Tokushima University / Educator and Researcher Directory --- Naniwa, Kohei

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Academic Paper (Judged Full Paper):

1.	Yoichiro Shirogane, Yu Usami, Masashi Okumura, Katsutoshi Hirose, Kohei Naniwa, Kazunori Ikebe and Satoru Toyosawa : Anti-VEGFR2 neutralising antibody slows the progression of multistep oral carcinogenesis, The Journal of Pathology, 264, 4, 423-433, 2024. (Summary) Angiogenesis plays an important role in cancer growth and metastasis, and it is considered a therapeutic target to control tumour growth following anti-angiogenic therapy. However, it is still unclear when tissues initiate angiogenesis during malignant transformation from premalignant condition and whether this premalignant condition could be a therapeutic target of anti-angiogenic therapy. In this study, we aimed to analyse the onset of angiogenesis by evaluating morphological and functional alterations of microvessels during oral multistep carcinogenesis using a 4-nitroquinoline 1-oxide (4NQO)-induced oral carcinogenesis mouse model. In the study, we initially confirmed that with the use of 4NQO, oral lesions develop in a stepwise manner from normal mucosa through oral epithelial dysplasia (OED) to oral squamous cell carcinoma (OSCC). Evaluation of CD31-immunostained specimens revealed that microvessel density (MVD) increases in a stepwise manner from OEDs. Histological and functional analyses revealed the structural abnormalities and leakage of blood vessels had already taken place in OED. Then we evaluated the expression profiles of Hif1a and Vegfa along with hypoxic status and found that OED exhibited increased Vegfa expression under hypoxic conditions. Finally, we tested the possibility of OEDs as a target of anti-angiogenic therapy and found that anti-VEGFR2 neutralising antibody in OED slowed the disease progression from OED to OSCC. These data indicate that an angiogenic switch occurs at the premalignant stage and morphological, and functional alterations of microvessels already exist in OED. These findings also elucidate the tumour microenvironment, which gradually develops along with carcinogenic processes, and highlight usefulness of the 4NQO-induced carcinogenesis model in the study of epithelial and stromal components, which will support epithelial carcinogenesis. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. (Keyword) angiogenesis / oral cancer / oral epithelial dysplasia / premalignant / tumour microenvironment (Link to Publication Site) ● Publication site (DOI): 10.1002/path.6357 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39462847 ● Summary page in Scopus @ Elsevier: 2-s2.0-85207574724 (DOI: 10.1002/path.6357, PubMed: 39462847, Elsevier: Scopus)
2.	Keiko Aota, 中原崇道, 金川裕子, 小野伸二, Kohei Naniwa, Hideyuki Takano, Kohichi Kani and Yukihiro Momota : 周術期口腔機能管理を契機に発見された口腔悪性腫瘍5例の臨床的検討, 日本口腔ケア学会雑誌 = Official publication of the Japanese Society of Oral Care, 19, 1, 24-31, 2024. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520019512840222720 (CiNii: 1520019512840222720)
3.	Keiko Aota, Kohichi Kani, Shinji Ono, Kohei Naniwa, Yukihiro Momota, Makoto Fukui, Naozumi Ishimaru and Masayuki Azuma : Activation of Janus kinase 2 contributes to the autoimmune pathology in the salivary glands of patients with Sjögren's syndrome, Oral Science International, 21, 3, 415-424, 2024. (Tokushima University Institutional Repository) ● Metadata: 2012013 (Link to Publication Site) ● Publication site (DOI): 10.1002/osi2.1241 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85190987753 (Tokushima University Institutional Repository: 2012013, DOI: 10.1002/osi2.1241, Elsevier: Scopus)
4.	Kohei Naniwa, Katsutoshi Hirose, Yu Usami, Kenji Hata, Rikita Araki, Narikazu Uzawa, Toshihisa Komori and Satoru Toyosawa : Fam20C overexpression in odontoblasts regulates dentin formation and odontoblast differentiation., Journal of Molecular Histology, 54, 4, 329-347, 2023. (Summary) FAM20C phosphorylates secretory proteins at S-x-E/pS motifs, and previous studies of Fam20C-dificient mice revealed that FAM20C played essential roles in bone and tooth formation. Inactivation of FAM20C in mice led to hypophosphatemia that masks direct effect of FAM20C in these tissues, and consequently the direct role of FAM20C remains unknown. Our previous study reported that osteoblast/odontoblast-specific Fam20C transgenic (Fam20C-Tg) mice had normal serum phosphate levels and that osteoblastic FAM20C-mediated phosphorylation regulated bone formation and resorption. Here, we investigated the direct role of FAM20C in dentin using Fam20C-Tg mice. The tooth of Fam20C-Tg mice contained numerous highly phosphorylated proteins, including SIBLINGs, compared to that of wild-type mice. In Fam20C-Tg mice, coronal dentin volume decreased and mineral density unchanged at early age, while the volume unchanged and the mineral density elevated at maturity. In these mice, radicular dentin volume and mineral density decreased at all ages, and histologically, the radicular dentin had wider predentin and abnormal apical-side dentin with embedded cells and argyrophilic canaliculi. Immunohistochemical analyses revealed that abnormal apical-side dentin had bone and dentin matrix properties accompanied with osteoblast-lineage cells. Further, in Fam20C-Tg mice, DSPP content which is important for dentin formation, was reduced in dentin, especially radicular dentin, which might lead to defects mainly in radicular dentin. Renal subcapsular transplantations of tooth germ revealed that newly formed radicular dentin replicated apical abnormal dentin of Fam20C-Tg mice, corroborating that FAM20C overexpression indeed caused the abnormal dentin. Our findings indicate that odontoblastic FAM20C-mediated phosphorylation in the tooth regulates dentin formation and odontoblast differentiation. (Keyword) Mice / Animals / Odontoblasts / Mice, Transgenic / Tooth / Cell Differentiation / Extracellular Matrix Proteins / Dentin / Phosphoproteins / Calcium-Binding Proteins (Link to Publication Site) ● Publication site (DOI): 10.1007/s10735-023-10123-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37357253 ● Summary page in Scopus @ Elsevier: 2-s2.0-85162896363 (DOI: 10.1007/s10735-023-10123-y, PubMed: 37357253, Elsevier: Scopus)
5.	Katsutoshi Hirose, Kohei Naniwa, Yu Usami, Masaharu Kohara, Toshihiro Uchihashi, Susumu Tanaka, Saori Yamada, Yuri Iwamoto, Shumei Murakami, Kaori Oya, Yasuo Fukuda, Yumiko Hori, Eiichi Morii and Satoru Toyosawa : Primary Alveolar Soft Part Sarcoma of Cheek: Report of a Case and Review of the Literature, Head and Neck Pathology, 15, 4, 1426-1431, 2021. (Summary) Alveolar soft part sarcoma (ASPS) is a rare soft tissue sarcoma characterized by an alveolar or organoid arrangement of polygonal tumour cells separated by fibrovascular septa. A specific fusion gene [ASPS critical region 1 (ASPSCR1)-TFE3] was detected in ASPS. Despite being a slow-growing tumour without pain and dysfunction, ASPS is characterized by early metastasis, which leads to poor prognosis. Herein, we report a rare case of primary ASPS of the cheek harbouring ASPSCR1 (exon 7)-TFE3 (exon 5) fusion gene in a 21 year-old woman. This tumour was a well-circumscribed, smooth, round mass that was clinically suspected as a benign tumour. However, histologically, it was observed that the polygonal tumour cells were arranged in solid and alveolar growth patterns. Post-operative examination of the whole body excluded the possibility of metastasis at other sites. Thus, careful immunohistochemical and genetic analyses, as well as whole-body examination, demonstrated that the tumour was a primary ASPS of the cheek. (Keyword) Alveolar soft part sarcoma / ASPS / ASPSCR1 / Cheek tumour / TFE3 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12105-021-01324-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33840045 ● Summary page in Scopus @ Elsevier: 2-s2.0-85104130265 (DOI: 10.1007/s12105-021-01324-6, PubMed: 33840045, Elsevier: Scopus)

Proceeding of International Conference:

1.	Katsutoshi Hirose, Kohei Naniwa, Miho Hyodo, Yu Usami, Makoto Abe, Kenji Hata, Toshihiro Inubushi and Satoru Toyosawa : Osteocytic constitutive activation of Gαs activity exerts an anabolic effect on the bone, ASBMR 2022 Annual Meeting, Sep. 2022.

Proceeding of Domestic Conference:

1.	Kohei Naniwa, 芳地浩彰, 大山博行, 西田真理, Hiroaki Tawara, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota and Keiko Aota : 下顎歯肉に転移した肺腺癌の1例, 第53回日本口腔外科学会中四国支部学術集会, Jun. 2025.
2.	Mami Sato-Fukuba, Kohei Naniwa, Kohichi Kani, Yukihiro Momota, Takaaki Tsunematsu and Keiko Aota : Elucidating the significance of fat infiltration into the salivary gland in Sjogren's syndrome, a lipidomics analysis by using saliva, 第79回NPO法人日本口腔科学会学術集会, May 2025.
3.	Kohei Naniwa, 金川裕子, Shinji Ono, 西田真理, 大山博行, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota, Hideyuki Takano and Keiko Aota : 整形外科インプラント手術術後創部感染症例3例の歯科的検討, 第21回日本口腔ケア学会総会・学術大会/第4回国際口腔ケア学会総会・学術大会, Apr. 2025.
4.	Kohei Naniwa, 大山博行, NISHIDA Mari, 芳地浩彰, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota and Keiko Aota : 当科で経験したAYA世代舌がんの3症例, 第54回日本口腔外科学会中四国支部学術集会, Apr. 2025.
5.	Mami Sato-Fukuba, Kohei Naniwa, Hiroaki Tawara, Kohichi Kani, Yukihiro Momota, Takaaki Tsunematsu and Keiko Aota : シェーグレン症候群の唾液腺組織における脂肪浸潤の意義の探索, ダイバーシティ推進研究交流発表会2024, Mar. 2025.
6.	Kohichi Kani, 西田真理, 大山博行, 芳地浩彰, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 当科外来抜歯における予防抗菌薬使用の現状, 第69回日本口腔外科学会総会, Nov. 2024.
7.	Hiroaki Tawara, Takaaki Tsunematsu, Shigefumi Matsuzawa, Ruka Nagao, Kohei Naniwa, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : 頭頸部扁平上皮癌の分化を決定づける転写ネットワークの解明, 第60回日本口腔組織培養学会総会・学術大会, Nov. 2024.
8.	大山博行, Kohichi Kani, 西田真理, 芳地浩彰, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 原発性肺動脈性肺高血圧の患者の埋伏智歯抜歯を行った1例, 第71回日本口腔科学会中国・四国地方部会, Oct. 2024.
9.	Kohei Naniwa, 大山博行, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota and Keiko Aota : 口腔病変を初発症状とした多発血管炎性肉芽腫症の1例, 第71回NPO法人日本口腔科学会中国・四国地方部会, Oct. 2024.
10.	NISHIDA Mari, Kunihiro Otsuka, Mami Sato-Fukuba, Kohei Naniwa, Kohichi Kani, Yukihiro Momota, RUKA Nagao, MATSUZAWA Shigefumi, Aya Ushio, Takaaki Tsunematsu, Naozumi Ishimaru and Keiko Aota : シェーグレン症候群における老化関連B細胞の動態と発生機序の検討, 第32回日本シェーグレン症候群学会学術集会, Sep. 2024.
11.	西田真理, Kunihiro Otsuka, Mami Sato-Fukuba, Kohei Naniwa, Kohichi Kani, Yukihiro Momota, Naozumi Ishimaru and Keiko Aota : 老化関連B細胞を介したシェーグレン症候群の病態形成機序の解明, 第78回NPO法人日本口腔科学会学術集会, Jul. 2024.
12.	Kohichi Kani, Masahiko Watanabe, 西田真理, 大山博行, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 便宜抜歯時の抗菌薬予防投与に関する検討 ―抜歯後感染への影響について―, 第78回日本口腔科学会総会, Jul. 2024.
13.	芳地浩彰, Kohichi Kani, 西田真理, 大山博行, Hiroaki Tawara, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 含歯性嚢胞の術後出血により判明した後天性凝固因子ⅩⅢ因子欠乏症の1例, 第53回日本口腔外科学会中国四国支部学術集会, Jun. 2024.
14.	Mami Sato-Fukuba, NISHIDA Mari, Masahiko Watanabe, Kohei Naniwa, Kohichi Kani, Yukihiro Momota and Keiko Aota : 1型糖尿病モデルマウス唾液腺における発現遺伝子の網羅的解析, 第21回日本口腔ケア学会総会・学術大会第4回国際口腔ケア学会総会・学術大会, Apr. 2024.
15.	Keiko Aota, Kohichi Kani, 西田真理, Mami Sato-Fukuba, Kohei Naniwa and Yukihiro Momota : JAK阻害薬バリシチニブは唾液腺導管細胞のIFN-γ誘導性CXCL10発現を抑制する, 第59回日本口腔組織培養学会総会・学術大会, Nov. 2023.
16.	Kohei Naniwa, Mami Sato-Fukuba, 西田真理, 大山博行, Kohichi Kani, Yukihiro Momota and Keiko Aota : 当科における自己免疫性水疱症の臨床的検討, 第68回日本口腔外科学会総会・学術大会, Nov. 2023.
17.	Kohichi Kani, 西田真理, 大山博行, Mami Sato-Fukuba, Kohei Naniwa, Hideyuki Takano, Yukihiro Momota and Keiko Aota : 上唇に発生した嚢胞腺腫の1例, 第68回口腔外科学会総会・学術大会, Nov. 2023.
18.	Mami Sato-Fukuba, Kohei Naniwa, Kohichi Kani, Yukihiro Momota and Keiko Aota : 不明熱を契機にシェーグレン症候群の診断に至った7歳女児例, 第70回 NPO法人日本口腔科学会中国・四国地方部会, Oct. 2023.
19.	Kohichi Kani, 西田真理, Masahiko Watanabe, 大山博行, Mami Sato-Fukuba, Kohei Naniwa, Yukihiro Momota and Keiko Aota : 急激な増大を呈した頬粘膜形質芽細胞性リンパ腫の1例, 第33回日本口腔内科学会・4学会合同学術大会, Sep. 2023.
20.	Kohei Naniwa, 大山博行, 西田真理, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota and Keiko Aota : 多形滲出性紅斑の1例, 第52回口腔外科学会中四国支部学術大会, Jul. 2023.
21.	Kohichi Kani, 西田真理, 大山博行, Kohei Naniwa, Yukihiro Momota, Fumihiro Matsumoto and Keiko Aota : 歯痛を初発症状とした傍咽頭間隙原発悪性リンパ腫の1例, 第77回口腔科学会総会, May 2023.
22.	Kohei Naniwa, 金川裕子, Shinji Ono, 西田真理, 大山博行, Kohichi Kani, Fumihiro Matsumoto, Yukihiro Momota, Hideyuki Takano and Keiko Aota : 整形外科インプラント手術における周術期口腔機能管理の有効性の検討, 第20回日本口腔ケア学会総会・学術大会, Apr. 2023.
23.	Kohei Naniwa, 廣瀬勝俊, 宇佐美悠, 小守壽文, 豊澤悟 and Keiko Aota : 象牙質形成におけるFam20Cによるリン酸化の役割について, 第58回日本口腔組織培養学会学術大会, Dec. 2022.
24.	Kohei Naniwa, 西田真理, 大山博行, Hideyuki Takano, Kohichi Kani, Yukihiro Momota, Fumihiro Matsumoto and Keiko Aota : メトトレキサート休薬により良好な結果が得られた医原性リンパ増殖性疾患の一例, 第69回日本口腔科学会中四国地方部会, Oct. 2022.
25.	Hideyuki Takano, Yukihiro Momota, Kohichi Kani, NISHIDA Mari, 大山博行, Shinji Ono, Kohei Naniwa, Fumihiro Matsumoto and Keiko Aota : 徳島県における南海トラフ大地震による歯科医院被害予測と大学歯科に期待される役割, 第69回日本口腔科学会中国四国地方部会, Oct. 2022.
26.	Kohei Naniwa : Fam20C overexpression in odontoblasts regulates dentin mineralization and odontoblast differentiation, 令和3年度大阪大学歯学会優秀海外発表大学院生奨励賞受賞講演, Jul. 2022.

Et cetera, Workshop:

1.	Kohei Naniwa, 金川裕子, Shinji Ono, 西田真理, 大山博行, Mami Sato-Fukuba, Kohichi Kani, Yukihiro Momota, Hideyuki Takano and Keiko Aota : 整形外科インプラント手術における周術期口腔機能管理の有効性の検討, 四国歯学会第63回例会, Mar. 2024.

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

免疫老化と唾液腺老化に着目した口腔乾燥症の新たな治療展開 (Project/Area Number: 25K13228 )
シェーグレン症候群におけるFam20Cおよびオステオポンチンの役割の解明と治療への応用 (Project/Area Number: 23K16119 )
Search by Researcher Number (40967866)

Assistant Professor : Naniwa, Kohei

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