department of Developmental and Urological-Reproductive Medicine, Pediatrics |
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Related SDGs |
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MORITAKE Hiroshi
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Research Areas 【 display / non-display 】
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Life Science / Embryonic medicine and pediatrics
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Life Science / Hematology and medical oncology
Papers 【 display / non-display 】
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Fauzi YR, Nakahata S, Shimoda K, Matsuura T, Hagiwara S, Inoue K, Moritake H, Morishita K
Biochemical and biophysical research communications 756 151564 2025.2
Language：English Publishing type：Research paper (scientific journal) Publisher：Biochemical and Biophysical Research Communications
Previously, we developed a complete human IgG TFR1 antibody (JST-TFR09/PPMX-T003) that showed a potentially practical therapeutic effect against adult T-cell leukemia/lymphoma (ATLL) in vitro and in vivo. In the present study, to elucidate the molecular mechanism underlying ATLL cell death induced by anti-TFR1 antibodies, we performed comprehensive gene expression analysis and mass spectrometry on ATLL cells treated with PPMX-T003 antibody. These results suggest that PPMX-T003 antibody treatment of ATLL cell lines induces ferroptosis mediated by ferritin degradation. PPMX-T003 antibody-treated ATLL cell lines showed a decrease in ferritin proteins, an increase in ferrous iron (Fe2+), reactive oxygen species (ROS) generation, and malondialdehyde as induction of lipid peroxidation. Moreover, treatment with a ferroptosis inhibitor (ferroportin-1) inhibited the cell death induced by PPMX-T003 antibody in ATLL cells. Furthermore, NCO4A and LC3-II were induced following antibody treatment, and ferritin degradation was inhibited by lysosomal inhibitors, suggesting that ferritin degradation depends on autolysosomal system activation. Here, we introduce ferroptosis as one of the potential mechanisms of PPMX-T003 antibody, which is promising for future therapeutic antibodies targeting a wide range of leukemia and cancers, including ATLL.
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Aoki Y., Kota Y., Shimada M., Taniguchi T., Yamauchi S., Matsusaka M., Hamasuna K., Watanabe Y., Kodama Y., Moritake H.
Children 12 ( 2 ) 2025.2
Language：English Publishing type：Research paper (scientific journal) Publisher：Children
Background: Preterm infants often have unstable vital signs and prolonged hospital stays that can hinder parent–infant bonding, especially under COVID-19 restrictions. This study aimed to evaluate whether listening to songs recorded by parents was effective in stabilizing the condition of premature infants. Methods: This randomized controlled study was conducted at the University of Miyazaki Hospital from October 2022 to March 2024 during the COVID-19 pandemic period. The participants were preterm infants born at less than 33 weeks gestation and their parents, all of whom recorded songs. The recorded songs were played daily to the infants in the intervention group, while the control group received usual care. Primary outcomes included vital signs (respiratory rate, pulse oximetry saturation, heart rate) and activity level. Results: Data for 33 preterm infants (intervention, n = 17 [total 749 sessions]; control, n = 16 [total 721 sessions]) were analyzed for changes in vital signs and activity levels. The intervention reduced infants’ respiratory rates (4.1 [95% CI: 2.5–5.6], p < 0.001) and slightly but statistically significantly increased pulse oximetry saturation (0.6 [95% CI: 0.02–1.2], p < 0.044). Conclusions: Recorded parental songs were found to safely stabilize the respiratory status of preterm infants and may serve as an accessible intervention to support parent–infant attachment, particularly in settings with restricted parental visitation.
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Yokoyama R., Kodama Y., Takamura K., Takahashi M., Tanaka M., Watanabe N., Moritake H.
Journal of Cardiology Cases 2025
Publishing type：Research paper (scientific journal) Publisher：Journal of Cardiology Cases
Exercise stress echocardiography (ESE) is a feasible and valuable tool for evaluating subclinical pulmonary hypertension (PH). However, its utility in patients with unilateral pulmonary branch stenosis remains unclear. We present a case involving a 17-year-old patient with left pulmonary branch stenosis who exhibited exercise-induced PH in the contralateral pulmonary artery as detected by ESE. Standard echocardiography was unable to visualize the left pulmonary artery clearly; therefore, computed tomography was performed, revealing a left pulmonary branch stenosis with a minimum diameter of 4.2 mm. Resting echocardiography showed a pressure gradient of 17 mmHg, calculated using the tricuspid regurgitant velocity. During ESE with a prone ergometer, the slope of the mean pulmonary arterial pressure to systemic cardiac output was 3.1 mmHg/L/min, meeting the diagnostic criteria for exercise-induced PH. The patient underwent stent implantation to treat the left pulmonary branch stenosis. Follow-up ESE demonstrated improvement, with the slope of the mean pulmonary arterial pressure to systemic cardiac output decreasing to 1.5 mmHg/L/min. These findings underscore that ESE is both feasible and effective for assessing subclinical unilateral pulmonary branch stenosis. Learning objective: Patients with congenital unilateral peripheral branch pulmonary artery stenosis usually do not have pulmonary hypertension at rest, and identifying patients who require treatment is challenging. Exercise stress echocardiography can detect latent pulmonary hypertension of the contralateral pulmonary artery in some patients, providing valuable insights for determining treatment indications and evaluating the efficacy of catheter interventions for the stenotic lesion.
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CFAP43 variant in persistent respiratory symptoms after hematopoietic cell transplantation Reviewed
Nagasawa S., Nishimura T., Yamada A., Kamimura S., Ishimura M., Moritake H.
Human Genome Variation 11 ( 1 ) 41 2024.12
Language：English Publishing type：Research paper (scientific journal) Publisher：Human Genome Variation
We describe a case of RAS-associated autoimmune leukoproliferative disease with primary ciliary dyskinesia (PCD)-like symptoms, such as recurrent pneumonia, sinusitis, and otitis media, that occurred 7 years after hematopoietic cell transplantation. Whole-exome sequencing revealed a heterozygous CFAP43 nonsense variant. Environmental factors related to hematopoietic cell transplantation may have led to PCD symptoms in this patient with this variant. Genetic screening can help avoid subsequent complications during patient management.
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Mitochondrial dynamics as a potential therapeutic target in acute myeloid leukemia Reviewed
Kinoshita M., Saito Y., Otani K., Uehara Y., Nagasawa S., Nakagawa M., Yamada A., Kamimura S., Moritake H.
International Journal of Hematology 120 ( 5 ) 601 - 612 2024.11
Language：English Publishing type：Research paper (scientific journal) Publisher：International Journal of Hematology
Acute myeloid leukemia (AML) cells are highly dependent on oxidative phosphorylation and the mitochondrial dynamics regulated by fusion-related genes MFN1, MFN2, and OPA1 and fission-related genes DNM1L and MFF. An analysis of previously published gene expression datasets showed that high expression of MFF was significantly associated with poor prognosis in patients with AML. Based on this finding, we investigated the impact of mitochondrial dynamics in AML. Transduction of shRNA against fission-related genes, DNM1L and MFF, inhibited growth and increased the mitochondrial area in AML cell lines. Extracellular flux analysis showed that deletion of mitochondrial dynamic regulators reduced mitochondrial respiration without significantly affecting glycolysis, except in shDNM1L-transfected cells. Immunodeficient NOG mice transplanted with DNM1L- or MFF-knockdown AML cells survived significantly longer than controls. Treatment of AML cell lines with Mdivi-1, which inhibits the DRP1 encoded by DNM1L, inhibited cell proliferation and oxidative phosphorylation. Our results show that mitochondrial dynamics play an important role in AML, and provide novel biological insights. The inhibition of mitochondrial dynamics induces unique mitochondrial alterations, which may be explored as a potential therapeutic target in AML.
Books 【 display / non-display 】
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今日の治療指針
盛武 浩（ Role： Joint author , 小児の白血病）
医学書院 2021 （ ISBN:978-4-260-04283-3 ）
Responsible for pages：1494-1495 Language：Japanese Book type：Textbook, survey, introduction
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血液専門医テキスト 改訂第3版
盛武 浩（ Role： Joint author , 小児の急性骨髄性白血病）
南江堂 2019
Responsible for pages：456-460 Language：Japanese Book type：Textbook, survey, introduction
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鉄欠乏性貧血. 小児疾患診療のための病態生理3 改訂第5版.
盛武 浩（ Role： Sole author）
東京医学社 2016
Language：Japanese Book type：Textbook, survey, introduction
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白血球と分画
盛武 浩（ Role： Sole author）
今日の小児診断指針 2004.7
Language：Japanese Book type：Scholarly book
MISC 【 display / non-display 】
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KRAS G12 mutations as adverse prognostic factors in KMT2A-rearranged acute myeloid leukemia Reviewed
Iyoda S., Yoshida K., Shoji K., Ito N., Tanaka M., Nannya Y., Yamato G., Tsujimoto S., Shiba N., Hayashi Y., Shiozawa Y., Shiraishi Y., Chiba K., Okada A., Tanaka H., Miyano S., Koga Y., Goto H., Moritake H., Terui K., Ito E., Kiyokawa N., Tomizawa D., Taga T., Tawa A., Takita J., Nishikori M., Adachi S., Ogawa S., Matsuo H.
Leukemia 38 ( 7 ) 1609 - 1612 2024
Language：English Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Leukemia
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Reduced-intensity therapy for relapsed Philadelphia chromosome-positive leukemia Reviewed
Nagasawa S., Yamada A., Nakagawa M., Kinoshita M., Koga Y., Ohga S., Moritake H.
Pediatric Blood and Cancer 71 ( 2 ) e30802 2023
Language：English Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Pediatric Blood and Cancer
DOI： 10.1002/pbc.30802
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Nagasawa S., Yamada A., Kinoshita M., Kamimura S., Moritake H.
Pediatrics International 64 ( 1 ) e14970 2022.1
Language：Japanese Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Pediatrics International
DOI： 10.1111/ped.14970
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Kinoshita M., Yamada A., Saito Y., Kamimura S., Moritake H.
Pediatrics International 64 ( 1 ) e14975 2022.1
Language：Japanese Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Pediatrics International
DOI： 10.1111/ped.14975
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Taga T., Tanaka S., Hasegawa D., Terui K., Toki T., Iwamoto S., Hiramatsu H., Miyamura T., Hashii Y., Moritake H., Nakayama H., Takahashi H., Shimada A., Taki T., Ito E., Hama A., Ito M., Koh K., Hasegawa D., Saito A.M., Adachi S., Tomizawa D.
Leukemia 35 ( 12 ) 3622 - 3624 2021.12
Language：Japanese Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Leukemia
Following the publication of this article, the authors noted an error in the data reported.
Presentations 【 display / non-display 】
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COVID-19 ワクチン接種後に発症した心膜心筋炎
二見 加菜、髙村 一成、山下 尚人、原田 雅子、澤 大介、盛武 浩
第91回日本小児科学会宮崎地方会, 宮崎
Event date： 2022.3.20
Presentation type：Oral presentation (general)
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発症早期に免疫修飾治療を開始したラスムッセン脳炎
山本 夏穂、 下田 貴史、 森 こずえ、 前田 謙一、 木許 恭宏、 池田 俊郎、 盛武 浩
第91回日本小児科学会宮崎地方会, 宮崎
Event date： 2022.3.20
Presentation type：Oral presentation (general)
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集団健診を契機に診断された頻拍誘発性心筋症２例
興梠 智子、髙村 一成、山下 尚人、原田 雅子、盛武 浩
第91回日本小児科学会宮崎地方会, 宮崎
Event date： 2022.3.20
Presentation type：Oral presentation (general)
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Clonal architecture and its prognostic significance in KMT2A-rearranged acute myeloid leukemia
Matsuo H, Yoshida K, Nannya Y, Kamikubo Y, Saito S, Koga Y, Moritake H, Terui K, Kawaguchi K, Okamoto Y,Nakayama H, Kanno M, Hino M, Akane Y, Inoue A, Shimada A, Goto H, Ueno H, Takita J, Yamato G, Shiba N, Hayashi Y, Shiraishi Y, Miyano S, Kiyokawa N, Tomizawa D, Taga T, Tawa A, Ogawa S, Adachi S
Event date： 2021.9.23 - 2021.9.25
Presentation type：Oral presentation (general)
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不明熱を呈し, リンパ節生検により診断に至ったTAFRO症候群の１例
小川 智香, 山元 綾子, 西村 豊樹, 盛武 浩
第90回日本小児科学会宮崎地方会, 宮崎
Event date： 2021.9.12
Presentation type：Oral presentation (general)
Awards 【 display / non-display 】
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日本白血病研究基金 一般研究賞（クレディセゾン賞）
2014.11 公益信託 日本白血病研究基金助成事業
盛武 浩
Award type：Award from publisher, newspaper, foundation, etc. Country：Japan
Grant-in-Aid for Scientific Research 【 display / non-display 】
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PDXマウスモデルを用いた再発難治小児急性骨髄性白血病の病態解明と新規治療法開発
Grant number：23K07337 2023.04 - 2026.03
独立行政法人日本学術振興会 科学研究費基金 基盤研究(C)
Authorship：Principal investigator
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Mfsd2遺伝子KOマウスを用いた、脳内ＤＨＡによるエネルギー代謝調節機構の解明
Grant number：16K09971 2018.04
科学研究費補助金 基盤研究(C)
KOマウスの脳の組織学的評価と、摂食行動およびエネルギー代謝特性、代謝関連遺伝子発現を評価する。
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網羅的遺伝子解析をとおして同定した家族性白血病原因遺伝子の機能解析
Grant number：16K10032 2016.04 - 2019.03
科学研究費補助金 基盤研究(C)
Authorship：Principal investigator
網羅的遺伝子解析をとおして同定した家族性白血病原因遺伝子と想定される2つの遺伝子変異の機能解析を行う
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家族性急性リンパ性白血病の原因遺伝子の探索
Grant number：25461600 2013.04 - 2016.03
科学研究費補助金 基盤研究(C)
Authorship：Principal investigator
家族性急性リンパ性白血病の原因遺伝子の探索
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Mfsd2遺伝子ノックアウトマウスにおけるエネルギー代謝特性の解明
Grant number：25461556 2013.04 - 2015.03
科学研究費補助金 基盤研究(C)
Authorship：Coinvestigator(s)
我々が作成したMfsd2遺伝子ノックアウトマウスにおけるエネルギー代謝特性を解析する