Tokushima University / Educator and Researcher Directory --- Morita, Yutaka

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Tokushima University ⟩ Graduate School of Biomedical Sciences ⟩ 医学域 ⟩ Endwed Collaborative Research ⟩ Contribution ⟩ 地域リウマチ・総合内科学 ⟩

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Academic Paper (Judged Full Paper):

1.	Noriko Bando, Hirokazu Ogino, Kojin Murakami, Masami Wadatsu, Yuki Tsukazaki, Yohei Yabuki, Tatsuya Kajimoto, Rikako Matsumoto, Saki Harada, Yutaka Morita, Ryohiko Ozaki, Atsushi Mitsuhashi, Seidai Satou, Satoshi Sakaguchi, Masaki Hanibuchi and Yasuhiko Nishioka : A case of thymic carcinoma harboring an FGFR3 S249C mutation with durable disease control on lenvatinib., International Cancer Conference Journal, 15, 1, 160-165, 2025. (Summary) Thymic carcinoma is a rare and aggressive malignancy with limited treatment options, resulting in a poor prognosis. Lenvatinib, a small-molecule inhibitor targeting multiple receptor tyrosine kinases, including fibroblast growth factor receptors (FGFRs), has been approved for thymic carcinoma that progresses following platinum-based chemotherapy. However, the identification of predictive biomarkers for its efficacy remains an unmet medical need. We herein present a case of 67-year-old man with advanced thymic carcinoma who was treated with carboplatin plus paclitaxel as first-line therapy. Lenvatinib, administered as second-line therapy, achieved a durable disease control that was maintained for over 20 months-exceeding the previously reported median progression-free survival. Comprehensive genomic profiling (CGP) using the FoundationOne® CDx assay identified an oncogenic FGFR3 S249C mutation. The case, together with supporting literature, suggests the potential role of FGFR3 mutations as therapeutic targets in thymic carcinoma. Furthermore, the presence of oncogenic mutations in lenvatinib-targeted genes may serve as predictive biomarkers for durable disease control. Given the limited availability of methods to detect oncogenic mutations, including FGFR3, in patients with thymic carcinoma, early implementation of CGP testing-even in the frontline setting-may be warranted in the future. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13691-025-00836-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 41589241 ● Search Scopus @ Elsevier (PMID): 41589241 ● Search Scopus @ Elsevier (DOI): 10.1007/s13691-025-00836-0 (DOI: 10.1007/s13691-025-00836-0, PubMed: 41589241)
2.	Atsushi Mitsuhashi, Kazuya Koyama, Hirokazu Ogino, Reona Matsuo, Na Nguyen Thi, Yohei Yabuki, Ryohiko Ozaki, Yuki Tsukazaki, Yutaka Morita, Aito Yoshida, Kojin Murakami, Seidai Satou, Hiroshi Kawano, Hiroshi Nokihara, Yutaka Inagaki, Tsutomu Shinohara, Masaki Hanibuchi, Hiromitsu Takizawa and Yasuhiko Nishioka : Clock pathway inhibitor overcomes tumor immune-exclusion via regulation of fibrocyte differentiation, NPJ Precision Oncology, 9, 1, 274, 2025. (Link to Publication Site) ● Publication site (DOI): 10.1038/s41698-025-01066-6 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-105012739596 (DOI: 10.1038/s41698-025-01066-6, Elsevier: Scopus)
3.	Keisuke Nakanishi, Hirokazu Ogino, Kojin Murakami, Yasuyo Saijo, Nobuhito Naito, Rikako Matsumoto, Yutaka Morita, Yuki Tsukazaki, Ryohiko Ozaki, Yohei Yabuki, Noriko Bando, Atsushi Mitsuhashi, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka : A favorable antitumor efficacy of sotorasib in a patient with KRAS G12C-mutated pulmonary large-cell neuroendocrine carcinoma., International Cancer Conference Journal, 14, 4, 374-380, 2025. (Summary) The recent studies with comprehensive genomic analyses demonstrated that a certain proportion of patients with pulmonary large-cell neuroendocrine carcinoma (LCNEC) harbors some driver gene alterations. We herein present a case of 79-year-old man with Kirsten rat sarcoma virus oncogene homologue G12C-mutated pulmonary LCNEC who were treated with chemo-immunotherapy in the first-line setting. Sotorasib which was administered as second-line therapy showed a favorable therapeutic efficacy of partial response. Although sotorasib induced severe hepatobiliary disorder which forced us to terminate the treatment, the antitumor response was sustained for up to 5.6 months which was almost comparable to the therapeutic efficacy reported in pivotal clinical trials. Our case and related literature review suggest that the multiplex genetic mutation-detection assay should be considered for patients with LCNEC. Furthermore, it also suggests that biomarkers which enable us to distinguish patients who are likely to harbor driver gene alterations are required in near future. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13691-025-00780-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 41395550 ● Search Scopus @ Elsevier (PMID): 41395550 ● Search Scopus @ Elsevier (DOI): 10.1007/s13691-025-00780-z (DOI: 10.1007/s13691-025-00780-z, PubMed: 41395550)
4.	Kaori Nii, Hirokazu Ogino, Hiroki Bando, Yuki Yamamoto, Koji Fujita, Hiroto Yoneda, Nobuhito Naito, Atsushi Mitsuhashi, Yutaka Morita, Yuki Tsukazaki, Yohei Yabuki, Ryohiko Ozaki, Seidai Satou, Masaki Hanibuchi, Yuishin Izumi and Yasuhiko Nishioka : Immune checkpoint inhibitor-associated paraneoplastic cerebellar degeneration in a case of extensive-stage small-cell lung cancer with pre-existing anti-SOX1 antibody, The Journal of Medical Investigation : JMI, 72, 1.2, 172-176, 2025. (Summary) Neurological immune-related adverse events can manifest as paraneoplastic neurological syndrome (PNS), especially in patients with small-cell lung cancer (SCLC). We herein report a 73-year-old man with SCLC treated with an immune checkpoint inhibitor (ICI) combined with chemotherapy. Although the chemo-immunotherapy induced a favorable response to SCLC, he later developed acute cerebellar ataxia. He was diagnosed with paraneoplastic cerebellar degeneration associated with anti-Sry-like high mobility group box 1 (SOX1) autoantibody. The antibody was also identified in serum collected at the diagnosis of SCLC and before ICI administration, which retrospectively suggested that the patient was at risk of ICI-induced PNS. J. Med. Invest. 72 : 172-176, February, 2025. (Keyword) anti-SOX1 autoantibody / immune checkpoint inhibitors / paraneoplastic cerebellar degeneration / small-cell lung cancer (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.72.172 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40268441 ● Summary page in Scopus @ Elsevier: 2-s2.0-105003981938 (DOI: 10.2152/jmi.72.172, PubMed: 40268441, Elsevier: Scopus)
5.	Yohei Yabuki, Atsushi Mitsuhashi, Hirokazu Ogino, Aito Yoshida, Thi Na Nguyen, Hiroto Yoneda, Ryohiko Ozaki, Yuki Tsukazaki, Yutaka Morita, Hiroshi Nokihara, Seidai Satou, Tsutomu Shinohara, Masaki Hanibuchi and Yasuhiko Nishioka : Hypoxia-inducible factor-targeting therapy augmented the sensitivity to programmed death ligand-1 blockade by enhancing interferon-γ-induced chemokines in tumor cells, International Journal of Cancer, 156, 9, 1814-1825, 2024. (Summary) Immune checkpoint inhibitors (ICIs) targeting programmed death ligand-1 (PD-L1) provide clinical benefits for various advanced malignancies. However, the predictive factors that determine sensitivity to ICIs have not been fully elucidated. We focused on tumor-derived CXCL10/11 as a pivotal factor that determines the response to PD-L1 blockade by regulating T cell accumulation and tumor angiogenesis. We previously reported that CXCL10/11 was upregulated by interferon (IFN)-γ in ICI-sensitive tumor cells but not in ICI-resistant cells, including mouse Lewis lung carcinoma (LLC). In the present study, gene silencing of tumor-derived CXCL10/11 induced resistance to PD-L1 blockade in AB1-HA mesothelioma cell-bearing mice. To identify the mechanisms underlying ICI resistance, we performed a microarray analysis to compare the IFN-γ-inducible genes between ICI-sensitive AB1-HA and ICI-resistant LLC in vitro. A pathway analysis based on microarray data indicated that hypoxia-inducible factor (HIF) 1A is the key signal that inhibits CXCL10/11 expression. We revealed that the HIF1A inhibitors echinomycin (EC) and YC-1 upregulated CXCL10/11 genes induced by IFN-γ in tumor cells in vitro. In addition, combination therapy with PD-L1 blockade and EC demonstrated synergistic antitumor effects in LLC-bearing mice. Combination therapy enhanced tumor infiltration of CD8 T cells and suppressed tumor angiogenesis. The present study suggests that HIF1A signaling in tumor cells dominates ICI resistance via the downregulation of tumor-derived CXCL10/11. (Keyword) angiogenesis / CXCL10/11 / HIF1A / immune checkpoint inhibitor / interferon-γ (Tokushima University Institutional Repository) ● Metadata: 2013332 (Link to Publication Site) ● Publication site (DOI): 10.1002/ijc.35301 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39686841 ● Summary page in Scopus @ Elsevier: 2-s2.0-85212305972 (Tokushima University Institutional Repository: 2013332, DOI: 10.1002/ijc.35301, PubMed: 39686841, Elsevier: Scopus)
6.	Yuki Tsukazaki, Hirokazu Ogino, Yoshio Okano, Soji Kakiuchi, Shoko Harada, Yuko Toyoda, Yugo Matsumura, Seiya Ichihara, Takeshi Imakura, Rikako Matsumoto, Ryohiko Ozaki, Ei Ogawa, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Hiroto Yoneda, Masaki Hanibuchi, Kayoko Hase, Eiji Takeuchi, Takashi Haku and Yasuhiko Nishioka : Granulocyte colony-stimulating factor has the potential to attenuate the therapeutic efficacy of chemo-immunotherapy for extensive-stage small-cell lung cancer, International Journal of Clinical Oncology, 29, 10, 1451-1460, 2024. (Summary) Granulocyte colony-stimulating factor (G-CSF) has the potential to attenuate the anti-tumor immune responses of T-cells by increasing immune suppressive neutrophils and myeloid-derived suppressor cells. However, the clinical impact of G-CSF on the efficacy of immunotherapy remains unknown. This multi-center retrospective analysis evaluated the impact of G-CSF in patients with extensive-stage small-cell lung cancer (ES-SCLC) treated with chemo-immunotherapy. We analyzed 65 patients with ES-SCLC who completed four cycles of induction chemo-immunotherapy and evaluated the effects of G-CSF on progression-free survival (PFS), overall survival (OS), and a durable response to immunotherapy (defined as PFS 12 months). Fifty patients (76.9%) received 1 dose of G-CSF. The PFS of the patients with G-CSF was poorer than that of the patients without G-CSF (median PFS 8.3 vs. 4.9 months, p = 0.009). The OS of the patients with G-CSF tended to be shorter, but not statistically significant, than that of the patients without G-CSF (median OS 24.3 vs. 16.4 months, p = 0.137). In the multivariate analysis, G-CSF administration was associated with poorer PFS (hazard ratio 2.78, 95% CI 1.36-5.69, p = 0.005) and was identified as a determinant of a durable response (odds ratio 0.18, 95% CI 0.04-0.80, p = 0.024). These results were consistent with other definitions of G-CSF administration (administration of 1 dose of pegfilgrastim, or either 5 doses of filgrastim or 1 dose of pegfilgrastim). G-CSF has the potential to attenuate the efficacy of immunotherapy; therefore, the indication for G-CSF during chemo-immunotherapy should be carefully considered for ES-SCLC. (Keyword) Chemo-immunotherapy / Extensive-stage small-cell lung cancer / Granulocyte colony-stimulating factor (Link to Publication Site) ● Publication site (DOI): 10.1007/s10147-024-02586-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39009900 ● Summary page in Scopus @ Elsevier: 2-s2.0-85198503607 (DOI: 10.1007/s10147-024-02586-0, PubMed: 39009900, Elsevier: Scopus)
7.	Kenya Miyamoto, Hirokazu Ogino, Takumi Kakimoto, Yugo Matsumura, Keiko Haji, Atsushi Mitsuhashi, Yutaka Morita, Yuki Tsukazaki, Yohei Yabuki, Ryohiko Ozaki, Hiroto Yoneda, Seidai Satou, Masaki Hanibuchi, Yoshimi Bando, Hiroshi Nokihara and Yasuhiko Nishioka : Transformation of epidermal growth factor receptor mutated lung adenocarcinoma to small-cell carcinoma long after the cessation of tyrosine kinase inhibitor treatment: A case series and literature review, Respiratory Medicine Case Reports, 51, 102076, 2024. (Keyword) Acquired resistance / Epidermal growth factor receptor / Non-small-cell lung cancer / Small-cell lung cancer transformation / Tyrosine kinase inhibitors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.rmcr.2024.102076 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85196709618 (DOI: 10.1016/j.rmcr.2024.102076, Elsevier: Scopus)

Proceeding of International Conference:

1.	Yuki Tsukazaki, Hirokazu Ogino, Yoshio Okano, Soji Kakiuchi, Shoko Harada, Yuko Toyoda, Yugo Matsumura, Seiya Ichihara, Takeshi Imakura, Rikako Matsumoto, Ryohiko Ozaki, Ei Ogawa, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Hiroto Yoneda, Masaki Hanibuchi, Kayoko Hase, Eiji Takeuchi, Takashi Haku and Yasuhiko Nishioka : The Conflicting Impacts of G-CSF on the Therapeutic Efficacy of Chemoimmunotherapy for Extensive Stage Small Cell Lung Cancer, 2024 World Conference on Lung Cancer, San Diego, Sep. 2024.

Proceeding of Domestic Conference:

1.	西村郁海, Yuya Yamashita, Keiko Haji, Tatsuya Kajimoto, Yutaka Morita, Asami Fukuya, Hirokazu Ogino, Hiroshi Kawano, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka : 肥大性骨関節症を合併したKRAS G12C変異陽性肺腺癌の一例, 第73回日本呼吸器学会中国・四国地方会, Dec. 2025.
2.	MATSUMOTO Rikako, Hirokazu Ogino, Yuya Yamashita, Tatsuya Kajimoto, Yutaka Morita, Atsushi Mitsuhashi, Yuki Tsukazaki, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka : 進展型小細胞肺癌に対する化学免疫療法の肝転移制御効果に関する後方視的検討, 第133回日本内科学会四国地方会, Nov. 2025.
3.	Atsushi Mitsuhashi, Hirokazu Ogino, Yuki Tsukazaki, Yutaka Morita, Hiroshi Nokihara, Masaki Hanibuchi and Yasuhiko Nishioka : 細胞外基質成分解析による免疫チェックポイント阻害薬耐性機序の解明, 第66回日本肺癌学会学術集会, Nov. 2025.
4.	Hirokazu Ogino, MATSUMOTO Rikako, Yuki Tsukazaki, Yutaka Morita, Tatsuya Kajimoto, Atsushi Mitsuhashi, Masaki Hanibuchi and Yasuhiko Nishioka : 肺癌に対するアムルビシン投与に伴う薬剤性肺障害の発症に関連するリスク因子について, 第66回日本肺癌学会学術集会, Nov. 2025.
5.	Yutaka Morita, Bayarmaa Agarzandan, Atsushi Mitsuhashi, YOSHIDA Aito, Hirokazu Ogino, Yuki Tsukazaki, MATSUMOTO Rikako, Hiroshi Nokihara, Masaki Hanibuchi and Yasuhiko Nishioka : 胸膜中皮腫に対する時計遺伝子阻害薬の血管新生制御を介した治療効果の検討, 第66回日本肺癌学会学術集会., Nov. 2025.
6.	MATSUMOTO Rikako, Hirokazu Ogino, Yuki Tsukazaki, Yutaka Morita, Tatsuya Kajimoto, Atsushi Mitsuhashi, Masaki Hanibuchi and Yasuhiko Nishioka : 肺癌に対するアムルビシンによる薬剤性肺障害発症リスクに関する後方視的検討, 第63回日本癌治療学会学術集会, Oct. 2025.
7.	Agarzandan Bayarmaa, Atsushi Mitsuhashi, Hirokazu Ogino, YOSHIDA Aito, Yuki Tsukazaki, Ryohiko Ozaki, Yutaka Morita, Masaki Hanibuchi and Yasuhiko Nishioka : 時計遺伝子阻害薬による胸膜中皮腫に対する血管新生抑制作用の検討, 第84回日本癌学会学術総会, Sep. 2025.
8.	Atsushi Mitsuhashi, YOSHIDA Aito, Hirokazu Ogino, Ryohiko Ozaki, Yuki Tsukazaki, Yutaka Morita, Agarzandan Bayarmaa, MATSUMOTO Rikako, Hiroshi Nokihara, Masaki Hanibuchi and Yasuhiko Nishioka : 細胞外基質成分解析によるがん免疫排除誘導機序の探索, 第84回日本癌学会学術総会, Sep. 2025.
9.	MIYAMOTO Kenya, Masaki Hanibuchi, Yuya Yamashita, Yutaka Morita, Takeshi Imakura, Hirokazu Ogino, Hiroshi Kawano, Seidai Satou and Yasuhiko Nishioka : 気管支鏡検査後の呼吸器感染症に対する予測因子の解析と予防的抗菌薬投与の意義, 第271回徳島医学会学術集会, Jul. 2025.
10.	Agarzandan Bayarmaa, Atsushi Mitsuhashi, Hirokazu Ogino, Yoshida Aito, Yuki Tsukazaki, Ryohiko Ozaki, Yutaka Morita, Masaki Hanibuchi and Yasuhiko Nishioka : The anti-angiogenic effects of clock gene inhibitors in malignant pleural mesothelioma, the 34th Annual Meeting and General Meeting of the Japanese Association for Cancer Metastasis, Jun. 2025.
11.	MATSUMOTO Rikako, Hirokazu Ogino, Yutaka Morita, Yuki Tsukazaki, Ryohiko Ozaki, Atsushi Mitsuhashi, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka : 進展型小細胞肺癌に対する化学免疫療法の遠隔転移制御効果に関する後方視的検討, 第65回日本呼吸器学会学術講演会, Apr. 2025.
12.	MATSUMOTO Rikako, Hirokazu Ogino, Yuki Tsukazaki, Yutaka Morita, Ryohiko Ozaki, Atsushi Mitsuhashi, Masaki Hanibuchi and Yasuhiko Nishioka : 進展型小細胞肺癌における化学免疫療法の遠隔転移制御効果に関する後方視的検討, 第22回日本臨床腫瘍学会学術集会, Mar. 2025.
13.	Ryohiko Ozaki, Hirokazu Ogino, Yutaka Morita, MATSUMOTO Rikako, Yuki Tsukazaki, Atsushi Mitsuhashi, Hiroshi Nokihara and Yasuhiko Nishioka : 進展型小細胞肺癌における二次化学療法を妨げる因子の検討, 第22回日本臨床腫瘍学会学術集会, Mar. 2025.
14.	Yutaka Morita, 村上行人, Hiroki Bando, 宮本憲哉, 磯村祐太, 梶本達也, 近藤圭大, Kozo Kagawa, Hirokazu Ogino, Seidai Satou, Masaki Hanibuchi and Yasuhiko Nishioka : 気管支鏡で診断した肺内神経鞘腫の一例, 第33回日本呼吸器内視鏡学会中国四国支部会, Nov. 2024.
15.	Yuki Tsukazaki, Hirokazu Ogino, 岡野義夫, Souji Kakiuchi, Yuko Toyoda, MATSUMOTO Rikako, Ryohiko Ozaki, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Masaki Hanibuchi, 長谷加容子, 竹内栄治, 葉久貴司 and Yasuhiko Nishioka : G-CSFが進展型小細胞肺癌における化学免疫療法の治療効果に及ぼす影響を検討した多施設共同後方視的解析, 第65回日本肺癌学会学術集会, Nov. 2024.
16.	Yuki Tsukazaki, Hirokazu Ogino, 岡野義夫, Souji Kakiuchi, Yuko Toyoda, MATSUMOTO Rikako, Ryohiko Ozaki, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Masaki Hanibuchi, 長谷加容子, 竹内栄治, 葉久貴司 and Yasuhiko Nishioka : G-CSF が進展型小細胞肺癌に対する化学免疫療法の治療効果に及ぼす影響に関する解析, 第62回日本癌治療学会学術集会, Oct. 2024.
17.	Atsushi Mitsuhashi, Kazuya Koyama, Hirokazu Ogino, Yohei Yabuki, Ryohiko Ozaki, Yuki Tsukazaki, Yutaka Morita, Aito Yoshida, Hiroshi Nokihara, Masaki Hanibuchi and Yasuhiko Nishioka : Fibrocyte 制御によるがん免疫排除克服に向けた治療戦略, 第83回日本癌学会学術総会, Sep. 2024.
18.	近藤圭大, 村上行人, Hiroki Bando, Yuki Tsukazaki, Hirokazu Ogino, 松本利加子, Yutaka Morita, Atsushi Mitsuhashi, Ryohiko Ozaki, Yohei Yabuki, Seidai Satou, Masaki Hanibuchi, 岡野義夫, Souji Kakiuchi, Yuko Toyoda, 長谷加容子, 竹内栄治, 葉久貴司 and Yasuhiko Nishioka : 進展型小細胞肺癌において顆粒球コロニー刺激因子が化学免疫療法の治療効果に及ぼす影響, 第269回徳島医学会学術集会, Jul. 2024.
19.	宮本憲哉, Masaki Hanibuchi, Yuta Isomura, Yutaka Morita, 村上行人, Hiroki Bando, Ryohiko Ozaki, Kozo Kagawa, Hiroto Yoneda, Hirokazu Ogino and Yasuhiko Nishioka : 気管支鏡後の呼吸器感染症ハイリスク症例における予防的抗菌薬投与の意義についての後方視的研究, 第47回日本呼吸器内視鏡学会学術集会, Jun. 2024.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

時計遺伝子による血管新生制御機序の解明と胸膜中皮腫への治療応用 (Project/Area Number: 26K11118 )
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