Current Affiliation Organization 【 display / non-display 】

Current Affiliation Organization 【 display / non-display 】

External Career 【 display / non-display 】

External Career 【 display / non-display 】

Research Interests 【 display / non-display 】

Research Interests 【 display / non-display 】

Research Areas 【 display / non-display 】

Research Areas 【 display / non-display 】

Published Papers 【 display / non-display 】

Published Papers 【 display / non-display 】

• Remarkable Responses to Chemoimmunotherapy in Ultra‐Rare Urachal Cancer: A Case Series and Reverse Translational Research

  Hiroshi Kotani, Shigeki Sato, Kazuyoshi Shigehara, Daisuke Saito, Hiroyuki Sakaguchi, Akihiro Nishiyama, Isao Matsumoto, Atsushi Mizokami, Seiji Yano, Hiroaki Taniguchi

  MedComm ( Wiley )  6 ( 12 )   2025.12 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• MET Enhances Amivantamab Binding to EGFR and Antibody-Dependent Cellular Toxicity

  Shigeki Sato, Neval Yilmaz, Sachiko Arai, Katsuya Sakai, Hiroki Sato, Yuya Murase, Tsukasa Ueda, Hayato Koba, Shigeki Nanjo, Yuichi Tambo, Hiroshi Kotani, Koji Fukuda, Hiroaki Taniguchi, Romain Amyot, Holger Flechsig, Hideko Isozaki, Kunio Matsumoto, Seiji Yano

  Cancer Science ( Wiley )    2025.11 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  ABSTRACT Amivantamab is a bispecific antibody against epidermal growth factor receptor (EGFR) and MET that has been approved for nonsmall cell lung cancer (NSCLC) with EGFR exon 20 insertion mutations and common EGFR mutations, such as exon 19 deletion and L858R. MET has attracted attention as a therapeutic target for lung cancer; however, its role in EGFR binding and amivantamab‐induced antibody‐dependent cellular toxicity (ADCC) remains unclear. We used high‐speed atomic force microscopy (HS‐AFM) to observe the real‐time binding of amivantamab to the EGFR‐extracellular domain (ECD) and MET‐ECD and visualized the binding of amivantamab to the EGFR domain 3 and MET Sema domain. Furthermore, we observed the trimer comprising amivantamab bound to EGFR and MET. Western blot analysis of the gel filtration fractions revealed that the MET‐ECD enhanced the binding of amivantamab to the EGFR‐ECD, which promoted trimer formation. Moreover, amivantamab‐induced mononuclear cell‐mediated ADCC in NSCLC cells with common EGFR mutations. ADCC activity was positively correlated with EGFR expression in tumor cells. Studies using MET‐knockout NSCLC cells revealed that MET enhanced ADCC activity with low concentrations of amivantamab. Thus, MET augments amivantamab binding to EGFR and augments ADCC activity at low amivantamab concentrations. These results indicate that binding to MET contributes to the increased efficacy of amivantamab in NSCLC with common EGFR mutations.

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• Limited SUMOylation inhibitor administration enhances eradication of Burkitt's lymphoma with CD19 CAR-T therapy

  Hiroshi Kotani, Shigeki Sato, Seiji Yano, Marco L. Davila, Hiroaki Taniguchi

  Signal Transduction and Targeted Therapy ( Springer Science and Business Media LLC )  10 ( 1 )   2025.10 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Targeting WEE1 to Overcome ARID1A Mutation-Driven Osimertinib Resistance in EGFR-Mutant Lung Cancer

  Koji Fukuda, Shigeki Nanjo, Shinji Takeuchi, Turja Chakrabarti, Tyiesha Brown, Sharon Wesley Dev Sahadevan, Sachiko Arai, Shigeki Sato, Hiroshi Kotani, Akihiro Nishiyama, Hiroyuki Sakaguchi, Koushiro Ohtsubo, Hiroaki Taniguchi, Collin M. Blakely, Trever G. Bivona, Seiji Yano

  Journal of Thoracic Oncology ( Elsevier BV )    2025.06 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Effectiveness of Additional Immunosuppressive Drugs for Corticosteroid-refractory Immune Checkpoint Inhibitor-induced Myocarditis: Two Case Reports

  Hiroyuki Sakaguchi, Shigeki Nanjo, Shigeki Sato, Hiroshi Kotani, Akihiro Nishiyama, Kaname Yamashita, Koushiro Ohtsubo, Chiaki Suzuki, Masaya Shimojima, Seiji Yano, Shinji Takeuchi

  Internal Medicine ( Japanese Society of Internal Medicine )  64 ( 8 ) 1205 - 1210   2025.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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Presentations 【 display / non-display 】

Presentations 【 display / non-display 】

• 膵胆道疾患患者血漿中の腫瘍抑制性miRNAのメチル化に関する応用研究(Application of Methylation of Tumor Suppressive miRNAs in Plasma from Patients with Pancreaticobiliary Diseases)

  Ohtsubo Koushiro, Miyake Kunio, Arai Sachiko, Fukuda Koji, Suzuki Chiaki, Kotani Hiroshi, Tanimoto Azusa, Nishiyama Akihiro, Nanjo Shigeki, Yamashita Kaname, Takeuchi Shinji, Yano Seiji

  膵臓  1900.01  -  1900.01 

• 新たながん分子標的療法の実現に向けた腫瘍の多様性と可塑性の理解　TP53変異型KRAS陽性非小細胞肺癌におけるWEE1を標的とした新規治療法の開発(Understanding tumor diversity, plasticity and evolution to develop the next-generation targeted therapies　Targeting WEE1 enhances the antitumor effect of KRAS-mutated non-small cell lung cancer harboring TP53 mutation)

  福田 康二, 竹内 伸司, 新井 祥子, 南條 成輝, 小谷 浩, 矢野 聖二

  日本癌学会総会記事  1900.01  -  1900.01 

• MYC発現型KRAS変異がんに対するSUMO化とMEKの二重阻害(Dual inhibition of SUMOylation and MEK for MYC-expressing KRAS mutant cancers)

  小谷 浩, 矢野 聖二

  日本癌学会総会記事  1900.01  -  1900.01 

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

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

• Development of novel treatments for MYC-associated malignancies based on SUMOylation inhibition

  Grant-in-Aid for Early-Career Scientists

  Project Year: 2023.04  -  2026.03 

  Direct: 3,600,000 (YEN)  Overheads: 4,680,000 (YEN)  Total: 1,080,000 (YEN)