Updated on 2025/07/02

写真a

 
Nonami Atsushi
 
Organization
Kyushu University Hospital Center for Clinical and Translational Research Information Counter Assistant Professor
School of Medicine Department of Medicine(Concurrent)
Title
Assistant Professor

Research Areas

  • Life Science / Hematology and medical oncology

  • Life Science / Immunology

  • Life Science / Biomaterials

Degree

  • MD, PhD ( 2005.3 Kyushu University )

Education

  • Kyushu University   医学部  

    1992.4 - 1998.3

Research Interests・Research Keywords

  • Research theme: Establishing optimal conditions for adherent cell growth via novel nanofabrication.

    Keyword: ナノ加工、細胞増殖

    Research period: 2022.4 - 2026.3

  • Research theme: Development of culturing system by a robot

    Keyword: xrobot, cell culture

    Research period: 2019.12 - 2026.3

  • Research theme: The effect of immuno-cell therapy on cancers

    Keyword: cancer, immuno-cell therapy

    Research period: 2018.4 - 2022.3

  • Research theme: Identification of therapeutic targets of MPN by analysis of signal transduction of mutant Calreticulin

    Keyword: MPN, Calreticulin, therapeutic targets

    Research period: 2015.4 - 2020.3

Awards

  • ASH Abstract Achievement Award

    2014.12   American Society of Hematology   2014年米国血液学会にて優秀演題として選出

  • ASH Abstract Achievement Award

    2013.12   American Society of Hematology   2013年米国血液学会にて優秀演題として選出

  • ASH Abstract Achievement Award

    2012.12   American Society of Hematology   2012年米国血液学会にて優秀演題として選出

Papers

  • Regulatory approval of CAR-T cell and BsAb products for lymphoid neoplasms in the US, EU, and Japan.

    Matsuda K, Nonami A, Shinohara K, Nagai.

    Clinical Pharmacolgy & Therapy   2025.7

  • Prospective study of adoptive activated abT lymphocyte immunotherapy for refractory cancers: development and validation of a response scoring system

    Nonami, A; Matsuo, R; Funakoshi, K; Nakayama, T; Goto, S; Iino, T; Takaishi, S; Mizuno, S; Akashi, K; Eto, M

    CYTOTHERAPY   25 ( 1 )   76 - 81   2023.1   ISSN:1465-3249 eISSN:1477-2566

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    Language:English   Publisher:Cytotherapy  

    Background aims: This prospective clinical study aimed to determine the efficacy and prognostic factors of adoptive activated αβT lymphocyte immunotherapy for various refractory cancers. The primary endpoint was overall survival (OS), and the secondary endpoint was radiological response. Methods: The authors treated 96 patients. Activated αβT lymphocytes were infused every 2 weeks for a total of six times. Prognostic factors were identified by analyzing clinical and laboratory data obtained before therapy. Results: Median survival time (MST) was 150 days (95% confidence interval, 105–191), and approximately 20% of patients achieved disease control (complete response + partial response + stable disease). According to the multivariate Cox proportional hazards model with Akaike information criterion–best subset selection, sex, concurrent therapy, neutrophil/lymphocyte ratio, albumin, lactate dehydrogenase, CD4:CD8 ratio and T helper (Th)1:Th2 ratio were strong prognostic factors. Using parameter estimates of the Cox analysis, the authors developed a response scoring system. The authors then determined the threshold of the response score between responders and non-responders. This threshold was able to significantly differentiate OS of responders from that of non-responders. MST of responders was longer than that of non-responders (317.5 days versus 74 days). The validity of this response scoring system was then confirmed by internal validation. Conclusions: Adoptive activated αβT lymphocyte immunotherapy has clinical efficacy in certain patients. The authors’ scoring system is the first prognostic model reported for this therapy, and it is useful for selecting patients who might obtain a better prognosis through this modality.

    DOI: 10.1016/j.jcyt.2022.09.007

    Web of Science

    Scopus

    PubMed

  • Immunomodulatory Cell Therapy Using αGalCer-Pulsed Dendritic Cells Ameliorates Heart Failure in a Murine Dilated Cardiomyopathy Model

    Ikeda Masataka, Ide Tomomi, Matsushima Shouji, Ikeda Soichiro, Okabe Kosuke, Ishikita Akihito, Tadokoro Tomonori, Sada Masashi, Abe Ko, Sato Midori, Hanada Akiko, Arai Shinobu, Ohtani Kisho, Nonami Atsushi, Mizuno Shinichi, Morimoto Sachio, Motohashi Shinichiro, Akashi Koichi, Taniguchi Masaru, Tsutsui Hiroyuki

    Circulation: Heart Failure   15 ( 12 )   1125 - 1139   2022.12   ISSN:19413289 eISSN:19413297

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    Language:English   Publisher:Wolters Kluwer Health  

    <jats:sec>
    <jats:title>Background:</jats:title>
    <jats:p>Dilated cardiomyopathy (DCM) is a life-threatening disease, resulting in refractory heart failure. An immune disorder underlies the pathophysiology associated with heart failure progression. Invariant natural killer T (iNKT) cell activation is a prospective therapeutic strategy for ischemic heart disease. However, its efficacy in nonischemic cardiomyopathy, such as DCM, remains to be elucidated, and the feasible modality for iNKT cell activation in humans is yet to be validated.</jats:p>
    </jats:sec>
    <jats:sec>
    <jats:title>Methods:</jats:title>
    <jats:p>
    Dendritic cells isolated from human volunteers were pulsed with α-galactosylceramide ex vivo, which were used as α-galactosylceramide-pulsed dendritic cells (αGCDCs). We treated DCM mice harboring mutated troponin T
    <jats:sup>ΔK210/ΔK210</jats:sup>
    with αGCDCs and evaluated the efficacy of iNKT cell activation on heart failure in DCM mice. Furthermore, we investigated the molecular basis underlying its therapeutic effects in these mice and analyzed primary cardiac cells under iNKT cell-secreted cytokines.
    </jats:p>
    </jats:sec>
    <jats:sec>
    <jats:title>Results:</jats:title>
    <jats:p>
    The number of iNKT cells in the spleens of DCM mice was reduced compared with that in wild-type mice, whereas αGCDC treatment activated iNKT cells, prolonged survival of DCM mice, and prevented decline in the left ventricular ejection fraction for 4 weeks, accompanied by suppressed interstitial fibrosis. Mechanistically, αGCDC treatment suppressed TGF (transforming growth factor)-β signaling and expression of fibrotic genes and restored vasculature that was impaired in DCM hearts by upregulating angiopoietin 1 (
    <jats:italic>Angpt1</jats:italic>
    ) expression. Consistently, IFNγ (interferon gamma) suppressed TGF-β-induced Smad2/3 signaling and the expression of fibrotic genes in cardiac fibroblasts and upregulated
    <jats:italic>Angpt1</jats:italic>
    expression in cardiomyocytes via Stat1.
    </jats:p>
    </jats:sec>
    <jats:sec>
    <jats:title>Conclusions:</jats:title>
    <jats:p>Immunomodulatory cell therapy with αGCDCs is a novel therapeutic strategy for heart failure in DCM.</jats:p>
    </jats:sec>

    DOI: 10.1161/circheartfailure.122.009366

    Web of Science

    Scopus

    PubMed

    CiNii Research

  • A case of a patient receiving combination therapy with paclitaxel plus bevacizumab and adoptive activated αβ T-cell immunotherapy in advanced breast cancer. Reviewed International journal

    Masuda T, Nonami A, Tanaka F, Ando Y, Eto M, Mimori K.

    The Breast Journal   2020.12

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Cell-based screen identifies a new potent and highly selective CK2 inhibitor for modulation of circadian rhythms and cancer cell growth Reviewed

    Tsuyoshi Oshima, Yoshimi Niwa, Keiko Kuwata, Ashutosh Srivastava, Tomoko Hyoda, Yoshiki Tsuchiya, Megumi Kumagai, Masato Tsuyuguchi, Teruya Tamaru, Akiko Sugiyama, Natsuko Ono, Norjin Zolboot, Yoshiki Aikawa, Shunsuke Oishi, Atsushi Nonami, Fumio Arai, Shinya Hagihara, Junichiro Yamaguchi, Florence Tama, Yuya Kunisaki, Kazuhiro Yagita, Masaaki Ikeda, Takayoshi Kinoshita, Steve A. Kay, Kenichiro Itami, Tsuyoshi Hirota

    Science Advances   5 ( 1 )   2019.1

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    Language:English   Publishing type:Research paper (scientific journal)  

    Compounds targeting the circadian clock have been identified as potential treatments for clock-related diseases, including cancer. Our cell-based phenotypic screen revealed uncharacterized clock-modulating compounds. Through affinity-based target deconvolution, we identified GO289, which strongly lengthened circadian period, as a potent and selective inhibitor of CK2. Phosphoproteomics identified multiple phosphorylation sites inhibited by GO289 on clock proteins, including PER2 S693. Furthermore, GO289 exhibited cell type–dependent inhibition of cancer cell growth that correlated with cellular clock function. The x-ray crystal structure of the CK2-GO289 complex revealed critical interactions between GO289 and CK2-specific residues and no direct interaction of GO289 with the hinge region that is highly conserved among kinases. The discovery of GO289 provides a direct link between the circadian clock and cancer regulation and reveals unique design principles underlying kinase selectivity.

    DOI: 10.1126/sciadv.aau9060

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Presentations

  • リンパ系腫瘍に対する新規免疫療法の米国承認ピボタル試験

    松田 健佑, 野波 篤, 篠原 加代, 永井 純正

    日本血液学会学術集会  2024.10  (一社)日本血液学会

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    Event date: 2024.10

    Language:English  

  • 悪性腫瘍に対する免疫細胞療法(αβT細胞療法、γδT 細胞療法、樹状細胞ワクチン療法)の有効性の解析

    野波 篤、後藤重則、近藤隆重、山下 陽子、中山智博、田村直久、飯野忠史、高石繁生、水野晋一 、 赤司浩一、江藤正俊

    免疫治療学会  2019.2 

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    Event date: 2019.2

    Language:Japanese  

    Venue:東京   Country:Japan  

MISC

  • Combination therapy with nilotinib for drug-sensitive and drug-resistant BCR-ABL-positive leukemia and other malignancies

    Ellen Weisberg, Atsushi Nonami, James D. Griffin

    Archives of Toxicology   2014.11

     More details

    Language:English  

    Despite the clinical efficacy achieved with frontline therapies for BCR-ABL-positive disease, such as imatinib and second-generation ABL inhibitors like nilotinib or dasatinib that were originally designed to override insensitivity to imatinib, drug resistance still remains a challenge, especially for patients with advanced-stage chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia. The discovery of BCR-ABL point mutations has been a great asset to furthering our understanding of a major cause of drug resistance, as has discovery of multidrug resistance proteins, dysregulation of signaling molecules downstream of BCR-ABL, and insights into the underlying causes of stromal-mediated chemoresistance. Such elucidation of mechanisms of resistance associated with leukemic cell survival is essential for the optimization of current therapies and enhancement of patient survival via delaying or preventing disease recurrence. Here, we present an overview of the use of nilotinib in combination with other agents against BCR-ABL-positive leukemia, as well as solid tumors, for the purpose of increasing clinical efficacy and overriding drug resistance.

    DOI: 10.1007/s00204-014-1385-5

Professional Memberships

  • American Society of Hematoogy

  • Japan Society for Hematopoietic Cell Transplantation

  • The Japan Society of Transfusion Medicine and Cell Therapy

  • The Japanese Society of Hematology

  • The Japanese Cancer Association

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Committee Memberships

  • 日本血液学会   Councilor   Domestic

    2018.4 - 2021.3   

Academic Activities

  • Screening of academic papers

    Role(s): Peer review

    2021

     More details

    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:3

  • Screening of academic papers

    Role(s): Peer review

    2019

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:6

Research Projects

  • 新規ナノ加工法による、付着細胞増殖の至適条件確立-素材表面と細胞形質の関連性より

    Grant number:23K23064  2022.4 - 2026.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    野波 篤, 中野 美紀, 穂苅 遼平, 栗原 一真

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    Grant type:Scientific research funding

    創薬・再生医療の分野において、付着細胞の接着・増殖を制御するバイオマテリアル部材の高機能化は、新たな医療技術開発に結びつき、再生医療の発展に重要な基盤技術となっている。
    この付着細胞の接着・増殖を決定する因子は、付着細胞と細胞の足場となる部材の表面物性の相互作用であると考えられているが、これらの相関関係やメカニズムは統計的に明らかでなく、細胞と培養素材選択の明確な指標が無い現状である。
    本研究では、医工連携により、大きく隔たりがある両学術領域の視点から研究を進め、細胞種に応じ最適な細胞の接着・増殖が可能な培養素材の設計指標の構築や培養素材の開発を行う。

    CiNii Research

  • 自動細胞ロボット増殖ユニットの開発

    2019.12 - 2026.3

    株式会社九州メディカルイノベーション  株式会社九州メディカルイノベーション  Joint research

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    Authorship:Coinvestigator(s)  Grant type:Other funds from industry-academia collaboration

  • 悪性腫瘍に対する免疫細胞療法(αβT細胞療法、γδT細胞療法、樹状細胞ワクチン療法)の効果に関する研究

    2018.4 - 2019.3

    株式会社メディネット  株式会社メディネット  Research commissions

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    Authorship:Coinvestigator(s)  Grant type:Other funds from industry-academia collaboration

  • 骨髄増殖性疾患における、CALR遺伝子変異によるJAK2活性化メカニズムの解明

    Grant number:16K09849  2016 - 2020

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 研究助成金

    2016

    新日本先進医療研究財団  新日本先進医療研究財団 

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    Grant type:Donation

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Educational Activities

  • 学部3年生に対する血液学講義

Class subject

  • 血液悪性腫瘍治療総論

    2021.4 - 2021.9   First semester

  • 血液悪性腫瘍治療総論

    2020.10 - 2021.3   Second semester

  • 血液悪性腫瘍治療総論

    2019.4 - 2020.3   Full year

Social Activities

  • 骨髄バンク ドナー調整医師

    骨髄バンク  九州大学病院、久留米大学病院  2015.4

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    Audience:General, Scientific, Company, Civic organization, Governmental agency

    Type:Other

Travel Abroad

  • 2008.6 - 2015.3

    Staying countory name 1:United States   Staying institution name 1:米国ブリガムアンドウイメンズ病院

    Staying institution name 2:米国ダナファーバー癌研究所

Specialized clinical area

  • Biology / Medicine, Dentistry and Pharmacy / Internal Medicine / Hematology

Clinician qualification

  • Certifying physician

    日本移植免疫細胞療法学会

  • Certifying physician

    日本再生医療学会

  • Preceptor

    The Japanese Society of Internal Medicine(JSIM)

  • Preceptor

    The Japanese Society of Hematology

  • Certifying physician

    日本輸血細胞治療学会

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Year of medical license acquisition

  • 1998