Tokushima University / Educator and Researcher Directory --- Tenshin, Hirofumi

Field of Study

Subject of Study

Book / Paper

Book:

1.	Eiji Tanaka, Akiko Oka, Daishi Arai and Hirofumi Tenshin : アンカースクリューを用いた上顎歯列全体の圧下によりガミースマイルを改善した症例．, Ishiyaku Publishers,Inc., Tokyo, Nov. 2019.
2.	Eiji Tanaka, Hirofumi Tenshin, Hiroki Mori and Keiichiro Watanabe : B-maxスクリュー Type-TKを用いた成人開咬の治療戦略, クインテッセンス出版株式会社, Tokyo, 2018.

Academic Paper (Judged Full Paper):

1.	Hirofumi Tenshin, Jesus Delgado-Calle, Jolene J Windle, G David Roodman, John M Chirgwin and Noriyoshi Kurihara : Osteocytes and Paget's Disease of Bone, Current Osteoporosis Reports, Vol.22, No.2, 266-272, 2024. (Summary) To describe the contributions of osteocytes to the lesions in Paget's disease, which are characterized by locally overactive bone resorption and formation. Osteocytes, the most abundant cells in bone, are altered in Paget's disease lesions, displaying increased size, decreased canalicular length, incomplete differentiation, and less sclerostin expression compared to controls in both patients and mouse models. Pagetic lesions show increased senescent osteocytes that express RANK ligand, which drives osteoclastic bone resorption. Abnormal osteoclasts in Paget's disease secrete abundant IGF1, which enhances osteocyte senescence, contributing to lesion formation. Recent data suggest that osteocytes contribute to lesion formation in Paget's disease by responding to high local IGF1 released from abnormal osteoclasts. Here we describe the characteristics of osteocytes in Paget's disease and their role in bone lesion formation based on recent results with mouse models and supported by patient data. (Keyword) Osteitis Deformans / Osteocytes / Humans / Animals / Osteoclasts / RANK Ligand / Bone Resorption / Mice / Insulin-Like Growth Factor I / Disease Models, Animal / Cellular Senescence (Link to Publication Site) ● Publication site (DOI): 10.1007/s11914-024-00863-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38457001 ● Search Scopus @ Elsevier (PMID): 38457001 ● Search Scopus @ Elsevier (DOI): 10.1007/s11914-024-00863-5 (DOI: 10.1007/s11914-024-00863-5, PubMed: 38457001)
2.	HANAWA Shigeki, Masahiro Hiasa, Akihiko Iwasa, Keiichiro Watanabe, Hirofumi Tenshin, Nao Kinouchi, Shinya Horiuchi and Eiji Tanaka : 上顎左側第二小臼歯先天欠如を伴う片側性唇顎口蓋裂患者に対して下顎左側第二小臼歯を移植した一症例．, The Journal of Chu-Shikoku Orthodontic Society, Vol.35, No.1, 67-76, 2023. (Keyword) 中・四国矯正歯科学会雑誌 35(1):67-76.
3.	Hirofumi Tenshin, Kazuaki Miyagawa, Patrick L. Mulcrone, Jesus Delgado-Calle, Mark A. Subler, Jolene J. Windle, John M. Chirgwin, G. David Roodman and Noriyoshi Kurihara : Osteoclast-derived IGF1 induces RANKL production in osteocytes and contributes to pagetic lesion formation, JCI Insight, Vol.8, No.14, e159838, 2023. (Summary) We previously reported that measles virus nucleocapsid protein (MVNP) expression in osteoclasts (OCLs) of patients with Paget disease (PD) or targeted to the OCL lineage in MVNP-transgenic mice (MVNP mice) increases IGF1 production in osteoclasts (OCL-IGF1) and leads to development of PD OCLs and pagetic bone lesions (PDLs). Conditional deletion of Igf1 in OCLs of MVNP mice fully blocked development of PDLs. In this study, we examined whether osteocytes (OCys), key regulators of normal bone remodeling, contribute to PD. OCys in PDLs of patients and of MVNP mice expressed less sclerostin, and had increased RANKL expression compared with OCys in bones from WT mice or normal patients. To test whether increased OCL-IGF1 is sufficient to induce PDLs and PD phenotypes, we generated TRAP-Igf1 (T-Igf1) transgenic mice to determine whether increased IGF1 expression in the absence of MVNP in OCLs is sufficient to induce PDLs and pagetic OCLs. We found that T-Igf1 mice at 16 months of age developed PD OCLs, PDLs, and OCys, with decreased sclerostin and increased RANKL, similar to MVNP mice. Thus, pagetic phenotypes could be induced by OCLs expressing increased IGF1. OCL-IGF1 in turn increased RANKL production in OCys to induce PD OCLs and PDLs. (Keyword) Animals / Mice / Bone and Bones / Gene Expression / Mice, Transgenic / Osteitis Deformans / Osteoclasts / Osteocytes (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.159838 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37338990 ● Search Scopus @ Elsevier (PMID): 37338990 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.159838 (DOI: 10.1172/jci.insight.159838, PubMed: 37338990)
4.	F Meo Di, A Iyer, K Akama, R Cheng, C Yu, A Cesarano, N Kurihara, Hirofumi Tenshin, A Aljoufi, S Marino, RK Soni, J Roda, J Sissons, LP Vu, M Guzman, K Huang, T Laskowski, HE Broxmeyer, DG Roodman and F Perna : A target discovery pipeline identified ILT3 as a target for immunotherapy of multiple myeloma, Cell Reports. Medicine, Vol.18, No.7, 101110, 2023. (Summary) Multiple myeloma (MM) is an incurable malignancy of plasma cells. To identify targets for MM immunotherapy, we develop an integrated pipeline based on mass spectrometry analysis of seven MM cell lines and RNA sequencing (RNA-seq) from 900+ patients. Starting from 4,000+ candidates, we identify the most highly expressed cell surface proteins. We annotate candidate protein expression in many healthy tissues and validate the expression of promising targets in 30+ patient samples with relapsed/refractory MM, as well as in primary healthy hematopoietic stem cells and T cells by flow cytometry. Six candidates (ILT3, SEMA4A, CCR1, LRRC8D, FCRL3, IL12RB1) and B cell maturation antigen (BCMA) present the most favorable profile in malignant and healthy cells. We develop a bispecific T cell engager targeting ILT3 that shows potent killing effects in vitro and decreased tumor burden and prolonged mice survival in vivo, suggesting therapeutic relevance. Our study uncovers MM-associated antigens that hold great promise for immune-based therapies of MM. (Keyword) Animals / Mice / Multiple Myeloma / Immunotherapy / T-Lymphocytes / Plasma Cells (Link to Publication Site) ● Publication site (DOI): 10.1016/j.xcrm.2023.101110 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37467717 ● Search Scopus @ Elsevier (PMID): 37467717 ● Search Scopus @ Elsevier (DOI): 10.1016/j.xcrm.2023.101110 (DOI: 10.1016/j.xcrm.2023.101110, PubMed: 37467717)
5.	Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, Sou Shimizu, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Eiji Tanaka and Masahiro Abe : Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors., International Journal of Hematology, 2023. (Summary) Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders. (Tokushima University Institutional Repository) ● Metadata: 118380 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03601-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37039914 ● Search Scopus @ Elsevier (PMID): 37039914 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03601-2 (Tokushima University Institutional Repository: 118380, DOI: 10.1007/s12185-023-03601-2, PubMed: 37039914)
6.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, Mariko Tanaka, Sooha Kim, Motosumi Nakagawa, Sou Shimizu, Kotaro Tanimoto, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : The Xanthine Oxidase Inhibitor Febuxostat Suppresses Adipogenesis and Activates Nrf2., Antioxidants, Vol.12, No.1, 2023. (Summary) Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine catabolism that acts as a novel regulator of adipogenesis. In pathological states, xanthine oxidoreductase activity increases to produce excess reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical inducer of antioxidants, which is bound and repressed by a kelch-like ECH-associated protein 1 (Keap1) in the cytoplasm. The Keap1-Nrf2 axis appears to be a major mechanism for robust inducible antioxidant defenses. Here, we demonstrate that febuxostat, a xanthine oxidase inhibitor, alleviates the increase in adipose tissue mass in obese mouse models with a high-fat diet or ovariectomy. Febuxostat disrupts in vitro adipocytic differentiation in adipogenic media. Adipocytes appeared at day 7 in absence or presence of febuxostat were 160.8 ± 21.2 vs. 52.5 ± 12.7 (p < 0.01) in 3T3L1 cells, and 126.0 ± 18.7 vs. 55.3 ± 13.4 (p < 0.01) in 10T1/2 cells, respectively. Adipocyte differentiation was further enhanced by the addition of hydrogen peroxide, which was also suppressed by febuxostat. Interestingly, febuxostat, but not allopurinol (another xanthine oxidase inhibitor), rapidly induced the nuclear translocation of Nrf2 and facilitated the degradation of Keap1, similar to the electrophilic Nrf2 activator omaveloxolone. These results suggest that febuxostat alleviates adipogenesis under oxidative conditions, at least in part by suppressing ROS production and Nrf2 activation. Regulation of adipocytic differentiation by febuxostat is expected to inhibit obesity due to menopause or overeating. (Tokushima University Institutional Repository) ● Metadata: 118313 (Link to Publication Site) ● Publication site (DOI): 10.3390/antiox12010133 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36670994 ● Search Scopus @ Elsevier (PMID): 36670994 ● Search Scopus @ Elsevier (DOI): 10.3390/antiox12010133 (Tokushima University Institutional Repository: 118313, DOI: 10.3390/antiox12010133, PubMed: 36670994)
7.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, Masahiro Hiasa, Hirofumi Tenshin, A Oda, A Seki, Y Inoue, Kotaro Tanimoto, Yoshiki Higa, M Oura, K Sogabe, Takeshi Harada, Ryohei Sumitani, T Maruhashi, H Yamagami, Y Sawa, Itsuro Endo, K Tsuneyama, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Aberrant upregulation of the endogenous PP2A inhibitor CIP2A is vital for myeloma cell growth and survival, International Journal of Myeloma, Vol.12, No.2, 14-23, 2022. (Summary) <p>The serine/threonine kinase TAK1 is constitutively overexpressed and auto-phosphorylated in multiple myeloma (MM) cells. Protein phosphatase 2A (PP2A) is a major serine/threonine phosphatase which dephosphorylates proteins phosphorylated by various serine/threonine kinases to regulate multiple cellular functions. We recently reported that the serine/threonine kinase TGF-β-activated kinase-1 (TAK1) is highly expressed and auto-phosphorylated to mediate critical growth and survival signaling in MM cells. We demonstrate here that regulation of PP2A activity inversely affects the phosphorylation levels of TAK1 in MM cells, and that MM cells aberrantly overexpress cancerous inhibitor of PP2A (CIP2A), an endogenous inhibitor for PP2A. <i>CIP2A</i> gene silencing as well as treatment with the CIP2A inhibitor TD52 potently induced MM cell death along with suppression of TAK1 expression in MM cells. These results suggest the critical role of PP2A inactivation via CIP2A upregulation in TAK1 phosphorylation and its protein expression and thereby MM cell growth and survival, posing the CIP2A-PP2A axis as an important therapeutic target.</p> (Keyword) multiple myeloma / TAK1 / CIP2A / PP2A (Tokushima University Institutional Repository) ● Metadata: 117150 (Link to Publication Site) ● Publication site (DOI): 10.57352/ijm.12.2_14 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390573947533793024 ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.12.2_14 (Tokushima University Institutional Repository: 117150, DOI: 10.57352/ijm.12.2_14, CiNii: 1390573947533793024)
8.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Mechanical unloading aggravates bone destruction and tumor expansion in myeloma., Haematologica, Vol.107, No.3, 744-749, 2022. (Keyword) Bone Resorption / Humans / Multiple Myeloma / Osteoclasts / Osteolysis (Tokushima University Institutional Repository) ● Metadata: 116715 (Link to Publication Site) ● Publication site (DOI): 10.3324/haematol.2021.278295 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34788982 ● Search Scopus @ Elsevier (PMID): 34788982 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2021.278295 (Tokushima University Institutional Repository: 116715, DOI: 10.3324/haematol.2021.278295, PubMed: 34788982)
9.	Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression., Clinical & translational immunology, Vol.11, No.1, 2022. (Summary) TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA. (Tokushima University Institutional Repository) ● Metadata: 117260 (Link to Publication Site) ● Publication site (DOI): 10.1002/cti2.1371 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379 ● Search Scopus @ Elsevier (PMID): 35079379 ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371 (Tokushima University Institutional Repository: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379)
10.	Shinya Horiuchi, Hiroko Sato, Akihiko Iwasa, Aki Ichihara, Hirofumi Tenshin, Keiichiro Watanabe, Masahiro Hiasa, Ichiro Hashimoto and Eiji Tanaka : Long-term Management of a Patient with Apert Syndrome., The Journal of Contemporary Dental Practice, Vol.22, No.10, 1184-1190, 2021. (Summary) The two-stage operation combining early distraction osteogenesis and postgrowth orthognathic surgery proves to be an effective therapy for correcting midfacial hypoplasia and skeletal mandibular protrusion caused by Apert syndrome. (Keyword) Acrocephalosyndactylia / Adolescent / Adult / Cephalometry / Humans / Infant / Male / Open Bite / Osteogenesis, Distraction / Osteotomy, Le Fort / Young Adult (Tokushima University Institutional Repository) ● Metadata: 117255 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35197388 ● Search Scopus @ Elsevier (PMID): 35197388 (Tokushima University Institutional Repository: 117255, PubMed: 35197388)
11.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Asuka Oda, Ariunzaya Bat-Erdene, Takeshi Harada, Shingen Nakamura, Mohannad Ashtar, Sou Shimizu, Masami Iwasa, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma, Haematologica, Vol.106, No.5, 1401-1413, 2021. (Summary) Along with the tumor progression, the bone marrow microenvironment is skewed in multiple myeloma (MM), which underlies the unique pathophysiology of MM and confers aggressiveness and drug resistance in MM cells. TGF-β-activated kinase-1 (TAK1) mediates a wide range of intracellular signaling pathways. We demonstrate here that TAK1 is constitutively overexpressed and phosphorylated in MM cells, and that TAK1 inhibition suppresses the activation of NF-κB, p38MAPK, ERK and STAT3 to decrease the expression of critical mediators for MM growth and survival, including PIM2, MYC, Mcl-1, IRF4, and Sp1, along with a substantial reduction in the angiogenic factor VEGF in MM cells. Intriguingly, TAK1 phosphorylation was also induced along with upregulation of vascular cell adhesion molecule-1 (VCAM-1) in bone marrow stromal cells (BMSCs) in cocultures with MM cells, which facilitated MM cell-BMSC adhesion while inducing IL-6 production and receptor activator of nuclear factor κ-Β ligand (RANKL) expression by BMSCs. TAK1 inhibition effectively impaired MM cell adhesion to BMSCs to disrupt the support of MM cell growth and survival by BMSCs. Furthermore, TAK1 inhibition suppressed osteoclastogenesis enhanced by RANKL in cocultures of bone marrow cells with MM cells, and restored osteoblastic differentiation suppressed by MM cells or inhibitory factors for osteoblastogenesis overproduced in MM. Finally, treatment with the TAK1 inhibitor LLZ1640-2 markedly suppressed MM tumor growth and prevented bone destruction and loss in mouse MM models. Therefore, TAK1 inhibition may be a promising therapeutic option targeting not only MM cells but also the skewed bone marrow microenvironment in MM. (Keyword) Animals / Bone Marrow Cells / MAP Kinase Kinase Kinases / Mice / Multiple Myeloma / NF-kappa B / Osteoclasts / Osteolysis / RANK Ligand / Tumor Microenvironment (Tokushima University Institutional Repository) ● Metadata: 116529 (Link to Publication Site) ● Publication site (DOI): 10.3324/haematol.2019.234476 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32273474 ● Search Scopus @ Elsevier (PMID): 32273474 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2019.234476 (Tokushima University Institutional Repository: 116529, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474)
12.	Sou Shimizu, Shinya Horiuchi, Hiroki Mori, Hirofumi Tenshin, Akihiko Iwasa, Keiichiro Watanabe, Toyoaki Takagi and Eiji Tanaka : 徳島大学病院矯正歯科における保険診療に関する実態調査-先天性疾患における裂奇形の併発について, The Journal of Chu-Shikoku Orthodontic Society, Vol.32, No.1, 87-92, 2020. (Summary) 矯正歯科治療に健康保険が導入されて約40年が経過し，唇顎口蓋裂と顎変形症の他に2018年現在53項目が保険治療の対象になっている．今回，我々は当科における矯正歯科治療の保険適用患者の実態を調査し，特に唇顎口蓋裂と他の先天性疾患との関連性について臨床統計学的検討を行ったので報告する．徳島大学病院病院情報システム・データウェアハウスを用い，2008年1月から2018年12月までの11年間に当院矯正歯科を受診した患者から保険治療を受けている患者を抽出し，顎変形症単独症例を除く先天性疾患患者について，電子カルテ全文検索システムを用いて臨床統計学的検討を行った．研究対象期間に当科にて保険治療を受けた矯正患者は345人で，そのうち，本研究対象患者は，顎変形症単独症例を除く207人であった．患者の内訳は，裂奇形を主徴候とする症例が全体の5割を占め最も多く，次いで，6歯以上の先天性部分性無歯症，ゴールデンハー症候群(鰓弓異常症を含む)，ダウン症候群の順であった．また，症候性疾患の中で裂奇形の併発は，ピエール・ロバン症候群，ダウン症候群，ゴールデンハー症候群の順に多く，その裂型は，口蓋裂(軟口蓋裂を含む)，唇顎口蓋裂，唇裂の順に多かった．以上のことから，当病院は裂奇形を併発した先天性疾患への専門的な対応が不可欠であり，希少疾患にも柔軟に対応できるよう複数の診療科，職種による診療科の枠組みを超えたチーム医療体制の構築が必要であることが示唆された． (Keyword) 先天性疾患 / 口唇裂・口蓋裂 / 臨床統計学的調査 / 合併症 (Tokushima University Institutional Repository) ● Metadata: 116914 (Tokushima University Institutional Repository: 116914)
13.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Ryohei Sumitani, Hirokazu Miki, Kengo Udaka, Mamiko Takahashi, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat., Cancers, Vol.12, No.4, 2020. (Summary) Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox's anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage. (Tokushima University Institutional Repository) ● Metadata: 115041 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers12040929 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32283857 ● Search Scopus @ Elsevier (PMID): 32283857 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers12040929 (Tokushima University Institutional Repository: 115041, DOI: 10.3390/cancers12040929, PubMed: 32283857)
14.	Masami Iwasa, Takeshi Harada, Asuka Oda, Ariunzaya Bat-Erdene, Jumpei Teramachi, Hirofumi Tenshin, Mohannad Ashtar, Masahiro Oura, Kimiko Sogabe, Kengo Udaka, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki and Masahiro Abe : PD-L1 upregulation in myeloma cells by panobinostat in combination with interferon-γ., Oncotarget, Vol.10, No.20, 1903-1917, 2019. (Summary) gene silencing abolished the PD-L1 upregulation by panobinostat and IFN-γ in combination, indicating a critical role for STAT1. These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-γ-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-γ. PD-L1 upregulation should be taken into account when combining immunotherapies with panobinostat. (Tokushima University Institutional Repository) ● Metadata: 113359 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.26726 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30956773 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062760316 (Tokushima University Institutional Repository: 113359, DOI: 10.18632/oncotarget.26726, PubMed: 30956773, Elsevier: Scopus)
15.	Dong Bingzi, Itsuro Endo, Ohnishi Yukoyo, Mitsui Yukari, Kiyoe Kurahashi, Mai Kanai, Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Persistent Activation of Calcium-Sensing Receptor Suppresses Bone Turnover, Increases Microcracks, and Decreases Bone Strength., JBMR Plus, Vol.3, No.7, e10182, 2019. (Summary) Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia type 1 (ADH1). Patients with ADH1 exhibit similar features to patients with hypoparathyroidism, including reduced serum parathyroid hormone (PTH) and Ca with low bone turnover. Although persistent suppression of bone turnover may increase bone fragility, bone strength in ADH1 patients has been unclear. We created knock-in mice harboring the A843E activating mutation of CaSR, mimicking severe features of ADH1 patients. The severe form of ADH1 model mice showed smaller body and bone size with lower bone mineral density (BMD) and cortical area of the femur compared with age-matched wild-type (WT) mice. Bone strength in the femur was lower in ADH1 mice even after correction by bone geometry and/or BMD. Microcracks were markedly increased in ADH1 mice, but were rarely detected in WT mice. There was a negative correlation between bone strength corrected by bone geometry and/or BMD and microcrack number or density in ADH1 and WT mice. Among ADH1 mice, negative correlation was still observed between bone strength and microcrack number or density. Microcracks increased with age in ADH1 mice, and were negatively correlated with bone strength. Treatment with PTH(1-34) or a calcilytic, JTT-305, increased bone turnover, reduced microcracks, and increased bone strength to similar levels to those in WT mice. The increase in microcracks was associated with a reduction in bone strength in ADH1 mice, and aging aggravates these changes. These results demonstrate that activating mutation of CaSR causes reduction in PTH secretion with suppressed bone turnover, that reduced bone turnover is associated with an age-dependent increase in microcracks with a reduction in bone strength, and that both PTH(1-34) and calcilytic ameliorate all these changes in bone turnover and strength. It is suggested that fracture susceptibility may be increased in severe types of ADH1 patients especially in the elderly. © 2019 The Authors. published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research. (Link to Publication Site) ● Publication site (DOI): 10.1002/jbm4.10182 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31372589 ● Search Scopus @ Elsevier (PMID): 31372589 ● Search Scopus @ Elsevier (DOI): 10.1002/jbm4.10182 (DOI: 10.1002/jbm4.10182, PubMed: 31372589)
16.	Ariunzaya Bat-Erdene, Shingen Nakamura, Asuka Oda, Masami Iwasa, Jumpei Teramachi, Mohannad Ashtar, Takeshi Harada, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Shiroh Fujii, Kimiko Sogabe, Masahiro Oura, Kengo Udaka, Kumiko Kagawa, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Class 1 HDAC and HDAC6 inhibition inversely regulates CD38 induction in myeloma cells via interferon-α and ATRA., British Journal of Haematology, 2018. (Tokushima University Institutional Repository) ● Metadata: 113393 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15673 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30474853 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057280798 (Tokushima University Institutional Repository: 113393, DOI: 10.1111/bjh.15673, PubMed: 30474853, Elsevier: Scopus)
17.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Takeshi Harada, Shingen Nakamura, Ryota Amachi, Hirofumi Tenshin, Masami Iwasa, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim-2 is a critical target for treatment of osteoclastogenesis enhanced in myeloma., British Journal of Haematology, Vol.180, No.4, 581-585, 2018. (Tokushima University Institutional Repository) ● Metadata: 112935 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.14388 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27748523 ● Search Scopus @ Elsevier (PMID): 27748523 ● Search Scopus @ Elsevier (DOI): 10.1111/bjh.14388 (Tokushima University Institutional Repository: 112935, DOI: 10.1111/bjh.14388, PubMed: 27748523)
18.	Shiroh Fujii, Shingen Nakamura, Asuka Oda, Hirokazu Miki, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Harada, Kumiko Kagawa, Michiyasu Nakao, Shigeki Sano and Masahiro Abe : Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity., British Journal of Haematology, Vol.180, No.2, 246-258, 2018. (Summary) Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned. (Keyword) Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Survival / Cell Transformation, Neoplastic / Disease Models, Animal / Humans / Hydrogen-Ion Concentration / Mice / Multiple Myeloma / Proteasome Inhibitors / Protein-Serine-Threonine Kinases / Proteolysis / Proto-Oncogene Proteins / Thiazolidinediones (Tokushima University Institutional Repository) ● Metadata: 112752 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15033 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29327347 ● Summary page in Scopus @ Elsevier: 2-s2.0-85040344893 (Tokushima University Institutional Repository: 112752, DOI: 10.1111/bjh.15033, PubMed: 29327347, Elsevier: Scopus)
19.	Hirokazu Miki, Shingen Nakamura, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kiyoe Kurahashi, Sumiko Yoshida, Kumiko Kagawa, Itsuro Endo, Aihara Kenichi, Mariko Ikuo, Kouji Itou, Koichiro Hayashi, Michihiro Nakamura and Masahiro Abe : Effective impairment of myeloma cells and their progenitors by hyperthermia., Oncotarget, Vol.9, No.12, 10307-10316, 2017. (Summary) Multiple myeloma (MM) remains incurable, and MM-initiating cells or MM progenitors are considered to contribute to disease relapse through their drug-resistant nature. In order to improve the therapeutic efficacy for MM, we recently developed novel superparamagnetic nanoparticles which selectively accumulate in MM tumors and extirpate them by heat generated with magnetic resonance. We here aimed to clarify the therapeutic effects on MM cells and their progenitors by hyperthermia. Heat treatment at 43°C time-dependently induced MM cell death. The treatment upregulated endoplasmic reticulum (ER) stress mediators, ATF4 and CHOP, while reducing the protein levels of Pim-2, IRF4, c-Myc and Mcl-1. Combination with the proteasome inhibitor bortezomib further enhanced ER stress to potentiate MM cell death. The Pim inhibitor SMI-16a also enhanced the reduction of the Pim-2-driven survival factors, IRF4 and c-Myc, in combination with the heat treatment. The heat treatment almost completely eradicated "side population" fractions in RPMI8226 and KMS-11 cells and suppressed their clonogenic capacity as determined by colony formation and tumorigenic capacity in SCID mice. These results collectively demonstrated that hyperthermia is able to impair clonogenic drug-resistant fractions of MM cells and enhance their susceptibility to chemotherapeutic drugs. (Tokushima University Institutional Repository) ● Metadata: 113059 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.23121 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29535808 ● Summary page in Scopus @ Elsevier: 2-s2.0-85041952629 (Tokushima University Institutional Repository: 113059, DOI: 10.18632/oncotarget.23121, PubMed: 29535808, Elsevier: Scopus)
20.	Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Ryota Amachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Keiichiro Watanabe, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Kenichi Aihara, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition subverts the osteoclastogenic action of TRAIL while potentiating its antimyeloma effects., Blood Advances, Vol.1, No.24, 2124-2137, 2017. (Summary) Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) agonists induce tumor-specific apoptosis indicating that they may be an attractive therapeutic strategy against cancers, including multiple myeloma (MM). Osteoclastogenesis is highly induced in MM, which in turn enhances MM growth, thereby forming a vicious cycle between MM tumor expansion and bone destruction. However, the effects of TRAIL on MM-enhanced osteoclastogenesis remain largely unknown. Here, we show that TRAIL induced apoptosis in MM cells, but not in osteoclasts (OCs), and that it rather facilitated receptor activator of NF-B ligand-induced osteoclastogenesis along with upregulation of cellular FLICE inhibitory protein (c-FLIP). TRAIL did not induce death-inducing signaling complex formation in OCs, but formed secondary complex (complex II) with the phosphorylation of transforming growth factor -activated kinase-1 (TAK1), and thus activated NF-B signaling. c-FLIP knockdown abolished complex II formation, thus permitting TRAIL induction of OC cell death. The TAK1 inhibitor LLZ1640-2 abrogated the TRAIL-induced c-FLIP upregulation and NF-B activation, and triggered TRAIL-induced caspase-8 activation and cell death in OCs. Interestingly, the TRAIL-induced caspase-8 activation caused enzymatic degradation of the transcription factor Sp1 to noticeably reduce c-FLIP expression, which further sensitized OCs to TRAIL-induced apoptosis. Furthermore, the TAK1 inhibition induced antiosteoclastogenic activity by TRAIL even in cocultures with MM cells while potentiating TRAIL's anti-MM effects. These results demonstrated that osteoclastic lineage cells use TRAIL for their differentiation and activation through tilting caspase-8-dependent apoptosis toward NF-B activation, and that TAK1 inhibition subverts TRAIL-mediated NF-B activation to resume TRAIL-induced apoptosis in OCs while further enhancing MM cell death in combination with TRAIL. (Tokushima University Institutional Repository) ● Metadata: 111724 (Link to Publication Site) ● Publication site (DOI): 10.1182/bloodadvances.2017008813 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29296860 ● Search Scopus @ Elsevier (PMID): 29296860 ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2017008813 (Tokushima University Institutional Repository: 111724, DOI: 10.1182/bloodadvances.2017008813, PubMed: 29296860)
21.	Ariunzaya Bat-Erdene, Hirokazu Miki, Asuko Oda, Shingen Nakamura, Jumpei Teramachi, Ryota Amachi, Hirofumi Tenshin, Masahiro Hiasa, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kimiko Sogabe, Kumiko Kagawa, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara and Masahiro Abe : Synergistic targeting of Sp1, a critical transcription factor for myeloma cell growth and survival, by panobinostat and proteasome inhibitors., Oncotarget, Vol.7, No.48, 79064-79075, 2016. (Summary) Panobinostat, a pan-deacetylase inhibitor, synergistically elicits cytotoxic activity against myeloma (MM) cells in combination with the proteasome inhibitor bortezomib. Because precise mechanisms for panobinostat's anti-MM action still remain elusive, we aimed to clarify the mechanisms of anti-MM effects of panobinostat and its synergism with proteasome inhibitors. Although the transcription factor Sp1 was overexpressed in MM cells, the Sp1 inhibitor terameprocol induced MM cell death in parallel with reduction of IRF4 and cMyc. Panobinostat induced activation of caspase-8, which was inversely correlated with reduction of Sp1 protein levels in MM cells. The panobinostat-mediated effects were further potentiated to effectively induce MM cell death in combination with bortezomib or carfilzomib even at suboptimal concentrations as a single agent. Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. The synergistic Sp1 reduction markedly suppressed Sp1-driven prosurvival factors, IRF4 and cMyc. Besides, the combinatory treatment reduced HDAC1, another Sp1 target, in MM cells, which may potentiate HDAC inhibition. Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination. (Tokushima University Institutional Repository) ● Metadata: 109988 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.12594 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27738323 ● Search Scopus @ Elsevier (PMID): 27738323 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.12594 (Tokushima University Institutional Repository: 109988, DOI: 10.18632/oncotarget.12594, PubMed: 27738323)

Academic Paper (Unrefereed Paper):

1.	Hirofumi Tenshin, Keiichiro Watanabe, Emiko Nakaue, Khurel-Ochir Tsendsuren, Masahiro Hiasa, Shinya Horiuchi and Eiji Tanaka : Identification of key determinant for predicting feasible mandibular molars distalization, Journal of Dental Sciences, 2022. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jds.2022.05.009 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85132231189 (DOI: 10.1016/j.jds.2022.05.009, Elsevier: Scopus)

Proceeding of International Conference:

1.	Hirofumi Tenshin, Windle J. Jolene, Subler A. Mark, Chirgwin M John, Roodman David G. and Kurihara Noriyoshi : OCL-IGF1-induced OCys senescence promotes RANKL production and induces pagetic bone lesions in Paget's disease, ASBMR, Oct. 2023.
2.	Hirofumi Tenshin, Jolene J. Windle, David W Dempster, John M Chirgwin, G. David Roodman and Noriyoshi Kurihara : Increased RANKL production by senescent osteocytes may contribute to Pagetic lesion formation in Paget's disease, ASBMR 2022, Sep. 2022.
3.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Mechanical unloading promotes bone destruction and myeloma tumor expansion, Cancer and bone society young investigator symposium, Online, Feb. 2022.
4.	Hirofumi Tenshin, Takeshi Harada, Yusuke Inoue, Jumpei Teramachi, Masahiro Hiasa, Sou Shimizu, Emiko Nakaue, Kotaro Tanimoto, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Targeting SLAMF7 to disrupt myeloma-osteoclast interaction: elotuzumabs ADCC activity with Th1-like gamma delta T cells towards osteoclasts and myeloma cells., Cancer and bone society young investigator symposium, Feb. 2022.
5.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Novel strategy of elotuzumab and zoledronic acid with Th1-like T cells against myeloma, 18th International Myeloma Workshop, Wien, Sep. 2021.
6.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Induction of elotuzumabs ADCC activity by Th1-like T cells towards osteoclasts as well as myeloma cells, EHA2021 Virtual Congress, Jun. 2021.
7.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The anti-SLAMF7 elotuzumab enhances ADCC activity with Th1-like γδT cells towards osteoclasts and myeloma cells., The European Calcified Tissue Society 2021 Digital Congress 2021, web, Mar. 2021.
8.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Eiji Tanaka, Kotaro Tanimoto, Sou Shimizu, Masahiro Oura, Kimiko Sogabe, Masahiro Abe, Toshio Matsumoto and Itsuro Endo : The novel therapeutic approaches with TAK1 inhibition against the aberrant NLRP3 inflammasome activation in rheumatoid arthritis, ECTS 2020 Digital Congress, Oct. 2020.
9.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Masahiro Abe and Eiji Tanaka : Immobilization accelerates bone loss and myeloma tumor expansion., 9th IOC, Yokohama, Oct. 2020.
10.	Mohannad Ashtar, Hirofumi Tenshin, Masahiro Abe and Eiji Tanaka : The effects of Febuxostat on RANKL-induced bone resorption., 9th IOC, Yokohama, Oct. 2020.
11.	Takeshi Harada, Asuka Oda, Hiroto Ohguchi, Yohann Grondin, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe : Novel therapeutic rationale for targeting HDAC1 and PIM2 in multiple myeloma, 61th ASH Annual Meeting & Exposition, Orlando, Dec. 2019. (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2019-127679 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2019-127679 (DOI: 10.1182/blood-2019-127679)
12.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Soh Shimizu, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The role of NLRP3 inflammasome activation in joint inflammation and destruction in rheumatoid arthritis: novel therapeutic approaches with TAK1 inhibition., 29th Australian and New Zealand Bone and Mineral Society Annual Scientific Meeting, Oct. 2019.
13.	Mai Kanai, Itsuro Endo, Yasuko Takahashi, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Establishment of model mice of FGF23-related hypophosphatemia induced by iron solution administration, ASBMR 2019, Orlando, Sep. 2019.
14.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption, American Society for Bone and Mineral Society Annual meeting 2019, Orlando, Florida, USA,, Sep. 2019.
15.	Jumpei Teramachi, Soh Shimizu, Hirofumi Tenshin, Bat-Erdene Ariunzaya, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Takeshi Harada, Mohannad Ashtar, Kotaro Tanimoto, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : A progressive auto-amplification loop in TAK1 expression and activation in MM cells., ASBMR 2019,, Orlando, Florida, USA., Sep. 2019.
16.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption., ASBMR 2019,, Orlando, Florida, USA., Sep. 2019.
17.	Takeshi Harada, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, C. Kenneth Anderson and Masahiro Abe : Targeting myeloma metabolisms regulated by HDAC1-IRF4 axis can be a novel therapeutic strategy, 17th International Myeloma Workshop, Sep. 2019.
18.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Masahiro Abe and Eiji Tanaka : Effective suppression of inflammasome-mediated joints destruction by TAK1 inhibition, 第97回IADR学術大会, Vancouver, Jun. 2019.
19.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Bat-Erdene Ariunzaya, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Peri-implantitis and the role of Febuxostat in osteoclast differentiation., AEEDC Dubai World Orthodontic Conference, Dubai, UAE, Feb. 2019.
20.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Disruption of a progressive vicious cycle between myeloma tumor growth and bone destruction by TAK1 inhibition, ASBMR 2018 Annual Meeting, Montreal, Sep. 2018.
21.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Iwasa Masami, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Opposite effects of TRAIL on the Sp-1-c-FLIP survival pathway in myeloma cells and osteoclasts., ASBMR 2018 Annual Meeting, Montreal, Sep. 2018.
22.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Tatsuji Haneji, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, 8th International Workshop on Advances in the Molecular Pharmacology and Therapeutics of Bone and other Musculoskeletal Diseases and Cancer and Bone Society 2018 Meeting, Oxford, Jun. 2018.
23.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation., 1st International Conference of Biophysical Technology in Dentistry (+10th International Scientific Meeting in Dentistry),, Makassar, Indonesia., Apr. 2018.
24.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation., The 4th ASEAN plus Tokushima Joint International Conference, Bali, Indonesia, Dec. 2017.
25.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma tumor growth and bone destruction, American Society for Bone and Mineral Research (ASBMR) 2017 Annual Meeting, Denver, Sep. 2017.
26.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, International Society for Experimental Hematology 46th Annual Scientific Meeting, Frankfurt, Aug. 2017.
27.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, A Baterdene, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Osteoclasts utilize TRAIL for their NF-B activation, but TAK1 inhibition resumes TRAIL-induced apoptosis in osteoclasts., Australian and New Zealand Bone and Mineral Society 2017, Brisbane, Australia., Jun. 2017.
28.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Akihito Yamamoto, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, Cancer and Bone Society Conference 2017, Indianapolis, May 2017.
29.	Ryota Amachi, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Jumpei Teramachi, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Osteoblast Creates a Non-permissive Niche for Myeloma Cells, 95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017.
30.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : TRAIL Stimulates Osteoclast Differentiation and Survival via TAK1 Activation., 95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017.
31.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma, American Society for Bone and Mineral Research 2016 Annual Meeting, Atlanta, Sep. 2016.
32.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Bingzi Dong, Masahiro Hiasa, Keiichiro Watanabe, Ryota Amachi, S Nakamura, H Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Osteoclasts utilize an apoptosis-inducer TRAIL as a stimulator for osteoclastogenesis Critical roles of the TAK-1-Pim-2 signaling induced by RANK ligand and TRAIL., ANZBMS 2016 Annual Meeting, Gold Coast, Aug. 2016.
33.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK-1 inhibition on tumor growth and bone destruction in myeloma, 21st Congress European Hematology Association, Copenhagen, Jun. 2016.
34.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Pim inhibition suppresses osteoclastogenesis and tumor growth in myeloma, 57th ASH Annual Meeting and Exposition, Orlando, Dec. 2015.
35.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, S Nakamura, H Miki, I Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAIL is not a proapoptotic but rather anti-apoptotic mediator for osteoclasts to stimulate their differentiation and survival, ASBMR 2015 Annual Meeting, Seattle, Oct. 2015.
36.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Asuka Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Up-regulation of the pH sensor TRPV1 in myeloma cells and their adaption to an acidic microenvironment, ASBMR 2015 Annual Meeting, Seattle, Oct. 2015.
37.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pivotal role of TAK-1 in tumor growth and bone destruction in myeloma: Therapeutic impact of TAK-1 inhibition, American Society for Bone and Mineral Research 2015 Annual Meeting, Oct. 2015.
38.	Hirokazu Miki, Shingen Nakamura, Hirofumi Tenshin, Ryota Amachi, Keiichiro Watanabe, Jumpei Teramachi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe : Effective impairment of myeloma progenitors by hyperthermia: augmentation with bortezomib and Pim inhibition in combination, Clinical Lymphoma, Myeloma & Leukemia, Vol.15, No.S3, e217-e218, Sep. 2015. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clml.2015.07.470 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.clml.2015.07.470 (DOI: 10.1016/j.clml.2015.07.470)
39.	Shingen Nakamura, Hirokazu Miki, Hirofumi Tenshin, Ryota Amachi, Keiichiro Watanabe, Jumpei Teramachi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe : Alteration of Pim-2 expression by clinically available anti-myeloma agents: combinatory anti-myeloma effects with Pim inhibition, Clinical Lymphoma, Myeloma & Leukemia, Vol.15, No.S3, e243, Sep. 2015. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clml.2015.07.517 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.clml.2015.07.517 (DOI: 10.1016/j.clml.2015.07.517)

Proceeding of Domestic Conference:

1.	Yoshiki Higa, Masahiro Hiasa, NAKAGAWA Motosumi, KIMU Suha, TANAKA Mariko, Emiko Nakaue, Sou Shimizu, Hirofumi Tenshin, Eiji Tanaka and Masahiro Abe : KEAP1-NRF2軸を介した脂肪細胞分化と骨芽細胞分化の制御機構, 第82回日本矯正歯科学会学術大会抄録集, 194, Nov. 2023.
2.	花輪茂己, Masahiro Hiasa, Akihiko Iwasa, Keiichiro Watanabe, Hirofumi Tenshin, Nao Kinouchi, Shinya Horiuchi and Eiji Tanaka : 上顎左側第二小臼歯先天性欠如を伴う片側性唇顎口蓋裂患者に対して下顎左側第二小臼歯を移植した一症例, The Journal of Chu-Shikoku Orthodontic Society, Vol.35, No.1, 67-75, Aug. 2023. (Summary) 口唇裂・口蓋裂患者では永久歯が先天性欠如する割合が高く,とくに複数歯が先天性欠如する症例の場合,マルチブラケット装置を用いた治療の際に咬合の確立に苦慮することは少なくない.今回,上顎左側側切歯および第二小臼歯の先天性欠如を伴う左側唇顎口蓋裂患者に対して,便宜抜去した下顎左側第二小臼歯を上顎左側第二小臼歯欠如部に移植し全顎的な矯正治療を行うことで良好な治療結果が得られたので報告する.初診時年齢0歳20日の女児で,左側唇顎口蓋裂を主訴に当院形成外科から紹介され来院した.12歳時,下顎歯列におけるarch length discrepancyの改善のために抜去した下顎左側第二小臼歯を上顎左側第二小臼歯欠如部へ移植した.12歳10ヵ月時,移植歯の歯根形成と根尖孔閉鎖が認められ,顎骨の成長がほぼ終了したため,二期治療としてマルチブラケット装置を用いて咬合の確立を図った.動的治療期間は5年0ヵ月で,1歯対2歯の緊密な咬合関係が獲得された.現在,保定後2年3ヵ月経過して安定した咬合を維持している.本症例では,便宜抜去した歯を移植することで,補綴処置を回避し,天然歯による緊密な咬合を獲得することができた.移植後2年経過した時点で歯根吸収は認めず,安定した経過をたどっている.しかしながら今後も長期的な観察が必要と考えられる.口唇裂・口蓋裂患者の歯の先天性欠如部位に対する治療法の一つとして歯の移植が有用であることが示唆された.(著者抄録) (Keyword) パノラマX線撮影法 X線診断自家移植下顎骨歯根吸収(合併症,X線診断,外科的療法) 上顎疾患(合併症,外科的療法,診断) 小臼歯(移植) 頭部計測法歯(移植) 無歯症(合併症,外科的療法,診断) 歯科矯正維持装置歯科矯正用ブラケット *唇顎口蓋裂(合併症,外科的療法,診断) ヒト新生児女歯学
3.	Kim SooHa, Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, TANAKA Mariko, NAKAGAWA Motosumi, Itsuro Endo, Takeshi Harada, Eiji Tanaka and Masahiro Abe : Molecular mechanisms for generation of non-permissive niche for myeloma cells by activated osteoblasts., The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 173, Jul. 2023.
4.	Takeshi Harada, Ryohei Sumitani, Asuka Oda, Yusuke Inoue, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : The therapeutic potential targeting ADAR1-dsRNA metabolism in myeloma cells with 1q amplification, The 84th Annual Meeting of the Japanese Society of Hematology, Oct. 2022.
5.	Keiichiro Watanabe, Hirofumi Tenshin, Emiko Nakaue, 塩屋園玲子 and Eiji Tanaka : 上顎歯列の全体的な圧下を行い骨格的な改善を図った，ガミースマイルを伴う成人骨格性上顎前突症例, 第81回日本矯正歯科学会学術大会, Oct. 2022.
6.	Yoshiki Higa, Masahiro Hiasa, KIMU Suha, TANAKA Mariko, Emiko Nakaue, Sou Shimizu, Kotaro Tanimoto, Hirofumi Tenshin, Eiji Tanaka and Masahiro Abe : キサンチンオキシダーゼ阻害薬febuxostatはKEAP1-NRF2軸を介し脂肪細胞分化と骨芽細胞分化を制御する, 第81回日本矯正歯科学会学術大会, Oct. 2022.
7.	Sou Shimizu, Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Yoshiki Higa, Emiko Nakaue, Masahiro Abe and Eiji Tanaka : 骨髄腫細胞の生存・増殖におけるTAK1-CIP2A経路の重要な役割, 第81回日本矯正歯科学会学術大会, Oct. 2022.
8.	Emiko Nakaue, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Yusuke Inoue, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : プロテアソーム阻害薬による骨髄腫骨病変部選択的骨形成誘導活性の検討, 第40回日本骨代謝学会学術集会, 141, Jul. 2022.
9.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : キサンチンオキシダーゼ(XO)阻害薬febuxostatによる脂肪細胞分化と骨芽細胞分化の制御機構, 第40回日本骨代謝学会学術集会, Jul. 2022.
10.	TANAKA Mariko, Masahiro Hiasa, Kotaro Tanimoto, Hirofumi Tenshin, Sou Shimizu, Yoshiki Higa, Emiko Nakaue, KIMU Suha, Jumpei Teramachi, Takeshi Harada, Shingen Nakamura, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動は骨髄腫骨病変部DPP-4発現増加と骨髄腫の腫瘍進展・髄外播種を加速させる, 第40回日本骨代謝学会学術集会, Jul. 2022.
11.	Takeshi Harada, Hirofumi Tenshin, Yusuke Inoue, Ryohei Sumitani, Emiko Nakaue, Jumpei Teramachi, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Production of SLAMF7 by osteoclasts and development of novel treatment targeting SLAMF7 against myeloma bone disease, 第40回日本骨代謝学会学術集会, Jul. 2022.
12.	Emiko Nakaue, Keiichiro Watanabe, Hirofumi Tenshin, Kaoru Yoshinaga, Yuta Matsuki, Masahiro Hiasa, Shinya Horiuchi and Eiji Tanaka : Identification of key determinant for predicting feasible mandibular molars distalization, The Journal of Chu-Shikoku Orthodontic Society, Jul. 2022.
13.	HANAWA Shigeki, Masahiro Hiasa, Akihiko Iwasa, Keiichiro Watanabe, Hirofumi Tenshin, Nao Kinouchi, Shinya Horiuchi and Eiji Tanaka : 上顎左側第二小臼歯先天欠損を伴う片側性唇顎口蓋裂患者に対して下顎左側第二小臼歯を移植した一症例, Journal fo Japanese Cleft Palate Association, Vol.47, No.2, 146, May 2022.
14.	KIMU Suha, Keiichiro Watanabe, Kaoru Yoshinaga, Hirofumi Tenshin, Emiko Nakaue, Yoshiki Higa, 坂本幸, 近藤英司, Aki Shimada, Kazuhide Mineda, Soushi Ishida, Aya Miyazaki, Takamasa Kitamura, Masahiro Hiasa, Shinya Horiuchi, Tomonori Iwasaki, Ichiro Hashimoto and Eiji Tanaka : 徳島大学病院における口唇口蓋裂センター設立前後での患者動向の変化金秀河(徳島大学大学院口腔科学教育部口腔顎顔面矯正学分野), 渡邉佳一郎, 吉永薫, 天眞寛文, 中上絵美子, 比嘉佳基, 坂本幸, 近藤英司, 島田亜紀, 峯田一秀, 石田創士, 宮嵜彩, 北村尚正, 日浅雅博, 堀内信也, 岩崎智憲, 橋本一郎, 田中栄二日本口蓋裂学会雑誌(0386-5185)47巻2号 Page135(2022.04), Journal fo Japanese Cleft Palate Association, Vol.47, No.2, 135, May 2022.
15.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, 菊池次郎, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐 and Masahiro Abe : Osteoclasts robustly express SLAMF7 and secrete soluble SLAMF7, The 47th Annual Meeting of the Japanese Society of Myeloma, May 2022.
16.	井上雄介, Takeshi Harada, Hirofumi Tenshin, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Leverage of Th1-like γδT cells into antibody-mediated immunotherapy against myeloma, The 47th Annual Meeting of the Japanese Society of Myeloma, May 2022.
17.	Takeshi Harada, Ryohei Sumitani, Asuka Oda, Inoue Yusuke, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Takahashi Mamiko, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Therapeutic impact of targeting RNA editing enzyme ADAR1 on myeloma cells with 1q amplification, 第47回日本骨髄腫学会学術集会, May 2022.
18.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, 小田明日香, Sou Shimizu, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Takeshi Harada and Masahiro Abe : TAK1 阻害は骨髄腫の細胞間相互作用による骨破壊と薬剤耐性を改善する, 第47回日本骨髄腫学会学術集会, May 2022.
19.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Kotaro Tanimoto, Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Critical role of the xanthine oxidase-ROS axis in perturbation of bone marrow milieu in myeloma, International Journal of Myeloma, Vol.12, No.3, 149, May 2022.
20.	Emiko Nakaue, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka and Masahiro Abe : The impact of pulsatile proteasome inhibitor on bone metabolism, International Journal of Myeloma, Vol.12, No.3, 152, May 2022. (Keyword) 骨髄腫-多発性(薬物療法,病理学) / 骨組織リモデリング / パルス療法(薬物療法) / Proteasome Inhibitors(治療的利用,薬理学) / Homo sapiens
21.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, 菊池次郎, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐 and Masahiro Abe : 破骨細胞はSLAMF7を強発現し可溶性SLAMF7を産生する(Osteoclasts robustly express SLAMF7 and secrete soluble SLAMF7), International Journal of Myeloma, Vol.12, No.3, 150, May 2022. (Keyword) 骨髄腫-多発性(遺伝学,病理学) 破骨細胞 Signaling Lymphocytic Activation Molecule Family(血液) SLAMF7 Protein(血液) ヒト
22.	Keiichiro Watanabe, Hirofumi Tenshin, Kaoru Yoshinaga, Emiko Nakaue, 坂本幸, Eiji Kondou, Aki Shimada, Kazuhide Mineda, Soushi Ishida, Masahiro Hiasa, Shinya Horiuchi, Tomonori Iwasaki, Ichiro Hashimoto and Eiji Tanaka : Pre-epiglottic baton plateによる保存的治療で重度気道閉塞の改善がみられたPierre Robin Sequenceの1例, Journal fo Japanese Cleft Palate Association, Vol.47, No.2, 116, Apr. 2022. (Keyword) Pierre Robin症候群(合併症) 気道閉塞(合併症,診断,予後) 呼吸障害(病因,予後) *保存的療法哺乳障害(病因,予後) ヒト新生児男歯学
23.	Hirofumi Tenshin, Keiichiro Watanabe, Emiko Nakaue and Eiji Tanaka : 歯科矯正用アンカースクリューを用いた積極的な臼歯圧下により治療を行なった成人骨格性開咬症例, 第80回日本矯正歯科学会学術大会, Oct. 2021.
24.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The critical roles of the TAK1-CIP2A axis in MM cell growth and survival and osteoclastogensis, 第83回日本血液学会学術集会, BPA-3-3, Sep. 2021.
25.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Resumption of myeloma cell sensitivity to proteasome inhibitors by PIM and Akt inhibition, The 83rd Annual Meeting of the Japanese Society of Hematology, Sep. 2021.
26.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, 大浦雅弘, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Critical roles of the XO-ROS axis in the pathology of bone loss in myeloma, 第83回日本血液学会学術集会, BPA-3-4, Sep. 2021.
27.	Hirofumi Tenshin, 寺町順平日浅雅博小田明日香原田武志, Masahiro Hiasa, 小田明日香, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Eiji Tanaka, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome aggravates osteoclastic bone destruction in myeloma, 日本血液学会学術集会83回 Page 83回 Page OS2-4B-4(2021.09), Sep. 2021.
28.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Extraosseous dissemination of myeloma by mechanical unloading, 日本血液学会学術集会83回 Page 83回 Page OS2-11C-3(2021.09), Sep. 2021.
29.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Expansion of γδT cells by CELMoDs and enhancement of their anti-myeloma effects by elotuzumab, The 83rd Annual Meeting of Japanese Society of Hematology, Sep. 2021.
30.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : PIMとAkt阻害による骨髄腫細胞のプロテアソーム阻害薬感受性の増強(Sensitization of myeloma cells to proteasome inhibitors by PIM and Akt inhibition), 日本血液学会学術集会, OS2-11D-3, Sep. 2021.
31.	Yuzo Hirai, Keiichiro Watanabe, Emiko Nakaue, Muneyuki Yoshimura, Hirofumi Tenshin, Masahiro Hiasa and Eiji Tanaka : 歯科矯正用アンカースクリューおよび周囲骨の応力分布に及ぼす植立深さの影響:有限要素法による解析, The Journal of Chu-Shikoku Orthodontic Society, Vol.33, No.1, 80, Jul. 2021.
32.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Development of combinatory treatment of Th1-like γδT cells with elotuzumab against osteoclasts as well as myeloma cells, 第46回日本骨髄腫学会学術集会, May 2021.
33.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, 李政樹, 飯田真介 and Masahiro Abe : 骨髄腫細胞のプロテアソーム阻害薬の耐性機序におけるPIM2とAkt活性およびNRF2蓄積の役割(Mechanisms for the resistance to proteasome inhibitors in myeloma cells: the role of PIM2 and Akt kinase activation and NRF2 accumulation), International Journal of Myeloma, Vol.11, No.2, 85, May 2021. (Keyword) 癌原遺伝子タンパク質骨髄腫-多発性(遺伝学,実験的) Protein-Serine-Threonine Kinases 抗腫瘍剤耐性 c-akt癌原遺伝子タンパク質 NF-E2-Related Factor 2 Proteasome Inhibitors(薬理学) *PIM2 Protein
34.	Keiichiro Watanabe, Hirofumi Tenshin, Kazuhide Mineda, Soushi Ishida, Kaoru Yoshinaga, Emiko Nakaue, Yoshiki Higa, Aya Miyazaki, Takamasa Kitamura, 坂本幸, Eiji Kondou, Aki Shimada, Masahiro Hiasa, Shinya Horiuchi, Ichiro Hashimoto and Eiji Tanaka : 当院における口腔内スキャナーを活用した哺乳床早期装着のための取り組み, Journal fo Japanese Cleft Palate Association, Vol.46, No.2, 123, Apr. 2021. (Keyword) 口蓋裂口唇裂歯科用機器母乳栄養ヒト乳児(1∼23ヶ月) 歯学
35.	Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Hirokazu Miki, 小田明日香, Takeshi Harada, Ryohei Sumitani, Masahiro Oura, Kumiko Kagawa, Hirofumi Tenshin, Jumpei Teramachi, Masaki Ri, Shinsuke Iida and Masahiro Abe : Immediate accumulation of anti-apoptotic PIM2 in myeloma cells by proteasome inhibitors, 第82回日本血液学会学術集会, Oct. 2020.
36.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 骨髄腫細胞のPP2A阻害因子CIP2A発現誘導を介するTAK1活性化増強機構, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 149, Oct. 2020.
37.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Mohannad Ashtar, Sou Shimizu, Yoshiki Higa, Jumpei Teramachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動は骨吸収と骨髄腫進展を促進させる, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 149, Oct. 2020.
38.	Hirofumi Tenshin, Mohannad Ashtar, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する:Xanthine oxidase阻害剤febuxostatの治療効果．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020.
39.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Ryohei Sumitani, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Versatile anti-myeloma effects by elotuzumab: impact on γδT cells and osteoclasts, The 82nd Annual Meeting of Japanese Soceity of Hematology, Oct. 2020.
40.	Hirofumi Tenshin, アシテルモハナッド, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, 比嘉佳基, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する Xanthine oxidase阻害剤febuxostatの治療効果, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020. (Keyword) Xanthine Oxidase(拮抗物質・阻害物質) / reactive oxygen species / 抗腫瘍剤(毒性・副作用) / 骨吸収(化学的誘発,薬物療法,実験的) / cell differentiation / osteoclast / 破骨細胞分化因子 / Febuxostat(治療的利用) / RAW264.7細胞 / マウス / animal
41.	Hirofumi Tenshin, Hiroko Sato, Akihiko Iwasa, Emiko Nakaue, Masaki Sawada, Daishi Arai, Shinya Horiuchi and Eiji Tanaka : 哺乳様式と不正咬合との関連性についての検討．, 第63回中・四国矯正歯科学会大会, Jul. 2020.
42.	Emiko Nakaue, Keiichiro Watanabe, Hiroki Mori, Hirofumi Tenshin, Shinya Horiuchi and Eiji Tanaka : カモフラージュ治療が行われた片側性完全唇顎口蓋裂患者の動的治療終了時の顎顔面形態の特徴, 第30回日本顎変形症学会総会・学術大会, Vol.30, No.2, 164, Jun. 2020.
43.	Takeshi Harada, Hirofumi Tenshin, Kotaro Tanimoto, Sou Shimizu and Masahiro Abe : MM cells overexpress SLAMF7 through HDAC1 and IRF4 upregulation, 第24回日本がん分子標的治療学会学術集会, Jun. 2020.
44.	Emiko Nakaue, Keiichiro Watanabe, Hiroki Mori, Hirofumi Tenshin, Shinya Horiuchi and Eiji Tanaka : カモフラージュ治療が行われた片側性完全唇顎口蓋裂患者の動的治療終了時の顎顔面形態の特徴, 第44回日本口蓋裂学会総会・学術集会, Jun. 2020.
45.	Chisato Okuzumi, Yuichi Nosaka, Ryotaroh Yamazaki, Hirofumi Tenshin, Hiroko Sato, Tsutomu Iwamoto and Eiji Tanaka : 哺乳様式と不正咬合との関連性についての検討．, 徳島県歯科医学大会, 36, Feb. 2020.
46.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Bat-Erdene Ariunzaya, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 190, Oct. 2019.
47.	Kotaro Tanimoto, Masahiro Hiasa, Akihiko Iwasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, 曾我部公子, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Oct. 2019.
48.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する．, 第37回日本骨代謝学会学術集会, Oct. 2019.
49.	谷本幸太朗, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, Kimiko Sogabe, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる, 第37回日本骨代謝学会学術集会, Oct. 2019.
50.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Soh Shimizu, Ashtar Mohannad, Takeshi Harada, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption in rheumatoid arthritis : the therapeutic roles of TAK1 inhibition, 16th Meeting of Bone Biology Forum, Aug. 2019.
51.	Sou Shimizu, Shinya Horiuchi, Hirofumi Tenshin, Akihiko Iwasa, Keiichiro Watanabe, Masahiro Hiasa, Tsutomu Iwamoto and Eiji Tanaka : 徳島大学病院矯正歯科における口唇裂・口蓋裂患者の合併先天異常に関する実態調査．, Journal fo Japanese Cleft Palate Association, May 2019.
52.	Takeshi Harada, Oda Asuka, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Masami Iwasa, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Teru Hideshima, Anderson C. Kenneth and Masahiro Abe : The novel therapeutic strategy targeting the HDAC1-IRF4-PIM2 pathway in myeloma cells, The 44th Annual Meeting of the Japanese Society of Myeloma, May 2019. (Keyword) Multiple myeloma / Class-I HDAC / IRF4 / Pim-2
53.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa and Masahiro Abe : TAK1阻害は腫瘍と微小環境との相互作用を遮断し腫瘍進展・骨破壊病変形成を抑制する, 第124回日本解剖学会総会・全国学術集会, Mar. 2019.
54.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Iwasa Masami, Shiroh Fujii, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Masahiro Oura, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Mechanisms of TAK1 over-activation in myeloma cells and TAK1-mediated myeloma growth and bone destruction, 第80回日本血液学会学術集会, Oct. 2018.
55.	Ashtar Mohannad, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Ariunzaya Erdene Bat, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Roles of ROS in induction of bone disease and cancer treatment-induced bone loss in myeloma., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
56.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Inverse regulation of c-FLIP-mediated survival in myeloma cells and osteoclasts by TRAIL., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
57.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Oda Asuka, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Kimiko Sogabe, Oura Masahiro, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Impact of denervation-induced paralysis and mechanical unloading on tumor expansion in myeloma., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
58.	Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Kotaro Tanimoto, Ariunzaya Bat-Erdene, Mohannad Ashtar, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Oda Asuka, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The effects of cathepsin K inhibition on osteocytes: its role in bone restoration in MM bone disease., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
59.	Itsuro Endo, 大西幸代, Kiyoe Kurahashi, Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : カルシウム感知受容体活性型変異マウスにおける骨強度の低下, 第36回日本骨粗鬆症学会各術集会, Jul. 2018.
60.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma growth and bone destruction, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2018.
61.	Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : カテプシンK阻害による多発性骨髄腫骨病変部の骨量回復プロセスにおける骨細胞の役割．, 第36回日本骨代謝学会学術集会, Jul. 2018.
62.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害はTRAILによる破骨細胞活性化作用を遮断させると同時にTRAILの抗骨髄腫作用を増強する, 第36回日本骨代謝学会学術集会, Jul. 2018.
63.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1による破骨細胞に対するTRAILの生存・細胞死シグナル制御機構．, 第4回日本骨免疫学会, Jun. 2018.
64.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Kimiko Sogabe, 大浦雅弘, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 神経切断による麻痺と免荷の骨髄腫の進展への影響．, 第4回日本骨免疫学会, Jun. 2018.
65.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Masami Iwasa, Masahiro Oura, Yusaku Maeda, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Disruption of myeloma cell-bone marrow interaction by TAK-1 inhibition, 第80回日本血液学会学術集会, Oct. 2017.
66.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Ariunzaya Baterdene, Masami Iwasa, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞を活性化させるが，TAK1阻害により骨髄腫細胞とともに破骨細胞にもTRAILのアポトーシス誘導活性が惹起できる, The 35th Annual Meeting of the Japanese Society for Bone and Mineral Research (oral talk), Jul. 2017.
67.	Daishi Arai, Keiichiro Watanabe, Islamy Rahma Hutami, Hirofumi Tenshin, Takehiro Shinohara, Nao Kinouchi and Eiji Tanaka : 矯正歯科患者における近年の永久前歯歯冠幅径の変化, 第60回中・四国矯正歯科学会大会学術口演, Jul. 2017.
68.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Baterdene Ariunzaya, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害はTRAILの抗骨髄腫作用を増強するともに骨吸収促進活性を抑制活性に変換する．, 第42回日本骨髄腫学会, May 2017.
69.	天知良太, Shingen Nakamura, Masahiro Hiasa, 小田明日香, バットエルデネアリウンザヤ, Jumpei Teramachi, Hirofumi Tenshin, Keiichiro Watanabe, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 骨形成誘導による骨髄腫細胞のエネルギー代謝の抑制, 第42回日本骨髄腫学会学術集会, May 2017.
70.	Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Hirohiko Okamura, Masahiro Abe and Tatsuji Haneji : 骨髄腫腫瘍進展と骨破壊病変形成におけるTAK-1の枢軸的役割, 第122回日本解剖学会総会・全国学術集会, Mar. 2017.
71.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 30. 天真寛文, 寺町順平, 小田明日香, 天知良太, , ,破骨細胞系細胞はアポトーシス誘引因子TRAILを生存促進・破骨細胞形成誘導因子として利用する:TAK1-Pim-2経路の役割, 第19回日本癌と骨病変研究会, Nov. 2016.
72.	Hirofumi Tenshin, Keiichiro Watanabe, Manami Shirai, Natsuko Hichijo and Eiji Tanaka : 新たな下顎臼歯の遠心移動量および移動様式の予測指標の開発-第2報-, 日本矯正歯科学会大会プログラム・抄録集. 第75回大会, Nov. 2016.
73.	Keiichiro Watanabe, Hirofumi Tenshin, Manami Shirai, Natsuko Hichijo and Eiji Tanaka : 新たな下顎臼歯の遠心移動量および移動様式の予測指標の開発-第1報-, 日本矯正歯科学会大会プログラム・抄録集. 第75回大会, Nov. 2016.
74.	Masahiro Hiasa, Ryota Amachi, Hirofumi Tenshin, Shinya Horiuchi, Masahiro Abe, Naozumi Ishimaru and Eiji Tanaka : RelBは古典的NF-κB経路の活性化を阻害し骨癒合不全と偽関節形成を予防する, 日本矯正歯科学会大会プログラム・抄録集., 192., Nov. 2016.
75.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition subverts TRAIL-mediated osteoclastogenesis., 第77回日本血液学会学術集会,, Oct. 2016.
76.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, 遠藤逸郎, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment., 第77回日本血液学会学術集会,, Oct. 2016.
77.	Keiichiro Watanabe, Jumpei Teramachi, Ryota Amachi, 小田明日香, Hirofumi Tenshin, 岩浅正美, Masahiro Hiasa, Shingen Nakamura, 遠藤逸郎, 川谷誠, 長田裕之, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Amelotin gene expression is temporarily being upregulated at the initiation of apoptosis induced by TGFb1 in mouse gingival epithelial cells, 第77回日本血液学会学術集会,, Oct. 2016.
78.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma, 第78回日本血液学会学術集会, Oct. 2016.
79.	Keiichiro Watanabe, Jumpei Teramachi, Ryota Amachi, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, 川谷誠, 長田裕之, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : リベロマイシンAによる酸性環境での骨髄腫細胞の治療抵抗性の克服, 日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, Jul. 2016.
80.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 破骨細胞はTAK1の発現誘導を介しアポトーシスを抑制しTRAILにより成熟活性化される, 日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, Jul. 2016.
81.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, 原田武志, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : 骨髄腫腫瘍進展と骨破壊病変形成におけるTAK1-Pim-2経路の役割, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2016.
82.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Hirofumi Tenshin, Shingen Nakamura, Ryota Amachi, Shiroh Fujii, Keiichiro Watanabe, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim-2は骨髄腫における破骨細胞形成促進の必須媒介因子である, 第41回日本骨髄腫学会学術集会, May 2016.
83.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞に細胞死を誘導せず，破骨細胞分化・生存を促進する., 第41回日本骨髄腫学会, May 2016.
84.	Shinya Horiuchi, Akihiro Yasue, Nobuhiko Kawai, Manami Shirai, Hirofumi Tenshin, Minami Sato, Minoru Sakama and Eiji Tanaka : 矯正歯科用接着剤のフッ素徐放機能に関する検討, 第74回日本矯正歯科学会大会プログラム・抄録集, 212, Nov. 2015.
85.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, A Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, H Miki, Kumiko Kagawa, Shiroh Fujii, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment, 第77回日本血液学会学術集会, Oct. 2015.
86.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Potent suppression of osteoclastogenesis in myeloma by Pim inhibition, 第77回日本血液学会学術集会, Oct. 2015.
87.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Tumor reduction and bone restoration in myeloma by TAK-1 inhibition, 第77回日本血液学会学術集会, Oct. 2015.
88.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim阻害による骨髄種骨病変の治療:破骨細胞形成の抑制, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2015.
89.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : 骨髄腫腫瘍進展と骨破壊病変形成における TAK-1の枢軸的役割, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2015.
90.	Hirofumi Tenshin, Keiichiro Watanabe, Natsuko Hichijo, Akiko Mino, Hiroki Mori, MANSJUR KARIMA QURNIA, Akihiro Yasue, Shingo Kuroda and Eiji Tanaka : 歯科矯正用アンカースクリューを用いた下顎臼歯遠心移動量および移動様式の治療前予測に関する検討, 第58回中·四国矯正歯科学会大会, 14, Jul. 2015.
91.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞分化・生存を促進する:TAK-1による生と死の運命制御, 第1回日本骨免疫学会, 137, Jul. 2015.
92.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Kumiko Kagawa, Hirokazu Miki, Shiroh Fujii, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 酸環境での骨髄腫細胞のDR4発現抑制:酸によるエピジェネティックな遺伝子発現制御, 第1回日本骨免疫学会, 108, Jul. 2015.
93.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Keiichiro Watanabe, Hirofumi Tenshin, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Takeshi Kondo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 酸性環境での骨髄腫細胞のTRPV1の発現亢進と酸環境への適応, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 165, Jul. 2015.
94.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : アポトーシス誘導因子TRAILによる破骨細胞分化・生存の促進, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 164, Jul. 2015.
95.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Ryota Amachi, Hirofumi Tenshin, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Pim阻害による骨髄腫骨吸収亢進の抑制, 第40回日本骨髄腫学会学術集会, May 2015.
96.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Ryota Amachi, Hirofumi Tenshin, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK-1は骨髄腫腫瘍進展と骨破壊病変形成の枢軸的な媒介因子である, 第40回日本骨髄腫学会学術集会, May 2015.

Et cetera, Workshop:

1.	Jumpei Teramachi, Hirofumi Tenshin, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : 骨髄腫特異的抗腫瘍活性と骨再生をもたらす新規分子標的薬の開発, 2018 先端医学交流セミナー, Aug. 2018.

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

加齢性歯槽骨吸収における骨細胞の役割の解明 (Project/Area Number: 24K23624 )
Investigation of the role of TAK1-NLRP3 inflammasome axis in rheumatoid arthritis (Project/Area Number: 20K18784 )
The novel therapeutic roles of TAK1 inhibition in rheumatoid arthritis (Project/Area Number: 19K21382 )
Search by Researcher Number (00829187)

Assistant Professor : Tenshin, Hirofumi

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