HARASHIMA Nanae

写真a

Title

Professor

Researcher Number(JSPS Kakenhi)

60345311
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Current Affiliation Organization 【 display / non-display 】

  • Duty   University of the Ryukyus   Faculty of Medicine   Health Sciences   Professor  

  • Concurrently   University of the Ryukyus   Graduate School of Health Sciences   Division of Health Sciences   Professor  

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University 【 display / non-display 】

  • 1997.04
    -
    2001.03

    Kurume University   Graduate School, Division of Medicine   Graduated

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Graduate School 【 display / non-display 】

  • 1995.04
    -
    1997.03

    University of the Ryukyus  Graduate School, Division of Health Care  Master's Course  Completed

  • 1997.04
    -
    2001.03

    Kurume University  Graduate School, Division of Medicine  Doctor's Course  Completed

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External Career 【 display / non-display 】

  • 2002.02
    -
    2005.07

     

  • 2005.07
    -
    2007.03

     

  • 2007.04
    -
    2017.03

    Shimane University Faculty of Medicine, School of Medicine  

  • 2007.04
    -
    2017.03

     

  • 2017.04
    　
    　

    University of the Ryukyus  

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Research Interests 【 display / non-display 】

  • 腫瘍免疫学

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Research Areas 【 display / non-display 】

  • Life Science / Tumor biology

  • Life Science / Pathological biochemistry

  • Life Science / Tumor diagnostics and therapeutics

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Published Papers 【 display / non-display 】

  • Fucoidan from brown algae Laminaria japonica trigger apoptosis in colon cancer cells

    Koya Shimabukuro, Ikuko Miyagi, Nanae Harashima

    bioRxiv     2026.06

    Type of publication: Research paper (scientific journal)

    • Access this article
      DOI

  • Differential Induction of Cancer Cell Death by Root, Leaf, and Flower Extract derived from Kalanchoe pinnata

    Mitsuki Maedomari, Sakura Kawada, Nanae Harashima

    bioRxiv     2026.05

    Type of publication: Research paper (scientific journal)

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      DOI

  • Novel drug-resistance mechanisms of pemetrexed-treated non-small cell lung cancer.

    Tanino R, Tsubata Y, Harashima N, Harada M, Isobe T

    Oncotarget ( Oncotarget )  9 ( 24 ) 16807 - 16821   2018.03 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

    　View Summary

    Pemetrexed (PEM) improves the overall survival of patients with advanced nonsmall cell lung cancer (NSCLC) when administered as maintenance therapy. However, PEM resistance often appears during the therapy. Although thymidylate synthase is known to be responsible for PEM resistance, no other mechanisms have been investigated in detail. In this study, we explored new drug resistance mechanisms of PEM-treated NSCLC using two combinations of parental and PEM-resistant NSCLC cell lines from PC-9 and A549. PEM increased the apoptosis cells in parental PC-9 and the senescent cells in parental A549. However, such changes were not observed in the respective PEM-resistant cell lines. Quantitative RT-PCR analysis revealed that, besides an increased gene expression of thymidylate synthase in PEM-resistant PC-9 cells, the solute carrier family 19 member1 (SLC19A1) gene expression was markedly decreased in PEM-resistant A549 cells. The siRNA-mediated knockdown of SLC19A1 endowed the parental cell lines with PEM resistance. Conversely, PEM-resistant PC-9 cells carrying an epidermal growth factor receptor (EGFR) mutation acquired resistance to a tyrosine kinase inhibitor erlotinib. Although erlotinib can inhibit the phosphorylation of EGFR and Erk, it is unable to suppress the phosphorylation of Akt in PEM-resistant PC-9 cells. Additionally, PEM-resistant PC-9 cells were less sensitive to the PI3K inhibitor LY294002 than parental PC-9 cells. These results indicate that SLC19A1 negatively regulates PEM resistance in NSCLC, and that EGFR-tyrosinekinase- inhibitor resistance was acquired with PEM resistance through Akt activation in NSCLC harboring EGFR mutations.

  • HIF-1 alpha-derived peptide capable of inducing cancer-reactive cytotoxic T lymphocytes from HLA-A24+patients with RCC

    Minami Takafumi, Sugimoto Koichi, Shimizu Nobutaka, De Velasco Marco, Nozawa Masahiro, Yoshimura Kazuhiro, Harashima Nanae, Harada Mamoru, Uemura Hirotsugu

    CANCER SCIENCE ( WILEY )  109   331 - 331   2018.01 [ Peer Review Accepted ]

    Type of publication: Research paper (other science council materials etc.)

  • Pemetrexed-Resistant Non-Small Cell Lung Cancer Cell Lines Have Novel Drug-Resistant Mechanisms

    Tanino, R; Tsubata, Y; Harashima, N; Harada, M; Isobe, T

    JOURNAL OF THORACIC ONCOLOGY   12 ( 11 ) S1949 - S1949   2017.11 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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Other Papers 【 display / non-display 】

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Presentations 【 display / non-display 】

  • Positive conversion of Tax specific CTL response in ATL patients after hematopoietic stem cell transplantation.

    Harashima N. N., Shimizu Y., Takamori A., Kurihara K., Utsunomiya A., Tanosak i R., Masuda M., Okamura J., and Kannagi M.

    AIDS Res. Hum. Retroviruses  2007.05  -  2007.05 

  • Positive conversion of Tax specific CTL response in ATL patients after hematopoietic stem cell transplantation.

    Harashima N. N, Shimizu Y, Takamori A, Kurihara K, Utsunomiya A, Tanosak i R, Masuda M, Okamura J, Kannagi M

    AIDS Res. Hum. Retroviruses  2007.05  -  2007.05 

  • Major target epitopes recognized by Tax specific CTL activated in ATL patients after hematopoietic stem cell transplantation.

    Harashima N. N., Kurihara K., Shimizu Y., Utsunomiya A., Tanosaki R., Masuda M., Miyazaki Y., Okamura J., and Kannagi M.

    AIDS Res. Hum. Retroviruses  2005  -  2005 

  • Major target epitopes recognized by Tax specific CTL activated in ATL patients after hematopoietic stem cell transplantation.

    Harashima N. N, Kurihara K, Shimizu Y, Utsunomiya A, Tanosaki R, Masuda M, Miyazaki Y, Okamura J, Kannagi M

    AIDS Res. Hum. Retroviruses  2005  -  2005 

  • Reactivation of stromg HTLV-I-specific CTL response in ATL patients following Non-myeloablative hematopoietic stem cell transplantation.

    AIDS Res. Hum. Retroviruses  1900.01  -  1900.01 

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Industrial Property 【 display / non-display 】

  • PEPTIDE HAVING HTLV-1-SPECIFIC CTL-INDUCING ACTIVITY

    Industrial Property No PCT/JP2004/005414  (2004.04.15)

    Patent No European Patent No. 1616950  (2008.06.25)

    HARASHIMA Nanae, KANNAGI Mari

  • COMPOSITIONS AND METHODS FOR PREVENTION OR TREATMENT OF NEOPLASTIC DISEASE IN A MAMMALIAN SUBJECT

    Industrial Property No US 14/549,296  (2014.12.08)

    Childs RW., Takahashi Y., Kajigaya S., Harashima N.

  • COMPOSITIONS AND METHODS FOR PREVENTION OR TREATMENT OF NEOPLASTIC DISEASE IN A MAMMALIAN SUBJECT.

    Industrial Property No US 14/549,296  (2014.12.08)

    Childs RW, Takahashi Y, Kajigaya S, Harashima N

  • PCT/JP2004/005414

    Industrial Property No PCT/JP2004/005414  (2004.04)

  • PEPTIDE HAVING HTLV-1-SPECIFIC CTL-INDUCING ACTIVITY

    Industrial Property No no_data  (1900.01.01)

    Unexpectedly No no_data  (1900.01.01)

    Patent No 特許1616950  (1900.01.01)

    HARASHIMA Nanae, KANNAGI Mari

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Grant-in-Aid for Scientific Research 【 display / non-display 】

  • Grant-in-Aid for Scientific Research(C)

    Project Year: 2013.04  -  2016.03 

    Direct: 4,100,000 (YEN) 

  • Grant-in-Aid for Young Scientists(B)

    Project Year: 2011.04  -  2013.03 

    Direct: 3,400,000 (YEN) 

  • Grant-in-Aid for Young Scientists(B)

    Project Year: 2008.04  -  2010.03 

    Direct: 3,300,000 (YEN) 

  • Anti-viral immuno therapeutic approaches for adult T-cell leukemia

    Grant-in-Aid for Scientific Research on Priority Areas

    Project Year: 2005  -  2009 

    Investigator(s): KANNAGI Mari, HARASHIMA Nanae 

    Direct: 48,500,000 (YEN)  Overheads: 48,500,000 (YEN) 

    　View Summary

    Our previous studies suggested that immunological approaches to activate HTLV-I-specific T-cell response potentially induce prophylactic and therapeutic effects on ATL. In order to verify this notion and apply for bedside, we indicated that vaccination reduced proviral load in a rat model, and that a subpopulation of HTLV-I-carriers showed weak HTLV-I-specific T-cell response and elevated proviral load. Moreover, we discovered an innate immune-mediated mechanism suppressing HTLV-I expression in vivo.

  • Grant-in-Aid for Scientific Research on Priority Areas

    Project Year: 2003  -  2003 

    Direct: 3,600,000 (YEN)  Overheads: 3,600,000 (YEN) 

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SDGs 【 display / non-display 】

  • 天然植物由来生理活性物質を応用したがん治療抵抗性克服

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