徳島大学 / 教育研究者総覧 --- 常松貴明

個人のホームページ

https://orcid.org/0000-0003-1043-2790 (ORCID)

専門分野

研究テーマ

著書・論文

著書:

1.	大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群の病理診断, 日本病理学会,
2.	常松貴明, 俵宏彰, 大塚邦紘, 牛尾綾, 石丸直澄 : ヒトパピローマウイルス陽性がんにおける脱ユビキチン化酵素の役割, 日本口腔組織培養学会, 2022年11月.
3.	大塚邦紘, 常松貴明, 牛尾綾, 佐藤真美, 石丸直澄 : シェーグレン症候群の病理, 2022年10月.

学術論文(審査論文):

1.	Daishiro Kobayashi, Masaya Denda, Junya Hayashi, Kohta Hidaka, Yutaka Kohmura, Takaaki Tsunematsu, Kohei Nishino, Harunori Yoshikawa, OHKAWACHI Kento, Kiyomi Nigorikawa, Tetsuro Yoshimaru, Naozumi Ishimaru, Wataru Nomura, Toyomasa Katagiri, Hidetaka Kosako and Akira Otaka : Sulfoxide-Mediated Cys-Trp-Selective Bioconjugation that Enables Protein Labeling and Peptide Heterodimerization, ChemistryEurope, Vol.2, No.3-4, 2024. (出版サイトへのリンク) ● Publication site (DOI): 10.1002/ceur.202400014 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1002/ceur.202400014 (DOI: 10.1002/ceur.202400014)
2.	Hiroaki Tawara, Takaaki Tsunematsu, Ruka Nagao, Shigefumi Matsuzawa, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : The noncanonical function of borealin, a component of chromosome passenger complex, promotes glycolysis via stabilization of survivin in squamous cell carcinoma cells., Biochemical and Biophysical Research Communications, Vol.706, 149741, 2024. (要約) The chromosome passenger complex (CPC) is a kinase complex formed by Aurora B, borealin, survivin and inner centromere protein (INCENP). The CPC is active during mitosis and contributes to proper chromosome segregation via the phosphorylation of various substrates. Overexpression of each CPC component has been reported in most cancers. However, its significance remains unclear, as only survivin is known to confer chemoresistance. This study showed that the overexpression of borealin, a CPC component, stabilized survivin protein depending on its interaction with survivin. Unexpectedly, the accumulation of survivin by borealin overexpression did not affect the well-characterized functions of survivin, such as chemoresistance and cell proliferation. Interestingly, the overexpression of borealin promoted lactate production but not the overexpression of the deletion mutant that lacks the ability to bind to survivin. Consistent with these findings, the expression levels of glycolysis-related genes were enhanced in borealin-overexpressing cancer cells. Meanwhile, the overexpression of survivin alone did not promote lactate production. Overall, the accumulation of the borealin-survivin complex promoted glycolysis in squamous cell carcinoma cells. This mechanism may contribute to cancer progression via excessive lactate production. (キーワード) Humans / Survivin / Centromere / Chromosomal Proteins, Non-Histone / Cell Cycle Proteins / Mitosis / Phosphorylation / Aurora Kinase B / Carcinoma, Squamous Cell / Lactates (徳島大学機関リポジトリ) ● Metadata: 119377 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2024.149741 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38471204 ● Search Scopus @ Elsevier (PMID): 38471204 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2024.149741 (徳島大学機関リポジトリ: 119377, DOI: 10.1016/j.bbrc.2024.149741, PubMed: 38471204)
3.	栗尾奈愛, 鎌田久美子, 上杉篤史, 常松貴明, 工藤保誠 : 頬粘膜に発生した基底細胞腺腫の1例, 四国歯学会誌, Vol.37, No.1, 18-23, 2024年.
4.	Shengjian Jin, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Hiroko Hagita, Motoharu Sarubo, Natsumi Fujiwara, Qi Guangying, Naozumi Ishimaru and Yasusei Kudo : Involvement of the OTUB1-YAP1 axis in driving malignant behaviors of head and neck squamous cell carcinoma., Cancer Medicine, Vol.12, No.24, 22156-22169, 2023. (要約) In HNSCC patients, USP10, USP14, OTUB1, and STAMBP among the screened DUBs were associated with a poor prognosis. Among them, OTUB1 showed the most aggressive characteristics in both in vitro and in vivo experiments. Additionally, OTUB1 regulated the stability and nuclear localization of YAP1, a substrate involved in cell proliferation and invasion. Notably, OTUB1 expression exhibited a positive correlation with the HNSCC-YAP score in HNSCC cells. (キーワード) deubiquitinating enzyme (DUB) / head and neck squamous cell carcinoma / invasion / OTUB1 / YAP (徳島大学機関リポジトリ) ● Metadata: 118778 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/cam4.6735 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37986681 ● CiNii @ 国立情報学研究所 (CRID): 1940583859514191616 ● Summary page in Scopus @ Elsevier: 2-s2.0-85177448617 (徳島大学機関リポジトリ: 118778, DOI: 10.1002/cam4.6735, PubMed: 37986681, CiNii: 1940583859514191616, Elsevier: Scopus)
5.	富田満, 小川博久, 常松貴明, 佐藤真美, 山下貴央, 北村嘉章, 石丸直澄, 常山幸一, 上原久典, 坂東良美 : 線維化と腫瘍随伴リンパ組織増生を伴う粘表皮癌の1例, 診断病理, Vol.40, No.4, 336-341, 2023年.
6.	Mami Sato-Fukuba, Rieko Arakaki, Aya Ushio, Kunihiro Otsuka, Ruka Nagao, Shigefumi Matsuzawa, Hiroaki Tawara, Takaaki Tsunematsu and Naozumi Ishimaru : CD4 T-cell-dependent differentiation of CD23 follicular B cells contributes to the pulmonary pathology in a primary Sjögren's syndrome mouse model., Frontiers in Immunology, Vol.14, 1217492, 2023. (要約) Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease that affects the function of exocrine glands, such as the lacrimal and the salivary glands. Extraglandular lesions and malignant lymphoma also occur during the progressive stage of pSS. We have, herein, focused on the pulmonary lesions of pSS and have aimed clarifying their pathophysiological mechanism by comparing the glandular with the extraglandular lesions observed in a mouse model of pSS. The histopathological analysis of lung tissues obtained from NFS/ mice that have undergone neonatal thymectomy was performed. Moreover, and experiments were conducted along with immunological analyses in order to characterize the unique phenotypes of the pulmonary lesions identified in these pSS model mice. Inflammatory lesions with a bronchus-associated lymphoid tissue-like structure were identified in the lungs of pSS model mice. In addition, relative to salivary gland lesions, pulmonary lesions showed increased CD23 follicular B (FB) cells. and pulmonary B cells were more readily driven to CD23 FB cell phenotype than salivary gland B cells in pSS model mice. Furthermore, the CD23 FB cell differentiation was found to be enhanced in a CD4 T-cell-dependent manner under a Th2-type condition in the lungs of herein examined pSS model mice. A Th2-type response in the pSS lung may promote the progression of autoimmune lesions through an enhanced abnormal differentiation of B cells. (キーワード) Mice / Animals / シェーグレン症候群 (Sjögren's syndrome) / 唾液腺 (salivary glands) / B-Lymphocytes / 細胞分化 (cell differentiation) / CD4-Positive T-Lymphocytes (徳島大学機関リポジトリ) ● Metadata: 118467 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2023.1217492 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37475871 ● Summary page in Scopus @ Elsevier: 2-s2.0-85165185874 (徳島大学機関リポジトリ: 118467, DOI: 10.3389/fimmu.2023.1217492, PubMed: 37475871, Elsevier: Scopus)
7.	Wenhua Shao, Takaaki Tsunematsu, Masaaki Umeda, Hiroaki Tawara, Natsumi Fujiwara, Yasuhiro Mouri, Rieko Arakaki, Naozumi Ishimaru and Yasusei Kudo : Cancer cell-derived novel periostin isoform promotes invasion in head and neck squamous cell carcinoma., Cancer Medicine, Vol.12, No.7, 8510-8525, 2023. (要約) It recently has been reported that partial-epithelial-mesenchymal transition (p-EMT) program is associated with metastasis in head and neck squamous cell carcinoma (HNSCC). We previously have identified POSTN (which encodes periostin) as an invasion-promoting molecule in HNSCC. Interestingly, POSTN expression is frequently observed in cancer cells with higher p-EMT score by using a previous single-cell transcriptomic data of HNSCC cases. Although it is known that POSTN has 11 splicing variants, the role of them has not been determined in HNSCC. Here, we found that HNSCC cells with EMT features expressed POSTN isoforms, Iso3 (lacking exon 17 and 21) and Iso5 (lacking exon 17), whereas fibroblast expressed Iso3 and Iso4 (lacking exon 17, 18, and 21). The expression of POSTN Iso3 and Iso4 are known to be widely observed in various cell types including stromal cells. Therefore, we focused on the role of novel cancer cell-derived POSTN isoform, Iso5, in HNSCC. Single overexpression of POSTN Iso5 as well as Iso3 promoted invasion. Surprisingly, Iso5 synergistically promoted invasion together with Iso3. Notably, Iso5 as well as Iso3 upregulated p-EMT-related genes. We suggest that a novel cancer-specific POSTN isoform lacking exon 17 (Iso5) can be a useful marker for detecting cancer cells undergoing p-EMT. Moreover, a POSTN Iso5 can be a novel target for diagnosis and therapy in HNSCC. (徳島大学機関リポジトリ) ● Metadata: 118312 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/cam4.5601 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36691359 ● Search Scopus @ Elsevier (PMID): 36691359 ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.5601 (徳島大学機関リポジトリ: 118312, DOI: 10.1002/cam4.5601, PubMed: 36691359)
8.	Mami Sato, Rieko Arakaki, Hiroaki Tawara, Ruka Nagao, Hidetaka Tanaka, Kai Tamura, Yuki Kawahito, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : Disturbed natural killer cell homeostasis in the salivary gland enhances autoimmune pathology via IFN-γ in a mouse model of primary Sjogren's syndrome., Frontiers in Medicine, Vol.9, 1036787, 2022. (要約) Innate lymphoid cells (ILCs), including natural killer (NK) cells, ILC1, ILC2, lymphoid tissue-inducer (LTi) cells, and ILC3 cell, play a key role in various immune responses. Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by chronic inflammation of exocrine glands, such as the lacrimal and salivary glands (SGs). The role of NK cells among ILCs in the pathogenesis of pSS is still unclear. In this study, the characteristics and subsets of NK cells in the salivary gland (SG) tissue were analyzed using a murine model of pSS. Multiple phenotypes and cytotoxic signature of the SG NK cells in control and pSS model mice were evaluated by flow cytometric analysis. Intracellular expression of interferon-γ (IFN-γ) among T cells and NK cells from the SG tissues was compared by experiments. In addition, pathological analysis was performed using anti-asialo-GM1 (ASGM1) antibody (Ab)-injected pSS model mice. The number of conventional NK (cNK) cells in the SG of pSS model mice significantly increased compared with that in control mice at 6 weeks of age. The production level of IFN-γ was significantly higher in SG NK cells than in SG T cells. The depletion of NK cells by ASGM1 Ab altered the ratio of tissue resident NK (rNK) cells to cNK cells, which inhibited the injury to SG cells with the recovery of saliva secretion in pSS model mice. The results indicate that SG cNK cells may enhance the autoreactive response in the target organ by upregulating of IFN-γ, whereas SG rNK cells protect target cells against T cell cytotoxicity. Therefore, the activation process and multiple functions of NK cells in the target organ could be helpful to develop potential markers for determining autoimmune disease activity and target molecules for incurable immune disorders. (徳島大学機関リポジトリ) ● Metadata: 118305 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fmed.2022.1036787 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36388880 ● Search Scopus @ Elsevier (PMID): 36388880 ● Search Scopus @ Elsevier (DOI): 10.3389/fmed.2022.1036787 (徳島大学機関リポジトリ: 118305, DOI: 10.3389/fmed.2022.1036787, PubMed: 36388880)
9.	Takaaki Tsunematsu, Rieko Arakaki, Mami Sato, Masako Saito, Kunihiro Otsuka, Furukawa Yusuke, Taquahashi Yuhji, Kanno Jun and Naozumi Ishimaru : Exposure to Multiwall Carbon Nanotubes Promotes Fibrous Proliferation by Production of Matrix Metalloproteinase-12 via NF-κB Activation in Chronic Peritonitis., The American Journal of Pathology, Vol.S0002-9440, No.22, 00240, 2022. (要約) The toxicologic effects of nanomaterials, such as carbon nanotubes (CNTs), on the immune system are considerably understood. However, the precise relationship between long-term exposure to CNTs and chronic inflammation remains unclear. In this study, a mouse model of chronic peritonitis was established using i.p. injection of multiwalled CNTs treated by the Taquann method with high dispersion efficiency. Chronic peritonitis with fibrosis was observed in Taquann-treated multiwalled CNT (T-CNT)-injected mice, but not in Taquann-treated titanium dioxide-injected mice. In vivo and in vitro experiments showed that matrix metalloproteinase-12 (MMP-12) of macrophages was up-regulated by T-CNT to enhance fibroblast activation and profibrotic molecule expression in fibroblasts. In addition, T-CNT-induced peritonitis reduced MMP-12 expression in Nfκb1 mice, suggesting that MMP-12-producing macrophages play a key role in chronic inflammation due to T-CNT exposure through NF-κB activation. The results of this study could be helpful in understanding the molecular toxicity of nanomaterial and chronic inflammation. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ajpath.2022.07.009 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35963465 ● Search Scopus @ Elsevier (PMID): 35963465 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ajpath.2022.07.009 (DOI: 10.1016/j.ajpath.2022.07.009, PubMed: 35963465)
10.	Kunihiro Otsuka, Mami Sato, Takaaki Tsunematsu and Naozumi Ishimaru : Virus Infections Play Crucial Roles in the Pathogenesis of Sjögren's Syndrome., Viruses, Vol.14, No.7, 1474, 2022. (要約) Sjögren's syndrome (SS) is an autoimmune disease especially targeting exocrine glands, such as the salivary and lacrimal glands. A radical therapy for SS based on its etiology has not been established because of the complex pathogenesis of the disease. Several studies have demonstrated a relationship between virus infection and SS pathogenesis. In particular, infection with the Epstein-Barr (EB) virus among others is a potent factor associated with the onset or development of SS. Specifically, virus infection in the target organs of SS triggers or promotes autoreactive responses involving the process of autoantigen formation, antigen-presenting function, or T-cell response. Our review of recent research highlights the crucial roles of virus infection in the pathogenesis of SS and discusses the critical association between virus infection and the etiology of autoimmunity in SS. (キーワード) Autoantigens / 自己免疫 (autoimmunity) / Herpesvirus 4, Human / Humans / シェーグレン症候群 (Sjögren's syndrome) / Virus Diseases (徳島大学機関リポジトリ) ● Metadata: 117727 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/v14071474 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35891453 ● Summary page in Scopus @ Elsevier: 2-s2.0-85133687255 (徳島大学機関リポジトリ: 117727, DOI: 10.3390/v14071474, PubMed: 35891453, Elsevier: Scopus)
11.	Mayuko Shimizu, Soichiroh Ishimaru, Wai Yee Yan Christine, Takeo Minamikawa, Takaaki Tsunematsu, Aiko Endoh, Takumi Kojima, Minoru Matsumoto, Tomoko Kobayashi, Satoshi Sumida, Takumi Kakimoto, MIYAGAMI Yuko, Hirohisa Ogawa, Takeshi Oya and Koichi Tsuneyama : Establishment of an epicutaneously sensitized murine model of shellfish allergy and evaluation of skin condition by Raman microscopy., Applied Sciences, Vol.12, No.3566, 2022. (徳島大学機関リポジトリ) ● Metadata: 117211 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/app12073566 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.3390/app12073566 (徳島大学機関リポジトリ: 117211, DOI: 10.3390/app12073566)
12.	Shu Chen, Naofumi Tamaki, Yasusei Kudo, Takaaki Tsunematsu, Kaname Miki, Naozumi Ishimaru and Hiro-O Ito : Protective effects of resveratrol against 5-fluorouracil-induced oxidative stress and inflammatory responses in human keratinocytes., Journal of Clinical Biochemistry and Nutrition, Vol.69, No.3, 238-246, 2021. (要約) -acetylcysteine reduced ROS levels without affecting the expression of pro-inflammatory cytokines. Resveratrol might be useful for preventing 5-FU-induced adverse effects by activating anti-oxidant and anti-inflammatory responses. (徳島大学機関リポジトリ) ● Metadata: 116380 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.21-23 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34857985 ● Search Scopus @ Elsevier (PMID): 34857985 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.21-23 (徳島大学機関リポジトリ: 116380, DOI: 10.3164/jcbn.21-23, PubMed: 34857985)
13.	Mami Sato, Rieko Arakaki, Hiroaki Tawara, Takaaki Tsunematsu and Naozumi Ishimaru : Formation of Autoimmune Lesions Is Independent of Antibiotic Treatment in NOD Mice., International Journal of Molecular Sciences, Vol.22, No.6, 3239, 2021. (要約) The relationship between autoimmunity and changes in intestinal microbiota is not yet fully understood. In this study, the role of intestinal microbiota in the onset and progression of autoimmune lesions in non-obese diabetic (NOD) mice was evaluated by administering antibiotics to alter their intestinal microenvironment. Flow cytometric analysis of spleen cells showed that antibiotic administration did not change the proportion or number of T and B cells in NOD mice, and pathological analysis demonstrated that autoimmune lesions in the salivary glands and in the pancreas were also not affected by antibiotic administration. These results suggest that the onset and progression of autoimmunity may be independent of enteral microbiota changes. Our findings may be useful for determining the appropriate use of antibiotics in patients with autoimmune diseases who are prescribed drugs to maintain systemic immune function. (キーワード) Animals / Anti-Bacterial Agents / Autoimmune Diseases / 自己免疫 (autoimmunity) / 細胞質分裂 (cytokinesis) / Disease Models, Animal / Disease Susceptibility / Immune System / Mice / Mice, Inbred NOD / Sialadenitis (徳島大学機関リポジトリ) ● Metadata: 117463 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/ijms22063239 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33810172 ● Search Scopus @ Elsevier (PMID): 33810172 ● Search Scopus @ Elsevier (DOI): 10.3390/ijms22063239 (徳島大学機関リポジトリ: 117463, DOI: 10.3390/ijms22063239, PubMed: 33810172)
14.	Takaaki Tsunematsu, Rieko Arakaki, Hidehiko Kawai, Jan Ruppert, Koichi Tsuneyama, Naozumi Ishimaru, C William Earnshaw, Michele Pagano and Yasusei Kudo : is required for the termination of chromosomal passenger complex activity upon mitotic exit., Journal of Cell Science, Vol.133, No.18, 2020. (要約) terminates CPC activity upon mitotic exit and thereby contributes to proper control of DNA replication. (徳島大学機関リポジトリ) ● Metadata: 115422 (出版サイトへのリンク) ● Publication site (DOI): 10.1242/jcs.251314 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32934012 ● Summary page in Scopus @ Elsevier: 2-s2.0-85091052907 (徳島大学機関リポジトリ: 115422, DOI: 10.1242/jcs.251314, PubMed: 32934012, Elsevier: Scopus)
15.	Satoru Kisoda, Wenhua Shao, Natsumi Fujiwara, Yasuhiro Mouri, Takaaki Tsunematsu, Shengjian Jin, Rieko Arakaki, Naozumi Ishimaru and Yasusei Kudo : Prognostic value of partial EMT-related genes in head and neck squamous cell carcinoma by a bioinformatic analysis., Oral Diseases, Vol.26, No.6, 1149-1156, 2020. (要約) Our findings suggest that p-EMT program may be involved in poor prognosis of HNSCC. SERPINE1, ITGA5, TGFBI, P4HA2, CDH13, and LAMC2 can be used for a prognostic marker. Moreover, HNSCC cells with p-EMT phenotype can be a useful model for investigating a nature of p-EMT. (徳島大学機関リポジトリ) ● Metadata: 114969 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/odi.13351 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32277532 ● Summary page in Scopus @ Elsevier: 2-s2.0-85083974773 (徳島大学機関リポジトリ: 114969, DOI: 10.1111/odi.13351, PubMed: 32277532, Elsevier: Scopus)
16.	Kunihiro Otsuka, Akiko Yamada, Masako Saito, Aya Ushio, Mami Sato, Satoru Kisoda, Wenhua Shao, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : Ascl2-Regulated Follicular Helper T Cells Promote Autoimmunity in a Murine Model for Sjögren's Syndrome., The American Journal of Pathology, Vol.189, No.12, 2414-2427, 2019. (要約) mice that received neonatal thymectomy treatment demonstrated that Ascl2 contributes to the Tfh cell differentiation associated with autoimmunity during the early stages independent of Bcl6. In conclusion, our results indicate that abnormal Tfh cell differentiation via Ascl2 regulation might contribute to the pathogenesis of autoimmunity. (キーワード) Animals / Autoantibodies / 自己免疫 (autoimmunity) / B-Lymphocytes / Basic Helix-Loop-Helix Transcription Factors / 細胞分化 (cell differentiation) / Cytokines / Disease Models, Animal / 女性 (female) / Germinal Center / Mice / Mice, Inbred C57BL / Proto-Oncogene Proteins c-bcl-6 / シェーグレン症候群 (Sjögren's syndrome) / T-Lymphocytes, Helper-Inducer (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ajpath.2019.08.008 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31539517 ● Summary page in Scopus @ Elsevier: 2-s2.0-85075213858 (DOI: 10.1016/j.ajpath.2019.08.008, PubMed: 31539517, Elsevier: Scopus)
17.	Aya Ushio, Rieko Arakaki, Kunihiro Ohtsuka, Akiko Yamada, Takaaki Tsunematsu, Yasusei Kudo, Keiko Aota, Masayuki Azuma and Naozumi Ishimaru : CCL22-Producing Resident Macrophages Enhance T Cell Response in Sjögren's Syndrome., Frontiers in Immunology, Vol.9, 2594, 2018. (要約) Macrophages (MΦs) are critical regulators of immune response and serve as a link between innate and acquired immunity. The precise mechanism of involvement of tissue-resident MΦs in the pathogenesis of autoimmune diseases is not clear. Here, using a murine model for Sjögren's syndrome (SS), we investigated the role of tissue-resident MΦs in the onset and development of autoimmunity. Two unique populations of CD11b and CD11b resident MΦs were observed in the target tissue of the SS model. Comprehensive gene expression analysis of chemokines revealed effective production of CCL22 by the CD11b MΦs. CCL22 upregulated the migratory activity of CD4 T cells by increasing CCR4, a receptor of CCL22, on T cells in the SS model. In addition, CCL22 enhanced IFN-γ production of T cells of the SS model, thereby suggesting that CCL22 may impair the local immune tolerance in the target organ of the SS model. Moreover, administration of anti-CCL22 antibody suppressed autoimmune lesions in the SS model. Finally, histopathological analysis revealed numerous CCL22-producing MΦs in the minor salivary gland tissue specimens of the SS patients. CCL22-producing tissue-resident MΦs may control autoimmune lesions by enhancing T cell response in the SS model. These results suggest that specific chemokines and their receptors may serve as novel therapeutic or diagnostic targets for SS. (徳島大学機関リポジトリ) ● Metadata: 113526 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fimmu.2018.02594 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30467506 ● Summary page in Scopus @ Elsevier: 2-s2.0-85056303968 (徳島大学機関リポジトリ: 113526, DOI: 10.3389/fimmu.2018.02594, PubMed: 30467506, Elsevier: Scopus)
18.	Kazuchika Nishitsuji, Syunsuke Watanabe, Jinzhong Xiao, Ryosuke Nagatomo, Hirohisa Ogawa, Takaaki Tsunematsu, Hitomi Umemoto, Yuki Morimoto, Hiroyasu Akatsu, Koichi Inoue and Koichi Tsuneyama : Effect of coffee or coffee components on gut microbiome and short-chain fatty acids in a mouse model of metabolic syndrome., Scientific Reports, Vol.8, No.1, 2018. (要約) We previously showed that male Tsumura Suzuki obese diabetes (TSOD) mice, a spontaneous mouse model of metabolic syndrome, manifested gut dysbiosis and subsequent disruption of the type and quantity of plasma short-chain fatty acids (SCFAs), and daily coffee intake prevented nonalcoholic steatohepatitis in this mouse model. Here, we present a preliminary study on whether coffee and its major components, caffeine and chlorogenic acid, would affect the gut dysbiosis and the disrupted plasma SCFA profile of TSOD mice, which could lead to improvement in the liver pathology of these mice. Three mice per group were used. Daily intake of coffee or its components for 16 wk prevented liver lobular inflammation without improving obesity in TSOD mice. Coffee and its components did not repair the altered levels of Gram-positive and Gram-negative bacteria and an increased abundance of Firmicutes in TSOD mice but rather caused additional changes in bacteria in six genera. However, caffeine and chlorogenic acid partially improved the disrupted plasma SCFA profile in TSOD mice, although coffee had no effects. Whether these alterations in the gut microbiome and the plasma SCFA profile might affect the liver pathology of TSOD mice may deserve further investigation. (徳島大学機関リポジトリ) ● Metadata: 114533 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-018-34571-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30385796 ● Search Scopus @ Elsevier (PMID): 30385796 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-34571-9 (徳島大学機関リポジトリ: 114533, DOI: 10.1038/s41598-018-34571-9, PubMed: 30385796)
19.	Kunihiro Ohtsuka, Kohichi Yamada, Yuhji Taquahashi, Rieko Arakaki, Aya Ushio, Masako Saito, Akiko Yamada, Takaaki Tsunematsu, Yasusei Kudo, Jun Kanno and Naozumi Ishimaru : Long-term polarization of alveolar macrophages to a profibrotic phenotype after inhalation exposure to multi-wall carbon nanotubes., PLoS ONE, Vol.13, No.10, e0205702., 2018. (要約) Nanomaterials are widely used in various fields. Although the toxicity of carbon nanotubes (CNTs) in pulmonary tissues has been demonstrated, the toxicological effect of CNTs on the immune system in the lung remains unclear. In this study, exposure to Taquann-treated multi-walled CNTs (T-CNTs) was performed using aerosols generated in an inhalation chamber. At 12 months after T-CNT exposure, alveolar inflammation with macrophage accumulation and hypertrophy of the alveolar walls were observed. In addition, fibrotic lesions were enhanced by T-CNT exposure. The macrophages in the bronchoalveolar lavage fluid of T-CNT-exposed mice were not largely shifted to any particular population, and were a mixed phenotype with M1 and M2 polarization. Moreover, the alveolar macrophages of T-CNT-exposed mice produced matrix metalloprotinase-12. These results suggest that T-CNT exposure promoted chronic inflammation and fibrotic lesion formation in profibrotic macrophages for prolonged periods. (徳島大学機関リポジトリ) ● Metadata: 113371 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0205702 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30372450 ● Summary page in Scopus @ Elsevier: 2-s2.0-85055616395 (徳島大学機関リポジトリ: 113371, DOI: 10.1371/journal.pone.0205702, PubMed: 30372450, Elsevier: Scopus)
20.	Hirohisa Ogawa, Masahiko Azuma, Takaaki Tsunematsu, Yuuki Morimoto, Mayo Kondo, Toshifumi Tezuka, Yasuhiko Nishioka and Koichi Tsuneyama : Neutrophils induce smooth muscle hyperplasia via neutrophil elastase-induced FGF-2 in a mouse model of asthma with mixed inflammation., Clinical and Experimental Allergy, Vol.48, No.12, 1715-1725, 2018. (要約) The IL-17/neutrophil axis may play an important role in airway remodelling by contributing to smooth muscle hypertrophy/hyperplasia in mixed allergic inflammation and accordingly represents an attractive therapeutic target for severe asthma. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/cea.13263 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30171733 ● Search Scopus @ Elsevier (PMID): 30171733 ● Search Scopus @ Elsevier (DOI): 10.1111/cea.13263 (DOI: 10.1111/cea.13263, PubMed: 30171733)
21.	Penkhae Utaijaratrasmi, Kulthida Vaeteewoottacharn, Takaaki Tsunematsu, Pranisa Jamjantra, Sopit Wongkham, Chawalit Pairojkul, Narong Khuntikeo, Naozumi Ishimaru, Yongyut Sirivatanauksorn, Ananya Pongpaibul, Peti Thuwajit, Chanitra Thuwajit and Yasusei Kudo : The microRNA-15a-PAI-2 axis in cholangiocarcinoma-associated fibroblasts promotes migration of cancer cells., Molecular Cancer, Vol.17, No.1, 2018. (要約) These findings highlight the miR-15a/PAI-2 axis as a potential therapeutic target in CCA patients. (徳島大学機関リポジトリ) ● Metadata: 113571 (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s12943-018-0760-x (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29347950 ● Search Scopus @ Elsevier (PMID): 29347950 ● Search Scopus @ Elsevier (DOI): 10.1186/s12943-018-0760-x (徳島大学機関リポジトリ: 113571, DOI: 10.1186/s12943-018-0760-x, PubMed: 29347950)
22.	Mie Kurosawa, Rieko Arakaki, Akiko Yamada, Takaaki Tsunematsu, Yasusei Kudo, J Sprent and Naozumi Ishimaru : NF κB2 Controls the Migratory Activity of Memory T Cells by Regulating Expression of CXCR4 in a Mouse Model of Sjögren's Syndrome, Arthritis & Rheumatology, Vol.69, No.11, 2193-2202, 2017. (要約) Dysregulated chemokine signaling contributes to autoimmune diseases by facilitating aberrant T cell infiltration into target tissues, but the specific chemokines, receptors, and T cell populations remain largely unidentified. The aim of this study was to examine the role of the potent chemokine CXCL12 and its receptor CXCR4 in the T cell autoimmune response, using alymphoplasia (aly)/aly mice, a model of Sjögren's syndrome (SS). T cell phenotypes in the salivary gland of aly/aly mice were evaluated using immunologic analysis. An in vitro migration assay was used to assess T cell migratory activity toward several chemokines. Gene expression of chemokine receptors and transforming growth factor β receptors (TGFβRs) was measured by quantitative reverse transcription-polymerase chain reaction. The CXCR4 antagonist AMD3100 was administered to the aly/aly mice in order to evaluate its suppressive effect on autoimmune lesions. Effector memory T (TEM) cells derived from aly/aly mice demonstrated higher in vitro migratory activity toward CXCL12 than did TEM cells from aly/+ mice. CXCL12 expression was specifically up-regulated in the SS target cells of aly/aly mice. TEM cells from RelB mice, but not Nfkb1 mice, also showed high migratory activity toward CXCL12, implicating a role of the nonclassical RelB/NF-κB2 pathway in the regulation of TEM cell migration. TEM cells from aly/aly mice also overexpressed TGFβR type I (TGFβRI) and TGFβRII. The CXCR4 antagonist AMD3100 suppressed autoimmune lesions in aly/aly mice by reducing TEM cell infiltration. Our results suggest that the RelB/NF-κB2 pathway regulates T cell migration to autoimmune targets through TGFβ/TGFβR-dependent regulation of CXCL12/CXCR4 signaling. This suggests that these signaling pathways are potential therapeutic targets for the treatment of autoimmune diseases. (キーワード) Animals / Chemokine CXCL12 / Chemotaxis, Leukocyte / Disease Models, Animal / Gene Expression Regulation / In Vitro Techniques / Mice / Mice, Knockout / NF-kappa B p52 Subunit / Receptors, CXCR4 / Sjogren's Syndrome / T-Lymphocytes / Transcription Factor RelB (徳島大学機関リポジトリ) ● Metadata: 111719 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/art.40230 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28804991 ● Summary page in Scopus @ Elsevier: 2-s2.0-85031674261 (徳島大学機関リポジトリ: 111719, DOI: 10.1002/art.40230, PubMed: 28804991, Elsevier: Scopus)
23.	Koichi Tsuneyama, Kazuchika Nishitsuji, Minoru Matsumoto, Tomoko Kobayashi, Yuki Morimoto, Takaaki Tsunematsu and Hirohisa Ogawa : Animal models for analyzing metabolic syndrome-associated liver diseases., Pathology International, Vol.67, No.11, 539-546, 2017. (要約) Metabolic syndrome (MS) is a worldwide healthcare issue and a dominant risk factor for the development of incurable diseases affecting the entire body. The hepatic manifestations of MS include nonalcoholic fatty liver disease (NAFLD) and its progressive variant, nonalcoholic steatohepatitis (NASH). NASH is known to progress to liver cirrhosis and hepatocellular carcinoma (HCC). Excellent animal models for determining the mechanism of pathogenesis and establishing therapeutic treatment of NASH/HCC are strongly required worldwide. We recently reported that two previously established mouse models of obesity and diabetes mellitus, namely, Tsumura-Suzuki Obese Diabetes (TSOD) mice and MSG mice, developed MS-associated NASH and that their clinical course and pathological characteristics closely mimicked those of human MS-NASH patients. Interestingly, most of the mice developed HCC with advancing age, and the pathological and functional characteristics of this condition were identical to those of human HCC. We further established a novel mouse model of HCC based on type 1 diabetes (DIAR-nSTZ mice) and reported its histopathological features. By comparing various aspects of these mouse models, specific and useful characteristics in a suitable model of MS-associated liver diseases, including hepato-carcinogenesis, can be highlighted. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/pin.12600 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29027308 ● Search Scopus @ Elsevier (PMID): 29027308 ● Search Scopus @ Elsevier (DOI): 10.1111/pin.12600 (DOI: 10.1111/pin.12600, PubMed: 29027308)
24.	Hidesuke Tada, Natsumi Fujiwara, Takaaki Tsunematsu, Yoshiko Tada, Rieko Arakaki, Naofumi Tamaki, Naozumi Ishimaru and Yasusei Kudo : Preventive effects of mouthguard use while sleeping on recurrent aphthous stomatitis: Preliminary interventional study., Clinical and Experimental Dental Research, Vol.3, No.5, 198-203, 2017. (要約) Recurrent aphthous stomatitis (RAS) is the most common inflammatory ulceration in the oral mucosa of otherwise healthy individuals and is often accompanied by severe pain. However, the etiology of RAS is not completely understood, and currently, no therapy can completely prevent RAS recurrence. In our clinical experience, we noticed that patients using a night guard, which is often used for bruxism treatment, did not develop RAS. Therefore, the aim of this study was to determine whether mouthguard use can suppress RAS development. The cohort of this interventional, prospective, single-center, and self-controlled study included 20 subjects who developed RAS at least once a month. The oral health of all the subjects was recorded for 60 days before and after intervention with a mouthguard. The average number of RAS incidences decreased from 5.5 to 1.0, the average days until healing decreased from 7.3 to 5.6, and the period with RAS decreased from 31.5 to 5.0 with mouthguard use. Mouthguard use may be beneficial for preventing RAS development. (徳島大学機関リポジトリ) ● Metadata: 111727 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/cre2.88 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29744201 ● Search Scopus @ Elsevier (PMID): 29744201 ● Search Scopus @ Elsevier (DOI): 10.1002/cre2.88 (徳島大学機関リポジトリ: 111727, DOI: 10.1002/cre2.88, PubMed: 29744201)
25.	Satoko Kujiraoka, Takaaki Tsunematsu, Yukiko Sato, Maki Yoshida, Ayataka Ishikawa, Rei Tohyama, Michio Tanaka, Yutaka Kobayashi, Tomoyuki Kondo, Aya Ushio, Kunihiro Otsuka, Mie Kurosawa, Masako Saito, Akiko Yamada, Rieko Arakaki, Hirokazu Nagai, Hiromasa Nikai, Kengo Takeuchi, Toshitaka Nagao, Youji Miyamoto, Naozumi Ishimaru and Yasusei Kudo : Establishment and characterization of a clear cell odontogenic carcinoma cell line with EWSR1-ATF1 fusion gene., Oral Oncology, Vol.69, 46-55, 2017. (要約) To the best of our knowledge, this is the first report on the establishment of a CCOC cell line. CCOC-T cells serve as a useful in vitro model for understanding the pathogenesis and nature of MOT. (徳島大学機関リポジトリ) ● Metadata: 111726 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.oraloncology.2017.04.003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28559020 ● Search Scopus @ Elsevier (PMID): 28559020 ● Search Scopus @ Elsevier (DOI): 10.1016/j.oraloncology.2017.04.003 (徳島大学機関リポジトリ: 111726, DOI: 10.1016/j.oraloncology.2017.04.003, PubMed: 28559020)
26.	Syunsuke Watanabe, Tetsuyuki Takahashi, Hirohisa Ogawa, Hisanori Uehara, Takaaki Tsunematsu, Hayato Baba, Yuki Morimoto and Koichi Tsuneyama : Daily Coffee Intake Inhibits Pancreatic Beta Cell Damage and Nonalcoholic Steatohepatitis in a Mouse Model of Spontaneous Metabolic Syndrome, Tsumura-Suzuki Obese Diabetic Mice., Metabolic Syndrome and Related Disorders, Vol.15, No.4, 170-177, 2017. (要約) A daily habit of drinking coffee could possibly play a role in the prevention of metabolic syndrome. (徳島大学機関リポジトリ) ● Metadata: 113349 (出版サイトへのリンク) ● Publication site (DOI): 10.1089/met.2016.0114 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28358620 ● Search Scopus @ Elsevier (PMID): 28358620 ● Search Scopus @ Elsevier (DOI): 10.1089/met.2016.0114 (徳島大学機関リポジトリ: 113349, DOI: 10.1089/met.2016.0114, PubMed: 28358620)
27.	Toshinori Ando, Yasusei Kudo, Shinji Iizuka, Takaaki Tsunematsu, Hanako Umehara, Madhu Shrestha, Toshihiro Matsuo, Tadahiko Kubo, Shouji Shimose, Koji Arihiro, Ikuko Ogawa, Mitsuo Ochi and Takashi Takata : Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to doxorubicin via Src-Stat3 inactivation in osteosarcoma., Scientific Reports, Vol.7, 40187, 2017. (要約) Ameloblastin (AMBN), the most abundant non-amelogenin enamel matrix protein, plays a role in ameloblast differentiation. Previously, we found that AMBN promoted osteogenic differentiation via the interaction between CD63 and integrin 1, leading to the inactivation of Src; however, how AMBN affects the malignant behavior of osteosarcoma is still unclear. Osteosarcoma affects the bone and is associated with poor prognosis because of the high rate of pulmonary metastases and drug resistance. Here we demonstrated that stable overexpression of AMBN induced apoptosis and suppressed colony formation and cell migration via the inactivation of Src-Stat3 pathway in human osteosarcoma cells. Moreover, AMBN induced chemosensitivity to doxorubicin. Thus, AMBN induced a tumor suppressive phenotype and chemosensitivity to doxorubicin via the AMBN-Src-Stat3 axis in osteosarcoma. Indeed, immunohistochemical expression of AMBN was significantly correlated with better outcome of osteosarcoma patients. Our findings suggest that AMBN can be a new prognostic marker and therapeutic target for osteosarcoma combined with conventional doxorubicin treatment. (徳島大学機関リポジトリ) ● Metadata: 112332 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/srep40187 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28054649 ● Summary page in Scopus @ Elsevier: 2-s2.0-85008395075 (徳島大学機関リポジトリ: 112332, DOI: 10.1038/srep40187, PubMed: 28054649, Elsevier: Scopus)
28.	Koichi Tsuneyama, Hayato Baba, Yuki Morimoto, Takaaki Tsunematsu and Hirohisa Ogawa : Primary Biliary Cholangitis: Its Pathological Characteristics and Immunopathological Mechanisms., The Journal of Medical Investigation : JMI, Vol.64, No.1.2, 7-13, 2017. (要約) Primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is an organ-specific autoimmune disease that predominantly affects middle-aged women and is characterized by the chronic progressive destruction of small intrahepatic bile ducts with portal inflammation and, ultimately, fibrosis. The serological hallmark of PBC is the presence of anti-mitochondrial autoantibodies (AMA). Several mechanisms have been proposed for immune-mediated bile duct damage in PBC, including the roles of T cells, B cells, other cell phenotypes, and AMA. A sign of fragility of biliary epithelial cells caused by apoptosis, senescence, and autophagy has also been noted. Several complex steps and mechanisms appear to be involved in the induction and progression of cholangitis and biliary degeneration in patients with PBC. J. Med. Invest. 64: 7-13, February, 2017. (徳島大学機関リポジトリ) ● Metadata: 111056 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.64.7 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373632 ● Search Scopus @ Elsevier (PMID): 28373632 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.7 (徳島大学機関リポジトリ: 111056, DOI: 10.2152/jmi.64.7, PubMed: 28373632)
29.	Takashi Izawa, Rieko Arakaki, Hiroki Mori, Takaaki Tsunematsu, Yasusei Kudo, Eiji Tanaka and Naozumi Ishimaru : The nuclear receptor AhR controls bone homeostasis by regulating osteoclast differentiation via the RANK/c-Fos signaling axis., The Journal of Immunology, Vol.197, No.12, 4639-4650, 2016. (要約) The aryl hydrocarbon receptor (AhR) pathway plays a key role in receptor activator of NF-κB ligand (RANKL)-mediated osteoclastogenesis. However, the mechanism underlying the regulation of AhR expression in osteoclasts and the signaling pathway through which AhR controls osteoclastogenesis remain unclear. We found that the expression of AhR in bone marrow-derived osteoclasts was upregulated by RANKL at an earlier stage than was the expression of signature osteoclast genes such as those encoding cathepsin K and NFAT, cytoplasmic, calcineurin-dependent 1. In response to RANKL, bone marrow macrophages isolated from AhR(-/-) mice exhibited impaired phosphorylation of Akt and MAPK as well as NF-κB, whereas their response to M-CSF remained unchanged. Osteoclast differentiation mediated by the AhR signaling pathway was also regulated in an RANKL/c-Fos-dependent manner. Furthermore, ligand activation of AhR by the smoke toxin benzo[a]pyrene accelerated osteoclast differentiation in a receptor-dependent manner, and AhR-dependent regulation of mitochondrial biogenesis in osteoclasts was observed. Moreover, AhR(-/-) mice exhibited impaired bone healing with delayed endochondral ossification. Taken together, the present results suggest that the RANKL/AhR/c-Fos signaling axis plays a critical role in osteoclastogenesis, thereby identifying the potential of AhR in treating pathological, inflammatory, or metabolic disorders of the bone. (出版サイトへのリンク) ● Publication site (DOI): 10.4049/jimmunol.1600822 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27849171 ● Search Scopus @ Elsevier (PMID): 27849171 ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1600822 (DOI: 10.4049/jimmunol.1600822, PubMed: 27849171)
30.	Takaaki Tsunematsu, Natsumi Fujiwara, Maki Yoshida, Yukihiro Takayama, Satoko Kujiraoka, Guangying Qi, Masae Kitagawa, Tomoyuki Kondo, Akiko Yamada, Rieko Arakaki, Mutsumi Miyauchi, Ikuko Ogawa, Yoshihiro Abiko, Hiroki Nikawa, Shinya Murakami, Takashi Takata, Naozumi Ishimaru and Yasusei Kudo : Human odontogenic epithelial cells derived from epithelial rests of Malassez possess stem cell properties., Laboratory Investigation; a Journal of Technical Methods and Pathology, 2016. (要約) Epithelial cell rests of Malassez (ERM) are quiescent epithelial remnants of the Hertwig's epithelial root sheath (HERS) that are involved in the formation of tooth roots. ERM cells are unique epithelial cells that remain in periodontal tissues throughout adult life. They have a functional role in the repair/regeneration of cement or enamel. Here, we isolated odontogenic epithelial cells from ERM in the periodontal ligament, and the cells were spontaneously immortalized. Immortalized odontogenic epithelial (iOdE) cells had the ability to form spheroids and expressed stem cell-related genes. Interestingly, iOdE cells underwent osteogenic differentiation, as demonstrated by the mineralization activity in vitro in mineralization-inducing media and formation of calcification foci in iOdE cells transplanted into immunocompromised mice. These findings suggest that a cell population with features similar to stem cells exists in ERM and that this cell population has a differentiation capacity for producing calcifications in a particular microenvironment. In summary, iOdE cells will provide a convenient cell source for tissue engineering and experimental models to investigate tooth growth, differentiation, and tumorigenesis.Laboratory Investigation advance online publication, 1 August 2016; doi:10.1038/labinvest.2016.85. (徳島大学機関リポジトリ) ● Metadata: 113576 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/labinvest.2016.85 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27479086 ● Search Scopus @ Elsevier (PMID): 27479086 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.2016.85 (徳島大学機関リポジトリ: 113576, DOI: 10.1038/labinvest.2016.85, PubMed: 27479086)
31.	Mariko Obayashi, Maki Yoshida, Takaaki Tsunematsu, Ikuko Ogawa, Tomonori Sasahira, Hiroki Kuniyasu, Issei Imoto, Yoshimitsu Abiko, Dan Xu, Saori Fukunaga, Hidetoshi Tahara, Yasusei Kudo, Toshitaka Nagao and Takashi Takata : microRNA-203 suppresses invasion and epithelial-mesenchymal transition induction via targeting NUAK1 in head and neck cancer., Oncotarget, Vol.7, No.7, 8223-8239, 2016. (要約) Head and neck squamous cell carcinoma (HNSCC) has a high capacity for invasion. To identify microRNAs (miRNAs) that regulate HNSCC invasion, we compared miRNA expression profiles between a parent HNSCC cell line and a highly invasive clone. The miR-200 family and miR-203 were downregulated in the clone. Here we focused on the role of miR-203 in invasion and epithelial-mesenchymal transition (EMT) induction in HNSCC. miR-203 was downregulated during EMT induction. Moreover, ectopic overexpression of miR-203 suppressed the invasion and induced mesenchymal-epithelial transition (MET) in HNSCC cells. Interestingly, we identified NUAK family SNF1-like kinase 1 (NUAK1) as a novel target gene of miR-203 by cyclopedic analysis using anti-Ago2 antibody. Increased expression of NUAK1 was observed during EMT induction, and ectopic expression of miR-203 delayed EMT induction by suppressing NUAK1 expression. Moreover, NUAK1 overexpression promoted the invasion of HNSCC cells. Importantly, NUAK1 expression was well correlated with poor differentiation, invasiveness, and lymph node metastasis in HNSCC cases. Overall, miR-203 has a tumor-suppressing role in invasion and EMT induction by targeting NUAK1 in HNSCC, suggesting miR-203 as a potential new diagnostic and therapeutic target for the treatment of HNSCC. (徳島大学機関リポジトリ) ● Metadata: 113044 (出版サイトへのリンク) ● Publication site (DOI): 10.18632/oncotarget.6972 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26882562 ● Summary page in Scopus @ Elsevier: 2-s2.0-84958781328 (徳島大学機関リポジトリ: 113044, DOI: 10.18632/oncotarget.6972, PubMed: 26882562, Elsevier: Scopus)
32.	Akiko Yamada, Aya Ushio, Rieko Arakaki, Takaaki Tsunematsu, Yasusei Kudo, Yoshio Hayashi and Naozumi Ishimaru : Impaired expansion of regulatory T cells in a neonatal thymectomy-induced autoimmune mouse model., The American Journal of Pathology, Vol.185, No.11, 2886-2897, 2015. (要約) Neonatal thymectomy in certain mouse strains is known to induce organ-specific autoimmunity due to impaired functions of T cells, including Foxp3(+) regulatory T (Treg) cells in the thymus. The precise mechanism underlying the induction of autoimmunity by neonatal thymectomy remains unclear. One possibility is that depletion of Treg cells breaks down peripheral tolerance. We examined the functions of Treg cells by using a murine Sjögren syndrome model of NFS/sld mice that underwent neonatal thymectomy. The ratio of Treg cells to effector memory phenotype T cells in thymectomy mice was significantly lower than that of nonthymectomy mice. In addition, in vitro induction of peripherally induced Treg cells by transforming growth factor-β (TGF-β) using naive T cells from Sjögren syndrome model mice was severely impaired. The mRNA expression of TGF-β receptor I and II and Smad3 and -4 in the TGF-β-induced signal transduction pathway of Treg cells in this Sjögren syndrome model were lower than those of control mice. In addition, Treg cells in this Sjögren syndrome model exhibited an interferon-γ-producing Th1-like phenotype that resembled effector T cells. In conclusion, these results suggest that abnormal expansion and differentiation of Treg cells and inflammatory cytokines produced by Treg cells contribute to the development of autoimmunity. (キーワード) Animals / Animals, Newborn / Autoimmunity / Cell Differentiation / Cytokines / Disease Models, Animal / Female / Interferon-gamma / Mice / Mice, Inbred C57BL / Mutation / Protein-Serine-Threonine Kinases / Receptors, Transforming Growth Factor beta / Specific Pathogen-Free Organisms / T-Lymphocytes, Regulatory / Thymectomy / Transforming Growth Factor beta (徳島大学機関リポジトリ) ● Metadata: 113529 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ajpath.2015.07.007 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26343329 ● Search Scopus @ Elsevier (PMID): 26343329 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ajpath.2015.07.007 (徳島大学機関リポジトリ: 113529, DOI: 10.1016/j.ajpath.2015.07.007, PubMed: 26343329)
33.	Takaaki Tsunematsu, Rieko Arakaki, Akiko Yamada, Naozumi Ishimaru and Yasusei Kudo : The non-canonical role of Aurora-A in DNA replication., Frontiers in Oncology, Vol.96, No.4, 468-480, 2015. (要約) Aurora-A is a well-known mitotic kinase that regulates mitotic entry, spindle formation, and chromosome maturation as a canonical role. During mitosis, Aurora-A protein is stabilized by its phosphorylation at Ser51 via blocking anaphase-promoting complex/cyclosome-mediated proteolysis. Importantly, overexpression and/or hyperactivation of Aurora-A is involved in tumorigenesis via aneuploidy and genomic instability. Recently, the novel function of Aurora-A for DNA replication has been revealed. In mammalian cells, DNA replication is strictly regulated for preventing over-replication. Pre-replication complex (pre-RC) formation is required for DNA replication as an initiation step occurring at the origin of replication. The timing of pre-RC formation depends on the protein level of geminin, which is controlled by the ubiquitin-proteasome pathway. Aurora-A phosphorylates geminin to prevent its ubiquitin-mediated proteolysis at the mitotic phase to ensure proper pre-RC formation and ensuing DNA replication. In this review, we introduce the novel non-canonical role of Aurora-A in DNA replication. (徳島大学機関リポジトリ) ● Metadata: 110980 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fonc.2015.00187 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26380219 ● Search Scopus @ Elsevier (PMID): 26380219 ● Search Scopus @ Elsevier (DOI): 10.3389/fonc.2015.00187 (徳島大学機関リポジトリ: 110980, DOI: 10.3389/fonc.2015.00187, PubMed: 26380219)

学術論文(紀要・その他):

1.	Daishiroh Kobayashi, Masaya Denda, JUNYA Hayashi, Kohta Hidaka, Yutaka Kohmura, Takaaki Tsunematsu, Kohei Nishino, Harunori Yoshikawa, OHKAWACHI Kento, Kiyomi Nigorikawa, Tetsuro Yoshimaru, Naozumi Ishimaru, Nomura Wataru, Toyomasa Katagiri, Hidetaka Kosako and Akira Otaka : Sulfoxide-mediated Cys-Trp-selective bioconjugation that enables protein labeling and peptide heterodimerization, ChemRxiv, 2024. (出版サイトへのリンク) ● Publication site (DOI): 10.26434/chemrxiv-2024-tkv7w-v2 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.26434/chemrxiv-2024-tkv7w-v2 (DOI: 10.26434/chemrxiv-2024-tkv7w-v2)

総説・解説:

1.	M Samadarani B S Siriwardena, Takaaki Tsunematsu, Guangying Qi, Naozumi Ishimaru and Yasusei Kudo : Invasion-Related Factors as Potential Diagnostic and Therapeutic Targets in Oral Squamous Cell Carcinoma-A Review., International Journal of Molecular Sciences, Vol.19, No.5, May 2018. (要約) It is well recognized that the presence of cervical lymph node metastasis is the most important prognostic factor in oral squamous cell carcinoma (OSCC). In solid epithelial cancer, the first step during the process of metastasis is the invasion of cancer cells into the underlying stroma, breaching the basement membrane (BM)-the natural barrier between epithelium and the underlying extracellular matrix (ECM). The ability to invade and metastasize is a key hallmark of cancer progression, and the most complicated and least understood. These topics continue to be very active fields of cancer research. A number of processes, factors, and signaling pathways are involved in regulating invasion and metastasis. However, appropriate clinical trials for anti-cancer drugs targeting the invasion of OSCC are incomplete. In this review, we summarize the recent progress on invasion-related factors and emerging molecular determinants which can be used as potential for diagnostic and therapeutic targets in OSCC. (徳島大学機関リポジトリ) ● Metadata: 112412 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/ijms19051462 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29758011 ● Summary page in Scopus @ Elsevier: 2-s2.0-85047065487 (徳島大学機関リポジトリ: 112412, DOI: 10.3390/ijms19051462, PubMed: 29758011, Elsevier: Scopus)
2.	Guangying Qi, Jing Liu, Sisi Mi, Takaaki Tsunematsu, Shengjian Jin, Wenhua Shao, Tian Liu, Naozumi Ishimaru, Bo Tang and Yasusei Kudo : Aurora Kinase Inhibitors In Head And Neck Cancer., Current Topics in Medicinal Chemistry, Vol.18, No.3, 199-213, Jan. 2018. (要約) Aurora kinases are a group of serine/threonine kinases responsible for the regulation of mitosis. In recent years, with the increase in Aurora kinase-related research, the important role of Aurora kinases in tumorigenesis has been gradually recognized. Aurora kinases have been regarded as a new target for cancer therapy, resulting in the development of Aurora kinase inhibitors. The study and application of these small-molecule inhibitors, especially in combination with chemotherapy drugs, represents a new direction in cancer treatment. This paper reviews studies on Aurora kinases from recent years, including studies of their biological function, their relationship with tumor progression, and their inhibitors. (徳島大学機関リポジトリ) ● Metadata: 113572 (出版サイトへのリンク) ● Publication site (DOI): 10.2174/1568026618666180112163741 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29332580 ● Summary page in Scopus @ Elsevier: 2-s2.0-85047777413 (徳島大学機関リポジトリ: 113572, DOI: 10.2174/1568026618666180112163741, PubMed: 29332580, Elsevier: Scopus)
3.	Yasusei Kudo, Tada Hidesuke, Natsumi Fujiwara, Tada Yoshiko, Takaaki Tsunematsu, Yoichiro Miyake and Naozumi Ishimaru : Oral environment and cancer, Genes and Environment, Vol.38, No.13, Aug. 2016. (要約) Cancer is now the leading cause of death in Japan. A rapid increase in cancer mortality is expected as Japan is facing a super-aged society. Many causes of cancer are known to be closely linked to life style factors, such as smoking, drinking, and diet. The oral environment is known to be involved in the pathogenesis and development of various diseases such as bronchitis, pneumonia, diabetes, heart disease, and dementia. Because the oral cavity acts as the bodily entrance for air and food, it is constantly exposed to foreign substances, including bacteria and viruses. A large number of bacteria are endemic to the oral cavity, and indigenous oral flora act to prevent the settlement of foreign bacteria. The oral environment is influenced by local factors, including dental plaque, tartar, teeth alignment, occlusion, an incompatible prosthesis, and bad lifestyle habits, and systemic factors, including smoking, consumption of alcohol, irregular lifestyle and eating habits, obesity, stress, hormones, and heredity. It has recently been revealed that the oral environment is associated with cancer. In particular, commensal bacteria in the oral cavity are involved in the development of cancer. Moreover, Candida, human papilloma virus and Epstein-Barr virus as well as commensal bacteria have been reported to be associated with the pathogenesis of cancer. In this review, we introduce recent findings of the correlation between the oral environment and cancer. (キーワード) 癌 (cancer) / Oral environment / 細菌 (bacteria) / Candida / Human papilloma virus / Epstein-Barr virus (徳島大学機関リポジトリ) ● Metadata: 114519 (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s41021-016-0042-z (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27482300 ● Search Scopus @ Elsevier (PMID): 27482300 ● Search Scopus @ Elsevier (DOI): 10.1186/s41021-016-0042-z (徳島大学機関リポジトリ: 114519, DOI: 10.1186/s41021-016-0042-z, PubMed: 27482300)
4.	Akiko Yamada, Rieko Arakaki, Masako Saito, Takaaki Tsunematsu, Yasusei Kudo and Naozumi Ishimaru : Role of regulatory T cell in the pathogenesis of inflammatory bowel disease., World Journal of Gastroenterology : WJG, Vol.22, No.7, 2195-2205, Feb. 2016. (要約) Regulatory T (Treg) cells play key roles in various immune responses. For example, Treg cells contribute to the complex pathogenesis of inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis during onset or development of that disease. Many animal models of IBD have been used to investigate factors such as pathogenic cytokines, pathogenic bacteria, and T-cell functions, including those of Treg cells. In addition, analyses of patients with IBD facilitate our understanding of the precise mechanism of IBD. This review article focuses on the role of Treg cells and outlines the pathogenesis and therapeutic strategies of IBD based on previous reports. (徳島大学機関リポジトリ) ● Metadata: 110976 (出版サイトへのリンク) ● Publication site (DOI): 10.3748/wjg.v22.i7.2195 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26900284 ● Summary page in Scopus @ Elsevier: 2-s2.0-84959872333 (徳島大学機関リポジトリ: 110976, DOI: 10.3748/wjg.v22.i7.2195, PubMed: 26900284, Elsevier: Scopus)

国際会議:

1.	Hirohisa Ogawa, Masahiko Azuma, Umeno Aya, Shimizu Mayuko, Takaaki Tsunematsu, Mayo Kondou, Murotomi Kazutoshi, Koichi Tsuneyama and Yasuhiko Nishioka : Nerve growth factor exacerbates airway hyperresponsiveness via epithelial damage by neutrophils-derived singlet oxygen in a mouse model of asthma with mixed inflammation, JSA/WAO Joint Congress 2020, WEB, Sep. 2020.
2.	Takaaki Tsunematsu, Naozumi Ishimaru and Yasusei Kudo : APC/CCdh1-mediated degradation of Borealin triggers differentiation of pluripotent stem cells., FASEB meeting Ubiquitin and Cellular Regulation, Snowmass Village, CO, USA, May 2018.
3.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Takaaki Tsunematsu, Rieko Arakaki, Yasusei Kudo, Hidehiro Kishimmoto and Naozumi Ishimaru : Analysis of follicular helper T cells in a mouse model for Sjogren's Syndorome., 11th International Congress of Autoimmunity, Lisbon, May 2018.
4.	Ayumi Sugitani, Mayuko Shimizu, Shu Taira, Takaaki Tsunematsu and Koichi Tsuneyama : Analysis of fibrogenic roles of liver infiltrating macrophages in a novel Non-alcoholic steatohepatitis (NASH) rat model with liver cirrhosis, Hepatology, Vol.66, No.S1, 1099A-1100A, Oct. 2017.
5.	Takaaki Tsunematsu, Naozumi Ishimaru and Yasusei Kudo : Chromosome passenger complex protein,Borealin is regulated by APC/C Cdh1 ubiquitin ligase complex, Cold Spring Harbor Laboratory Meeting:The Ubiquitin Family, New York, Apr. 2017.
6.	Takaaki Tsunematsu, Naozumi Ishimaru and Yasusei Kudo : The APC/C-Cdh1-Borealin axis has critical role in the maintenance of undifferentiated state in embryonal carcinoma cells, 8th International Conference SUMO, Ubiquitin, UBL Proteins- Implications for Human Diseases, Shanghai, Oct. 2016.
7.	Yasusei Kudo, Takaaki Tsunematsu and Naozumi Ishimaru : Chromosome passenger complex protein,Borealin is regulated by APC/C-Cdh1 ubiquitin ligase complex, FASEB Ubiquitin & Cellular Regulation, Montana, Jun. 2016.

国内講演発表:

1.	新垣理恵子, 常松貴明, 木曽田暁, 石丸直澄, 牛尾綾 : Effect of inhalation exposure to acrbon nanotubes and titanium dioxide on alveolar macrophages, (キーワード) nanoparticle / alveolar macrophage
2.	西田真理, 大塚邦紘, 福場真美, 浪花耕平, 可児耕一, 桃田幸弘, 永尾瑠佳, 松澤鎮史, 牛尾綾, 常松貴明, 石丸直澄, 青田桂子 : 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, 2024年9月.
3.	福場真美, 俵宏彰, 常松貴明, 青田桂子 : Association of salivary gland adipocytes and age-related inflammation, 徳島大学先端酵素学研究所シンポジウム, 2024年8月.
4.	永尾瑠佳, 山本安希子, 牛尾綾, 大塚邦紘, 松澤鎮史, 常松貴明, 石丸直澄 : シェーグレン症候群におけるT Cell Receptor Associated Transmembrane Adaptor 1 (Trat1)を介した活性化T細胞抑制機構の解明, 第22回四国免疫フォーラム, 2024年6月.
5.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : 新生仔の胸腺におけるオートファジーとシェーグレン症候群の関係性, 第113回日本病理学会総会, 2024年3月.
6.	藤丸良, 常松貴明, 常山幸一, 山下理子 : 重症低血糖を呈したIGF-2 産生肝細胞癌の1例, 日本病理学会会誌, 2024年3月.
7.	永尾瑠佳, 山本安希子, 牛尾綾, 大塚邦紘, 松澤鎮史, 常松貴明, 石丸直澄 : シェーグレン症候群の病態形成におけるT細胞の共抑制性受容体役割の解析, 第113回日本病理学会総会, 2024年3月.
8.	牛尾綾, 大塚邦紘, 常松貴明, 高橋祐次, 菅野純, 石丸直澄 : The influence of multi-walled carbon nanotube for immune systems., 第113回日本病理学会総会, 2024年3月.
9.	富田満, 堀口英久, 小川博久, 上原久典, 坂東良美, 常松貴明, 佐藤真美, 石丸直澄, 常山幸一 : CRTC1::MAML2融合遺伝子の検出で確定診断に至った粘表皮癌の2例, 第113回日本病理学会総会, 2024年3月.
10.	俵宏彰, 常松貴明, 永尾瑠佳, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : Borealin-Survivin複合体は頭頸部扁平上皮癌の分化を直接的に制御する, 第113回日本病理学会総会, 2024年3月.
11.	常松貴明, 𠮷川治孝, 永尾瑠, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : がん特殊化リボソームの同定と機能解析, 第113回日本病理学会総会, 2024年3月.
12.	永尾瑠佳, 常松貴明, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : 下顎骨腫瘍, 第143回日本病理学会中国四国支部学術集会, 2024年2月.
13.	松澤鎮史, 常松貴明, 永尾瑠佳, 大塚邦紘, 牛尾綾, 尾矢剛志, 石丸直澄 : 歯肉腫瘍, 日本病理学会中国四国支部学術集会(第143回スライドカンファレンス), 2024年2月.
14.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : 新生仔胸腺におけるT細胞の分化・成熟とオートファジーの関連についての検討, 2023年度感染・免疫クラスター・ミニリトリート, 2024年2月.
15.	MATSUZAWA Shigefumi, Aya Ushio, RUKA Nagao, TAWARA Hiroaki, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Investigation of the relationship between T cell differation and autophagy in the neonatal thymus., 第52回日本免疫学会総会・学術集会, Jan. 2024.
16.	RUKA Nagao, 山本安希子, Aya Ushio, Kunihiro Otsuka, TAWARA Hiroaki, MATSUZAWA Shigefumi, Kai Tamura, KAWAHITO Yuki, Takaaki Tsunematsu and Naozumi Ishimaru : Analysis of the suppression mechanism for activated T cells via co-inhibitory receptors in Sjogrens syndrome, 第52回日本免疫学会総会・学術集会, Jan. 2024.
17.	Kai Tamura, KAWAHITO Yuki, Mami Sato, Kunihiro Otsuka, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : Pathological analysis of nasal lesions with aging in murine models of Sjögrens syndrome, 第52回日本免疫学会総会・学術集会, Jan. 2024.
18.	KAWAHITO Yuki, Tamura Kai, Mami Sato, Kunihiro Otsuka, Aya Ushio, Takaaki Tsunematsu and Naozumi Ishimaru : The Relation between the Reduction of Mucin 19 and the Onset of Sjögrens syndrome in a Mouse Model, 第52回日本免疫学会総会・学術集会, Jan. 2024.
19.	Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, Kunihiro Otsuka, Aya Ushio and Naozumi Ishimaru : The molecular mechanism of Cancer cell cannibalism and its significance in cancer progression, 第52回日本免疫学会総会・学術集会, Jan. 2024.
20.	富田満, 堀口英久, 常松貴明, 石丸直澄, 常山幸一 : 顎下腺腫瘍, 日本病理学会中国四国支部学術集会(第142回スライドカンファレンス, 2023年11月.
21.	常松貴明, 俵宏彰, 石丸直澄 : DNA損傷シグナルによってがん細胞が獲得する新たな機能, 第59回日本口腔組織培養学会総会・学術大会, 2023年11月.
22.	俵宏彰, 常松貴明, 大塚邦紘, 牛尾綾, 石丸直澄 : 口腔扁平上皮癌におけるSurvivinの核内蓄積がもたらす新たな機能, 第59回日本口腔組織培養学会総会・学術大会, 2023年11月.
23.	松澤鎮史, 牛尾綾, 永尾瑠佳, 大塚邦紘, 俵宏彰, 常松貴明, 石丸直澄 : シェーグレン症候群と胸腺におけるT細胞の分化・成熟の関連についての検討, 第31回日本シェーグレン症候群学会学術集会, 2023年9月.
24.	Jin Shengjian, 常松貴明, 堀口大吾, 毛利安宏, 卲文華, 三好圭子, 水澤典子, Hagita Hiroko, 猿棒元陽, 吉田佳世, 吉田賀弥, 藤原奈津美, 尾崎和美, 石丸直澄, 工藤保誠 : 頭頸部扁平上皮癌(HNSCC)の進行における脱ユビキチン化酵素 OTUB1 の役割, 第82回日本癌学会学術集会, 2023年9月.
25.	俵宏彰, 常松貴明, 大塚邦紘, 牛尾綾, 石丸直澄 : 頭頚部扁平上皮癌における染色体パッセンジャー複合体非依存的なBorealin-Survivin相互作用がもたらす新たな機能, 第65回歯科基礎医学会学術大会, 2023年9月.
26.	常松貴明, 石丸直澄 : ``がんの共食い``の分子機構とその生物学的意義の解明, 2023年度徳島大学先端酵素学研究所シンポジウム, 2023年9月.
27.	TAWARA Hiroaki, Takaaki Tsunematsu, RUKA Nagao, MATSUZAWA Shigefumi, Aya Ushio, Kunihiro Otsuka and Naozumi Ishimaru : Novel role of nuclear Survivin in head and neck squamous carcinoma, 2023 Tokushima Bioscience Retreat, Sep. 2023.
28.	俵宏彰, 常松貴明, 永尾瑠佳, 松澤鎮史, 大塚邦紘, 牛尾綾, 石丸直澄 : 染色体パッセンジャー複合体構成因子Borealin-Survivin相互作用は頭頚部扁平上皮癌の代謝を制御する, 第34回日本臨床口腔病理学会総会・学術大会, 2023年8月.
29.	藤丸良, 山下理子, 常松貴明, 福田いずみ, 玉木克佳, 常山幸一 : 腫瘍随伴症状としての NICTH を伴う IGF-2 産生性肝細胞癌, 第267回徳島医学会学術集会, 2023年8月.
30.	常松貴明, 石丸直澄 : ``がんの共食い''の分子機構とその生物学的意義の解明, 第40回分子病理学研究会, 2023年7月.
31.	田村海, 川人祐樹, 佐藤真美, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群モデルマウスにおける加齢に伴う鼻腔病変の病態解析, 第112回日本病理学会総会, 2023年4月.
32.	川人祐樹, 田村海, 佐藤真美, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群疾患モデルマウスにおけるMucin19の異常と病態との関連性の解析, 第112回日本病理学会総会, 2023年4月.
33.	常松貴明, 俵宏彰, 佐藤真美, 福田一稀, 大塚邦紘, 牛尾綾, 石丸直澄 : DNA損傷シグナルによって誘導されるがん細胞の新たな機能とその分子機構, 第112回日本病理学会総会, 2023年4月.
34.	俵宏彰, 常松貴明, 福田一稀, 永尾瑠佳, 佐藤真美, 大塚邦紘, 牛尾綾, 石丸直澄 : 染色体パッセンジャー複合体構成因子Borealin-Survivin相互作用は頭頸部扁平上皮癌の代謝を制御する, 第112回日本病理学会総会, 2023年4月.
35.	永尾瑠佳, 山本安希子, 大塚邦紘, 牛尾綾, 俵宏彰, 田中秀卓, 大塚邦紘, 常松貴明, 石丸直澄 : T細胞の共抑制性受容体を介したシェーグレン症候群の発症機序の解析, 第112回日本病理学会総会, 2023年4月.
36.	牛尾綾, 松田-Lennikov 真実, 大塚邦紘, 常松貴明, 石丸直澄, 高浜洋介 : 自己免疫疾患発症における多様性胸腺髄質上皮細胞の相乗的制御機構, 第112回日本病理学会総会, 2023年4月.
37.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hiroko Hagita, YOSHIDA Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of Deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第61回四国歯学会, Mar. 2023.
38.	常松貴明, 俵宏彰, 石丸直澄 : HPV陽性癌における新規脱ユビキチン化酵素複合体の分子機構の解明, 第58回日本口腔組織培養学会学術大会・総会, 2022年12月.
39.	俵宏彰, 常松貴明, 永尾瑠佳, 福田一稀, 佐藤真美, 大塚邦紘, 牛尾綾, 石丸直澄 : 頭頸部扁平上皮癌における染色体パッセンジャー複合体構成因子Borealinの高発現がもたらす新たな役割, 第58回日本口腔組織培養学会学術大会・総会, 2022年12月.
40.	Mami Sato, Aya Ushio, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Th2 response enhances the differentiation into follicular B cells to progress the pulmonary autoimmune lesions in a mouse model of Sjögrens syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
41.	Kai Tamura, Yuki KAWAHITO, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Pathological analysis of nasal tissue in a murine model of Sjögrens syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
42.	Yuki KAWAHITO, Kai Tamura, Mami Sato, Kunihiro Otsuka, Takaaki Tsunematsu and Naozumi Ishimaru : Role of Mucin 19 in Pathogenesis of a Mouse Model for Sjögren's Syndrome, 第51回日本免疫学会学術集会, Dec. 2022.
43.	Takaaki Tsunematsu, Rieko Arakaki, Mami Sato, Kunihiro Otsuka and Naozumi Ishimaru : Exposure to Multi-Wall Carbon Nanotubes Promotes Fibrous Proliferation by Production of Matrix Metalloproteinase-12 via NF-κB Activation in Chronic Peritonitis, 第51回日本免疫学会学術集会, Dec. 2022.
44.	俵宏彰, 常松貴明, 永尾瑠佳, 佐藤真美, 大塚邦紘, 石丸直澄 : がんにおける染色体パッセンジャー複合体構成因子Borealinの高発現がもたらす新たな機能, 第45回日本分子生物学学会年会, 2022年12月.
45.	Takaaki Tsunematsu and Naozumi Ishimaru : Cell Cycle machinery unravels the molecular mechanism of Cancer cell cannibalism, 第45回日本分子生物学学会年会, Nov. 2022.
46.	福田直志, 髙丸菜都美, 秋田和也, 工藤景子, 常松貴明, 石丸直澄, 宮本洋二 : 超選択的動脈塞栓術を併用して治療した上顎中心性巨細胞肉芽腫の1例, 第67回日本口腔外科学会総会・学術大会, 2022年11月.
47.	大塚邦紘, 近藤博之, 九十九伸一, 新垣理恵子, 佐藤真美, 常松貴明, 石丸直澄, 安友康二 : シングルセルRNA-seqとマルチプレックスSpatial解析を基盤としたシェーグレン症候群の標的臓器微小環境変化の解明, 第33回日本臨床口腔病理学会, 2022年9月.
48.	常松貴明, 俵宏彰, 佐藤真美, 新垣理恵子, 大塚邦紘, 牛尾綾, 石丸直澄 : 頭頸部扁平上皮癌における染色体パッセンジャー複合体構成因子Borealinの新たな機能, 第64回歯科基礎医学会学術大会, 2022年9月.
49.	川人祐樹, 田村海, 佐藤真美, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群モデルマウスであるNFS/sldマウスの変異遺伝子Mucin19の発現解析と病態との関連性, 第64回歯科基礎医学会学術大会, 2022年9月.
50.	大塚邦紘, 九十九伸一, 近藤博之, 佐藤真美, 俵宏彰, 常松貴明, 石丸直澄, 安友康二 : シングルセルRNA-seqで紐解くシェーグレン症候群モデルに特徴的に出現するT細胞集団の解析, 第64回歯科基礎医学会学術大会, 2022年9月.
51.	田村海, 川人祐樹, 佐藤真美, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群モデルマウスにおける鼻腔組織の病態解析, 第64回歯科基礎医学会学術大会, 2022年9月.
52.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群モデルマウス肺病変におけるケモカインの機能分析, 第64回歯科基礎医学会学術大会, 2022年9月.
53.	shengjian jin, Takaaki Tsunematsu, Taigo Horiguchi, Naozumi Ishimaru and Yasusei Kudo : 脱ユビキチン化酵素OTUB1の頭頸部扁平上皮癌の進展における役割, 第64回歯科基礎医学会学術大会, Sep. 2022.
54.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 石丸直澄 : シェーグレン症候群疾患モデルマウスの肺病変における濾胞B細胞の自己反応性獲得機構の解明, 先端歯学国際教育研究ネットワーク先端歯学スクール, 2022年8月.
55.	常松貴明, 石丸直澄 : 頭頚部扁平上皮癌における染色体パッセンジャー複合体構成因子Borealinの新たな機能, 第39回分子病理研究会内灘かほくシンポジウム, 2022年7月.
56.	Mami Sato, Aya Ushio, Kazuki FUKUTA, Hiroaki TAWARA, Kunihiro Otsuka, Takaaki Tsunematsu, Rieko Arakaki and Naozumi Ishimaru : Extraglandular lesions in Sjogren's syndorome model mice., 第20回四国免疫フォーラム, Jun. 2022.
57.	佐藤真美, 牛尾綾, 大塚邦紘, 常松貴明, 新垣理恵子, 石丸直澄 : シェーグレン症候群モデルマウス肺病変に対するケモカイン群の機能的解析, 第20回四国免疫フォーラム, 2022年6月.
58.	常松貴明, 石丸直澄 : 口腔扁平上皮癌におけるchromosome passenger complex構成因子Borealinが誘導するSurvivin安定化機構の解明, 第76回日本口腔科学会学術集会, 2022年4月.
59.	常松貴明, 俵宏彰, 田中秀卓, 福田一稀, 佐藤真美, 大塚邦紘, 新垣理恵子, 石丸直澄 : 口腔扁平上皮癌におけるBorealinの高発現がもたらすSurvivin安定化機構の解明, 第111回日本病理学会総会, 2022年4月.
60.	佐藤真美, 新垣理恵子, 常松貴明, 工藤保誠, 石丸直澄 : シェーグレン症候群疾患モデルにおける肺病変発症へのCCL6の役割, 第111回日本病理学会総会, 2022年4月.
61.	工藤保誠, 常松貴明, 毛利安宏 : Aurora-Bキナーゼ阻害剤による多能性幹細胞の分化誘導, 第95回日本薬理学会年会, 2022年3月.
62.	佐藤真美, 常松貴明, 大塚邦紘, 石丸直澄 : 下顎骨病変, 日本病理学会中国四国支部学術集会 (第 137 回スライドカンファレンス), 2022年2月.
63.	新垣理恵子, 常松貴明, 石丸直澄 : Pulmonary immune response and molecular mechanism of fibrosis by inhalation exposure to nanomaterials, 第50回日本免疫学会学術集会, 2021年12月.
64.	常松貴明, 新垣理恵子, 石丸直澄 : HPV陽性癌細胞の増殖に必須の脱ユビキチン化酵素の同定とその分子メカニズムの解明, 第57回口腔組織培養学会学術大会, 2021年11月.
65.	常松貴明, 石丸直澄 : がん細胞の老化細胞様変化による新たな機能の獲得とその分子機構, 第63回歯科基礎医学会学術大会アップデートシンポジウム「がん研究の新たな潮流~歯学基礎研究からの発信~」, 2021年10月.
66.	佐藤真美, 牛尾綾, 福田一稀, 俵宏彰, 大塚邦紘, 常松貴明, 新垣理恵子, 石丸直澄 : シェーグレン症候群モデルマウスにおける肺病変の病態探索, 第29回日本シェーグレン症候群学会学術集会, 2021年9月.
67.	常松貴明 : 頭頸部癌におけるDUBsを介したシンセティックリーサリティーの確立への挑戦, 第32回日本臨床口腔病理学会学術大会若手シンポジウム2(口腔腫瘍研究の最前線), 2021年8月.
68.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 佐藤真美, 木曽田暁, 卲文華, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : Achaete-Scute Homologue 2-Regulated Follicular Helper T Cells Promote Autoimmunity in a Murine Model for Sjögren Syndrome., 第32回日本臨床口腔病理学会奨励賞(実験病理分野), 2021年8月.
69.	石丸直澄, 新垣理恵子, 常松貴明, 高橋祐次, 菅野純 : ナノマテリアルの吸入暴露による肺免疫応答と線維化の分子機構, 第48回日本毒性学会学術年会, 2021年7月.
70.	佐藤真美, 牛尾綾, 福田一稀, 俵宏彰, 大塚邦紘, 常松貴明, 新垣理恵子, 石丸直澄 : シェーグレン症候群モデルマウスにおける腺外病変, 第19回四国免疫フォーラム, 2021年6月.
71.	常松貴明, 北川巧, 工藤保誠, 石丸直澄 : 口腔扁平上皮癌の進展におけるPeriostinスプライシングバリアントの新たな役割, 第75回日本口腔科学会学術集会, 2021年5月.
72.	佐藤真美, 牛尾綾, 常松貴明, 新垣理恵子, 石丸直澄 : シェーグレン症候群モデルマウスにおける肺病変の解析, 第110回日本病理学会学術集会, 2021年4月.
73.	新垣理恵子, 清水朱里, 佐藤真美, 俵宏彰, 常松貴明, 石丸直澄 : 唾液腺における常在型自然リンパ球の同定とシェーグレン症候群病態への関与, 第110回日本病理学会学術集会, 2021年4月.
74.	常松貴明, 北川巧, 佐藤真美, 新垣理恵子, 石丸直澄 : HPV陽性扁平上皮癌細胞の生存に必須な脱ユビキチン化酵素の同定とその役割の解明, 第110回日本病理学会総会, 2021年4月.
75.	佐藤真美, 牛尾綾, 新垣理恵子, 俵宏彰, 常松貴明, 石丸直澄 : シェーグレン症候群モデルマウスにおける腺外病変の発症機序, 四国歯学会第57回例会, 2021年3月.
76.	佐藤真美, 常松貴明, 大塚邦紘, 石丸直澄 : 下顎骨病変, 日本病理学会中国四国支部学術集会第 137 回スライドカンファレンス, 2021年2月.
77.	木曽田暁, 卲文華, Jin Shengjian, 常松貴明, 石丸直澄, 工藤保誠 : 頭頸部扁平上皮癌の予後を予測する新規システムの構築, 第79回日本癌学会学術総会, 2020年10月.
78.	常松貴明, 工藤保誠, 石丸直澄 : 多角的アプローチによる口腔癌の発生・進展の分子機構の解明, 第62回歯科基礎医学会学術大会先端歯学国際教育研究ネットワーク・シンポジウム「歯学研究の今昔と次世代研究」, 2020年9月.
79.	Wenhua Shao, Umeda Masaaki, Takaaki Tsunematsu, Kisoda Satoru and Naozumi Ishimaru : Novel periostin inform promotes invasion and metastasis in head and neck squamous cell carcinoma., 第109回日本病理学会総会, Jul. 2020.
80.	常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : 染色体パッセンジャー複合体による胎児性癌の未分化性維持機構, 第109回日本病理学会総会, 2020年7月.
81.	木曽田暁, 邵文華, 常松貴明, 石丸直澄, 工藤保誠 : 口腔癌におけるpartial EMTに関連する遺伝子の悪性度への関与, 第78回日本癌学会学術総会, 2019年9月.
82.	木曽田暁, 卲文華, 常松貴明, 石丸直澄, 工藤保誠 : 口腔癌におけるpartial-EMTに関連する遺伝子の悪性度への関与, 第78回日本癌学会学術総会, 2019年9月.
83.	Takaaki Tsunematsu, Naozumi Ishimaru and Yasusei Kudo : The maintenance of pluripotency by chromosome passenger complex in pluripotent stem cells., 日本RNAi研究会, Aug. 2019.
84.	常松貴明, 石丸直澄, 工藤保誠 : 染色体パッセンジャー複合体によるAurora-B活性を介した多能性幹細胞の未分化能維持機構, 第16回日本病理学会カンファレンス, 2019年8月.
85.	常松貴明, 石丸直澄, 工藤保誠 : 染色体パッセンジャー複合体による未分化能維持機構, 第135回日本薬理学会近畿部会, 2019年6月.
86.	常松貴明, 河合秀彦, 石丸直澄, Willium C Earnshaw, Michele Pagano, 工藤保誠 : 染色体パッセンジャー複合体による多能性幹細胞の未分化能維持機構, 第36回染色体ワークショップ, 2019年1月. (キーワード) 細胞周期 (cell cycle) / 人工多能性幹細胞 (induced pluripotent stem cells)
87.	Rieko Arakaki, Nakayama Shinichiro, Aya Ushio, Otsuka Kunihiro, Kisoda Satoshi, Takaaki Tsunematsu, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : The role of the cleaved from IL-33 in pathogenesis of Sjogren's syndorome(SS), Proceedings of the Japanese Society for Immunology, Dec. 2018.
88.	Kunihiro Ohtsuka, Akiko Yamada, Masako Saito, Aya Ushio, Satoru Kisoda, Takaaki Tsunematsu, Yasusei Kudo, Rieko Arakaki and Naozumi Ishimaru : A crucial role of follicular helper T cells in autoimmunity of a mouse model for Sjogren's syndorome., Proceedings of the Japanese Society for Immunology, Dec. 2018.
89.	常松貴明, 石丸直澄, 工藤保誠 : 多能性幹細胞においてAPC/CCdh1によるBorealinの分解は分化を誘発する, 第41回日本分子生物学会年会, 2018年11月. (キーワード) 細胞周期 (cell cycle) / 人工多能性幹細胞 (induced pluripotent stem cells)
90.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本シェーグレン症候群学会, 2018年9月.
91.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本歯科基礎医学会誌, 2018年9月.
92.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : Asc/2を介した濾胞ヘルパーT細胞分化異常が自己免疫疾患の病態形成に関与する．, 日本臨床口腔病理学会, 2018年8月.
93.	清水真祐子, 西辻和親, 清水金忠, 小川博久, 常松貴明, 梅本ひとみ, 森本友樹, 赤津裕康, 井之上浩一, 常山幸一 : TSODマウスにおけるNAFLDの発症およびコーヒーの投与による腸内細菌叢および短鎖脂肪酸プロファイルの変化, 第5回肝臓と糖尿病・代謝研究会, 2018年7月. (キーワード) TSOD mice / short chain fatty acid / microbiota / coffee
94.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 木曽田暁, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 分子病理学研究会, 2018年7月.
95.	中山慎一朗, 新垣理恵子, 牛尾綾, 大塚邦紘, 常松貴明, 工藤保誠, 石丸直澄 : シェーグレン症候群モデルマウス唾液腺におけるIL-33の発現とその役割, 日本病理学会会誌, Vol.107, 2018年6月.
96.	西條早紀, 大塚邦紘, 常松貴明, 大塚邦紘, 牛尾綾, 新垣理恵子, 工藤保誠, 石丸直澄 : Emi1の過剰発現による人工口腔癌幹細胞の作成, 日本病理学会会誌, Vol.107, 2018年6月.
97.	沼田雪乃, 大塚邦紘, 山田安希子, 牛尾綾, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルにおけるNotchシグナルの役割, 日本病理学会会誌, Vol.107, 2018年6月.
98.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群疾患モデルの自己免疫病変における濾胞ヘルパーT細胞の役割, 日本病理学会会誌, Vol.107, 2018年6月.
99.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 鯨岡聡子, 黒澤実愛, 常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : シェーグレン症候群疾患モデルにおける胚中心反応の解析, 第28回日本臨床口腔病理学会, Vol.28, 2017年8月.
100.	新垣理恵子, 山田耕一, 齋藤雅子, 大塚邦紘, 山田安希子, 常松貴明, 工藤保誠, 菅野純, 石丸直澄 : Chronic influence of Multi-walled carbon nanotubes (MWCNT) on immune system, 第106回日本病理学会総会, Vol.106, 2017年4月.
101.	常松貴明, 工藤保誠, 山田安希子, 新垣理恵子, 小川博久, 常山幸一, 石丸直澄 : 胎児性癌細胞におけるユビキチンプロテアソーム経路による未分化性維持機構, 第106回日本病理学会総会, Vol.106, 2017年4月.
102.	牛尾綾, 新垣理恵子, 山田安希子, 大塚邦紘, 鯨岡聡子, 常松貴明, 工藤保誠, 石丸直澄 : シェーグレン症候群の唾液腺におけるマクロファージサブセットと病態への関与, 第106回日本病理学会総会, Vol.106, 2017年4月.
103.	鯨岡聡子, 工藤保誠, 常松貴明, 牛尾綾, 大塚邦紘, 山田安希子, 新垣理恵子, 石丸直澄 : 歯原性明細胞癌細胞株の樹立とその性状解析, 第106回日本病理学会総会, Vol.106, 2017年4月.
104.	梅田将旭, 常松貴明, 齋藤雅子, 山田安希子, 新垣理恵子, 工藤保誠, 石丸直澄 : 口腔癌におけるPeriostinスプライシングバリアントの新たな役割, 第106回日本病理学会総会, Vol.106, 2017年4月.
105.	大塚邦紘, 山田安希子, 齋藤雅子, 牛尾綾, 黒澤実愛, 鯨岡聡子, 常松貴明, 工藤保誠, 新垣理恵子, 石丸直澄 : シェーグレン症候群モデルマウスにおける濾胞ヘルパーT細胞の解析, 第106回日本病理学会総会, Vol.106, 2017年4月.
106.	Ayumi Sugitani, Ryusei Takahashi, Kohki Kai, Mayuko Shimizu, 平修, 川口誠, Hirohisa Ogawa, Takaaki Tsunematsu, Koichi Tsuneyama, 野本一博 and Koichi Tsuneyama : A case of lipid-rich carcinoma of the breast with numerous hyaline globules, Proceedings of the Japanese Society of Pathology, Vol.106, No.1, 492-493, Mar. 2017.
107.	常松貴明, 工藤保誠, 山田安希子, 新垣理恵子, 小川博久, 常山幸一, 石丸直澄 : 胎児性癌細胞におけるユビキチンプロテアソーム経路による未分化性維持機構, 日本病理学会会誌, Vol.106, No.1, 356, 2017年3月.
108.	常山幸一, 渡邊俊介, 高橋徹行, 馬場逸人, 森本友樹, 常松貴明, 小川博久 : 自然発症メタボリックシンドローム-NASHモデル動物を用いた少量のコーヒー摂取による病態抑制効果の検討, 日本病理学会会誌, Vol.106, No.1, 441, 2017年3月.
109.	小川博久, 常松貴明, 森本友樹, 常山幸一 : IL-17/好中球は気道粘膜上皮透過性を増加させFGF-2産生を介した気道平滑筋肥厚を誘導する, 日本病理学会会誌, Vol.106, No.1, 474, 2017年3月.
110.	杉谷鮎美, 高橋立成, 甲斐幸樹, 清水真祐子, 平修, 川口誠, 小川博久, 常松貴明, 常山幸一, 野本一博, 常山幸一 : A case of lipid-rich carcinoma of the breast with numerous hyaline globules(和訳中), 日本病理学会会誌, Vol.106, No.1, 492-493, 2017年3月.
111.	Rieko Arakaki, Kohichi Yamada, Aya Ushio, Mie Kurosawa, Kunihiro Ohtsuka, Masako Saito, Takaaki Tsunematsu, Akiko Yamada, Yasusei Kudo and Naozumi Ishimaru : Immunological and toxicological effect of multi-wall carbon nanotubes by whole body inhalation exposure in B6 mice, 第45回日本免疫学会学術集会, Vol.45, Dec. 2016.
112.	Akiko Yamada, Rieko Arakaki, Aya Ushio, Takaaki Tsunematsu, Yasusei Kudo and Naozumi Ishimaru : 1)Impaired Expansion of Regulatory T cells in a Murine model of Neonatal Thymectomy-induced Sjogrens Syndrome, 第45回日本免疫学会学術集会, Vol.45, Dec. 2016.
113.	牛尾綾, 工藤保誠, 鯨岡聡子, 大塚邦紘, 常松貴明, 山田安希子, 石丸直澄 : 上顎骨腫瘍, 日本臨床口腔病理学会総会・学術集会, Vol.27, 2016年8月.
114.	鯨岡聡子, 工藤保誠, 常松貴明, 牛尾綾, 大塚邦紘, 山田安希子, 石丸直澄 : 小児に発生した歯原性下顎骨腫瘍の1例, 日本臨床口腔病理学会総会・学術集会, Vol.27, 2016年8月.
115.	梅田将旭, 常松貴明, 齋藤雅子, 山田安希子, 新垣理恵子, 工藤保誠, 石丸直澄 : 口腔扁平上皮癌におけるPeriostinスプライシングバリアントの新たな役割, 第27回日本臨床口腔病理学会総会・学術大会, 2016年8月.
116.	新垣理恵子, 常松貴明, 山田安希子, 齋藤雅子, 工藤保誠, 石丸直澄 : 全身吸入暴露による多層化カーボンナノチューブの免疫システムへの影響, 第105回日本病理学会総会, Vol.105, No.1, 2016年5月.
117.	鯨岡聡子, 工藤保誠, 常松貴明, 近藤智之, 牛尾綾, 大塚邦紘, 山田安希子, 新垣理恵子, 石丸直澄 : 顎骨中心性明細胞性腫瘍からの細胞株の樹立とその性状, 第105回日本病理学会総会, Vol.105, No.1, 2016年5月.
118.	常山幸一, 小川博久, 常松貴明, 上原久典 : 新生児期ストレプトゾトシン投与4CS系マウスは通常食飼育によって持続高血糖なしに肝腫瘍を発症する, 日本病理学会会誌, Vol.105, No.1, 384, 2016年4月.
119.	小川博久, 常松貴明, 上原久典, 常山幸一 : ダニ抗原経鼻感作はIL-17/好中球を増加させ平滑筋肥厚を伴う気道リモデリングを誘導する, 日本病理学会会誌, Vol.105, No.1, 386, 2016年4月.
120.	上原久典, 小川博久, 常松貴明, 常山幸一 : 前立腺癌細胞の骨内増殖におけるlipolysis stimulated lipoprotein receptorの役割, 日本病理学会会誌, Vol.105, No.1, 466, 2016年4月.
121.	常松貴明, 工藤保誠, 山田安希子, 新垣理恵子, 小川博久, 上原久典, 石丸直澄, 常山幸一 : 染色体パッセンジャー複合体タンパク質Borealinのユビキチン分解の意義とその癌化への関与, 日本病理学会会誌, Vol.105, No.1, 548, 2016年4月.
122.	良祐別所, 常松貴明, 小川博久, 上原久典, 常山幸一 : 自然発症2型糖尿病モデルマウスにおける膵島の外分泌腺組織への変化がβ細胞の機能不全に果たす役割, 日本病理学会会誌, Vol.105, No.1, 595, 2016年4月.
123.	新垣理恵子, 牛尾綾, 黒澤実愛, 大塚邦紘, 山田安希子, 齋藤雅子, 常松貴明, 工藤保誠, 石丸直澄 : Analysis of function of macrophages in murine models of Sjogren's syndorome., 日本免疫学会総会·学術集会記録, 2015年11月.
124.	黒澤実愛, 山田安希子, 新垣理恵子, 齋藤雅子, 常松貴明, 工藤保誠, 石丸直澄 : Migratory activity of memory T cells in aly/aly mice., 日本免疫学会総会·学術集会記録, 2015年11月.
125.	近藤智之, 常松貴明, 工藤保誠, 石丸直澄 : 自己免疫疾患モデルにおける腫瘍増殖の亢進, 第74回日本癌学会学術総会, 2015年10月.
126.	常松貴明, 工藤保誠, 近藤智之, 牛尾綾, 鯨岡聡子, 山田安希子, 新垣理恵子, 石丸直澄 : 染色体パッセンジャー複合体タンパク質Borealinのユビキチン分解とその癌化への関与, 日本病理学会会誌, Vol.104, No.1, 504, 2015年5月.
127.	鯨岡聡子, 工藤保誠, 常松貴明, 近藤智之, 牛尾綾, 山田安希子, 新垣理恵子, 石丸直澄 : 口腔癌細胞におけるペリオスチンのスプライシングバリアントの発現とその意義, 日本病理学会会誌, Vol.104, No.1, 497, 2015年4月.
128.	近藤智之, 常松貴明, 鯨岡聡子, 鯨岡聡子, 牛尾綾, 山田安希子, 新垣理恵子, 工藤保誠, 石丸直澄 : 自己免疫疾患モデルを用いた腫瘍増殖制御機構の解明, 日本病理学会会誌, Vol.104, No.1, 497, 2015年4月.
129.	牛尾綾, 新垣理恵子, 近藤智之, 鯨岡聡子, 常松貴明, 山田安希子, 工藤保誠, 石丸直澄 : Analysis of macrophages in the pathogenesis of a murine for Sjogren's syndorome., 日本病理学会会誌, Vol.104, No.1, 450, 2015年4月.
130.	工藤保誠, 常松貴明, 鯨岡聡子, 近藤智之, 牛尾綾, 山田安希子, 新垣理恵子, 石丸直澄 : 顎骨中心性粘表皮癌細胞株の樹立とその性状, 日本病理学会会誌, Vol.104, No.1, 401, 2015年4月.
131.	新垣理恵子, 常松貴明, 山田安希子, 工藤保誠, 菅野純, 石丸直澄 : 自己免疫疾患モデルマウスを利用した多層化カーボンナノチューブの免疫システムへの影響, 日本病理学会会誌, Vol.104, No.1, 380, 2015年4月.

その他・研究会:

1.	木曽田暁, 邵文華, 常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : 口腔癌における上皮-間葉移行の関与, 徳島県歯科医学大会(四国歯学会第56回例会), 2020年2月.
2.	邵文華, Takaaki Tsunematsu, 梅田将旭, 木曽田暁, Rieko Arakaki, Yasusei Kudo and Naozumi Ishimaru : 口腔癌の進展に関わる新規ペリオスチンスプライシングバリアントの同定, 徳島県歯科医学大会(四国歯学会第56回例会), Feb. 2020.
3.	林亜門, 清水朱里, 中西美緒, 山内加奈, 佐藤真美, 邵文華, 木曽田暁, 福井仁美, 木野倫子, 牛尾綾, 山田安希子, 常松貴明, 新垣理恵子, 工藤保誠, 石丸直澄 : 口腔分子病態学分野における免疫・癌研究, 徳島県歯科医学大会(四国歯学会第56回例会), 2020年2月.
4.	常松貴明, 石丸直澄, 工藤保誠 : 染色体パッセンジャー複合体による多能性幹細胞の未分化能維持機構, 第37回染色体ワークショップ・第18回核ダイナミクス研究会, 2019年12月.
5.	常松貴明, 石丸直澄, 工藤保誠 : 染色体パッセンジャー複合体によるAurora-B活性を介した多能性幹細胞の未分化能維持機構, 第16回日本病理学会カンファレンス, 2019年8月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

共食い口腔がん細胞による新たな腫瘍免疫逃避機構の同定 (研究課題/領域番号: 24K22189 )
免疫難病における自己抗体産生機構の解明と多角的臨床応用 (研究課題/領域番号: 23K18361 )
免疫チューニング分子を基盤とした自己免疫疾患の新たな病因論の確立と治療戦略 (研究課題/領域番号: 23H00438 )
DNA損傷が司る”がんの共食い”を介した口腔がんの新たな高悪性化機構の解明 (研究課題/領域番号: 22K19630 )
定量プロテオミクスが紐解く新規タンパク質複合体によるHPV陽性癌の新たな病因論 (研究課題/領域番号: 23K24547 )
DUBによる頭頸部癌のシンセティックリーサリティーの確立と革新的治療法の開発 (研究課題/領域番号: 20KK0378 )
唾液腺ムチンタンパクの糖鎖形成異常を介した自己免疫疾患の新たな発症機序の解明 (研究課題/領域番号: 21K19605 )
相同組み換え修復を制御するUSP26を標的とした頭頸部癌新規治療戦略 (研究課題/領域番号: 20K18480 )
臓器間コミュニケーションを介した自己免疫疾患発症機序の解明 (研究課題/領域番号: 19H01070 )
顎顔面領域骨代謝性疾患におけるエピゲノム制御による新規骨リモデリング機構の解明 (研究課題/領域番号: 18H03011 )
病態解明と新規治療薬開発を可能にする口腔扁平上皮癌高転移モデルマウスの創出 (研究課題/領域番号: 17K19761 )
人工口腔癌幹細胞の作製とその性状解析による新たな研究基盤の確立 (研究課題/領域番号: 17K19760 )
過剰なDNA複製を抑制する分子機構の同定とその破綻による発癌機構の解明 (研究課題/領域番号: 16H06271 )
染色体パッセンジャー複合体タンパクの分解とその破綻による口腔発癌機構の解明と制御 (研究課題/領域番号: 16H05542 )
口腔癌のEMTを制御するマスター遺伝子の探索と新規口腔癌治療戦略 (研究課題/領域番号: 15K15740 )
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准教授 : 常松貴明