Tokushima University / Educator and Researcher Directory --- Fujii, Shiroh

Field of Study

○	Medicine

Subject of Study

○

Book / Paper

Book:

1.	Kumiko Kagawa, 前田悠作, Masahiro Oura, Kimiko Sogabe, 藤野ひかる, 髙橋真美子, 丸橋朋子, 岩佐昌美, 宇高憲吾, Takeshi Harada, Takayuki Ise, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shusuke Yagi, Kyoko Takeuchi, Shuji Ozaki, Masahiro Abe and 藤野ひかる : Analysis of long-term survivors with cardiac AL amyloidosis, The Japanese Society of Hematology, Oct. 2017. (Summary) <p>Cardiac AL amyloidosis (CA) is generally known as a severe disease with very poor prognosis. Here we retrospectively examined seven patients with CA in our cohort who achieved long-term survival. All six patients who underwent high-dose melphalan and autologous stem cell transplantation (ASCT) survived for >3 years, whereas four patients survived for >5 years. Patients who underwent ASCT had prompt hematological responses, and five patients showed organ responses. ASCT helps to achieve a quick and deep hematological response required for long-term survival in patients with CA. New agents have been implemented for the treatment of CA. However, the risks and benefits of each treatment modality should be considered according to patient condition, thus making the best use of ASCT in combination with new agents for the treatment of CA.</p> (Keyword) Cardiac AL amyloidosis / Autologous hematopoietic stem cell transplantation / Long-term survival (Link to Publication Site) ● Publication site (DOI): 10.11406/rinketsu.58.2197 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680011466240 ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.58.2197 (DOI: 10.11406/rinketsu.58.2197, CiNii: 1390282680011466240)

Academic Paper (Judged Full Paper):

1.	Mamiko Takahashi, Shin Kondo, Kumiko Kagawa, Masafumi Nakamura, Yusaku Maeda, Ryohei Sumitani, Hikaru Yagi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Itsuro Endo, Masahiro Abe and Shingen Nakamura : Skeletal muscle mass during chemotherapy for haematological malignancies: a retrospective study., BMJ Supportive & Palliative Care, Vol.14, No.2, 195-199, 2024. (Summary) This study investigated whether baseline or alteration in muscle mass affects complications during chemotherapy or overall survival (OS) in haematological malignancies. Skeletal Muscle Index (SMI) was evaluated by bioimpedance analysis before and after chemotherapy in patients with haematological malignancies, and the association between muscle mass and clinical data was retrospectively analysed. Exactly 104 patients were enrolled, with a mean age of 62.2 years. SMI was 7.85 and 6.08 in male and female patients under 65 years and 7.10 and 5.92 over 65 years, before chemotherapy, respectively. Lower baseline SMI was not correlated with worse OS in total patients (p=0.915). After a median measurement interval of 30 days after chemotherapy (n=67), body weight and SMI decreased by 2.73% and 2.87% (mean), respectively. The decrease in body weight correlated with the loss of trunk muscle mass (R=0.2107) but was more strongly associated with the loss of lower limbs muscle mass (R=0.3985). The muscle mass of lower limbs significantly decreased in lymphoma patients who experienced febrile neutropenia (-0.42% vs -6.04%, p=0.040). OS significantly decreased in lymphoma patients with loss of lower limbs muscle ≥2.8% (p=0.0327). Muscle loss occurred following anticancer treatments, significantly contributing to worse outcomes. Body composition assessment and relevant multimodal prevention of muscle loss may be vital for patients receiving chemotherapy for haematological malignancies. (Keyword) Humans / Male / Female / Retrospective Studies / Middle Aged / Hematologic Neoplasms / Muscle, Skeletal / Aged / Adult / Antineoplastic Agents / Aged, 80 and over / Body Composition / Sarcopenia (Tokushima University Institutional Repository) ● Metadata: 119635 (Link to Publication Site) ● Publication site (DOI): 10.1136/spcare-2024-004870 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38569748 ● Search Scopus @ Elsevier (PMID): 38569748 ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-004870 (Tokushima University Institutional Repository: 119635, DOI: 10.1136/spcare-2024-004870, PubMed: 38569748)
2.	Shingen Nakamura, Keijiro Hara, Tomoko Kobayashi, Ryohei Sumitani, Masahiro Oura, Yusaku Maeda, Kimiko Sogabe, Hikaru Yagi, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Yoshimi Bando, Masahiro Abe and Hirokazu Miki : Tl uptake and retention mimicking malignant lymphoma in a patient with human immunodeficiency virus infection., Parasitology International, Vol.101, 102895, 2024. (Summary) Various opportunistic infections develop during immunodeficiency due to human immunodeficiency virus (HIV) infection. The treatment options for malignant lymphoma (ML) and toxoplasmic encephalitis (TE) are completely different; therefore, their discrimination is critical. A 25-year-old female of foreign nationality had been experiencing headaches for several weeks and suddenly developed convulsions. Brain computed tomography revealed multiple intracranial lesions; therefore, the patient was referred to the neurosurgery department. Brain magnetic resonance imaging (MRI) revealed multiple masses with surrounding edema, accompanied by enhanced contrast. The largest mass (2 cm) in the left occipital lobe exhibited ringed contrast enhancement. Her blood test results showed a CD4 count of 40/μL, positive HIV Ag/Ab, HIV-RNA level of 56 × 10 copies/mL, positive anti-Toxoplasma IgG (63 IU/mL), and negative anti-Toxoplasma IgM. Tl- single photon emission computed tomography (Tl-SPECT) revealed abnormal accumulation only in the tumor in the left occipital lobe (early T/N ratio, 3.034; delayed T/N ratio, 2.738; retention index, 0.9), which was suspected to be a ML. Both tumors, with or without high accumulation of Tl, were subjected to craniotomy biopsy. Pathological examination revealed infiltration of small lymphocytes with a necrotic background. The patient was diagnosed with TE based on a positive result of a tissue polymerase chain reaction test for Toxoplasma gondii. Two weeks after sulfamethoxazole and trimethoprim combination therapy, MRI imaging showed dramatic improvement in multiple brain tumors. This case is atypical because ML was ruled out despite high Tl-SPECT uptake and retention. Careful diagnosis through pathological examination and DNA testing is important. (Keyword) Humans / Female / Adult / Toxoplasmosis, Cerebral / Lymphoma / HIV Infections / Magnetic Resonance Imaging / Diagnosis, Differential / Tomography, Emission-Computed, Single-Photon / Toxoplasma (Tokushima University Institutional Repository) ● Metadata: 119634 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.parint.2024.102895 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38614255 ● Search Scopus @ Elsevier (PMID): 38614255 ● Search Scopus @ Elsevier (DOI): 10.1016/j.parint.2024.102895 (Tokushima University Institutional Repository: 119634, DOI: 10.1016/j.parint.2024.102895, PubMed: 38614255)
3.	Tomoko Maruhashi, Hirokazu Miki, Kimiko Sogabe, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Acute suppression of translation by hyperthermia enhances anti-myeloma activity of carfilzomib, International Journal of Hematology, Vol.119, No.3, 291-302, 2024. (Summary) Hyperthermia is a unique treatment option for cancers. Multiple myeloma (MM) remains incurable and innovative therapeutic options are needed. We investigated the efficacy of hyperthermia and carfilzomib in combination against MM cells. Although MM cell lines exhibited different susceptibilities to pulsatile carfilzomib treatment, mild hyperthermia at 43℃ induced MM cell death in all cell lines in a time-dependent manner. Hyperthermia and carfilzomib cooperatively induced MM cell death even under suboptimal conditions. The pro-survival mediators PIM2 and NRF2 accumulated in MM cells due to inhibition of their proteasomal degradation by carfilzomib; however, hyperthermia acutely suppressed translation in parallel with phosphorylation of eIF2α to reduce these proteins in MM cells. Recovery of β5 subunit enzymatic activity from its immediate inhibition by carfilzomib was observed at 24 h in carfilzomib-insusceptible KMS-11, OPM-2, and RPMI8226 cells, but not in carfilzomib-sensitive MM.1S cells. However, heat treatment suppressed the recovery of β5 subunit activity in these carfilzomib-insusceptible cells. Therefore, hyperthermia re-sensitized MM cells to carfilzomib. Our results support the treatment of MM with hyperthermia in combination with carfilzomib. Further research is warranted on hyperthermia for drug-resistant extramedullary plasmacytoma. (Keyword) Humans / Multiple Myeloma / Oligopeptides / Hyperthermia, Induced (Tokushima University Institutional Repository) ● Metadata: 119321 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03706-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38252236 ● Search Scopus @ Elsevier (PMID): 38252236 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03706-8 (Tokushima University Institutional Repository: 119321, DOI: 10.1007/s12185-023-03706-8, PubMed: 38252236)
4.	Kimiko Sogabe, Shingen Nakamura, Yoshiki Higa, Hirokazu Miki, Asuka Oda, Tomoko Maruhashi, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Masafumi Nakamura, Yusaku Maeda, Tomoyo Hara, Hiroki Yamagami, Shiroh Fujii, Kumiko Kagawa, Shuji Ozaki, Kiyoe Kurahashi, Itsuro Endo, Ken-ichi Aihara, Emiko Nakaue, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada and Masahiro Abe : Acute accumulation of PIM2 and NRF2 and recovery of β5 subunit activity mitigate multiple myeloma cell susceptibility to proteasome inhibitors., International Journal of Hematology, Vol.119, No.3, 303-315, 2024. (Summary) Resistance to proteasome inhibitors (PIs) has emerged as an important clinical issue. We investigated the mechanisms underlying multiple myeloma (MM) cell resistance to PIs. To mimic their pharmacokinetic/pharmacodynamic (PK/PD) profiles, MM cells were treated with bortezomib and carfilzomib for 1 h at concentrations up to 400 and 1,000 nM, respectively. Susceptibility to these PIs markedly varied among MM cell lines. Pulsatile treatments with PIs suppressed translation, as demonstrated by incorporation of puromycin at 24 h in PI-susceptible MM.1S cells, but not PI-resistant KMS-11 cells. Inhibition of β5 subunit activity decreased at 24 h in KMS-11 cells, even with the irreversible PI carfilzomib, but not under suppression of protein synthesis with cycloheximide. Furthermore, the proteasome-degradable pro-survival factors PIM2 and NRF2 acutely accumulated in MM cells subjected to pulsatile PI treatments. Accumulated NRF2 was trans-localized into the nucleus to induce the expression of its target gene, HMOX1, in MM cells. PIM and Akt inhibition restored the anti-MM effects of PIs, even against PI-resistant KMS-11 cells. Collectively, these results suggest that increased synthesis of β5 proteasome subunit and acute accumulation of PIM2 and NRF2 reduce the anti-MM effects of PIs. (Keyword) Humans / Proteasome Inhibitors / NF-E2-Related Factor 2 / Multiple Myeloma / Proteasome Endopeptidase Complex / Drug Resistance, Neoplasm / Cell Line, Tumor / Bortezomib / Antineoplastic Agents / Proto-Oncogene Proteins / Protein Serine-Threonine Kinases (Tokushima University Institutional Repository) ● Metadata: 119384 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03705-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38245883 ● Search Scopus @ Elsevier (PMID): 38245883 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03705-9 (Tokushima University Institutional Repository: 119384, DOI: 10.1007/s12185-023-03705-9, PubMed: 38245883)
5.	Masahiro Oura, Takeshi Harada, Asuka Oda, Jumpei Teramachi, Atsushi Nakayama, Ryohei Sumitani, Yusuke Inoue, Yusaku Maeda, Kimiko Sogabe, Maruhashi Tomoko, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shingen Nakamura, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Itsuro Endo, Hiroo Hasegawa, Hiroshi Fujiwara and Masahiro Abe : Therapeutic efficacy of the resorcylic acid lactone LL-Z1640-2 for adult T-cell leukaemia/lymphoma, eJHaem, Vol.4, No.3, 667-678, 2023. (Summary) Adult T-cell leukaemia/lymphoma (ATL) remains incurable. The NF-κB and interferon regulatory factor 4 (IRF4) signalling pathways are among the critical survival pathways for the progression of ATL. TGF-β-activated kinase 1 (TAK1), an IκB kinase-activating kinase, triggers the activation of NF-κB. The resorcylic acid lactone LL-Z1640-2 is a potent irreversible inhibitor of TAK1/extracellular signal-regulated kinase 2 (ERK2). We herein examined the therapeutic efficacy of LL-Z1640-2 against ATL. LL-Z1640-2 effectively suppressed the in vivo growth of ATL cells. It induced in vitro apoptosis and inhibited the nuclear translocation of p65/RelA in ATL cells. The knockdown of strongly induced ATL cell death while downregulating MYC. LL-Z1640-2 as well as the NF-κB inhibitor BAY11-7082 decreased the expression of IRF4 and MYC at the protein and mRNA levels, indicating the suppression of the NF-κB-IRF4-MYC axis. The treatment with LL-Z1640-2 also mitigated the phosphorylation of p38 MAPK along with the expression of CC chemokine receptor 4. Furthermore, the inhibition of STAT3/5 potentiated the cytotoxic activity of LL-Z1640-2 against IL-2-responsive ATL cells in the presence of IL-2. Therefore, LL-Z1640-2 appears to be an effective treatment for ATL. Further studies are needed to develop more potent compounds that retain the active motifs of LL-Z1640-2. (Link to Publication Site) ● Publication site (DOI): 10.1002/jha2.758 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37601887 ● Search Scopus @ Elsevier (PMID): 37601887 ● Search Scopus @ Elsevier (DOI): 10.1002/jha2.758 (DOI: 10.1002/jha2.758, PubMed: 37601887)
6.	Takeshi Harada, Hiroto Ohguchi, Asuka Oda, Michiyasu Nakao, Jumpei Teramachi, Masahiro Hiasa, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Shigeki Sano, Teru Hideshima and Masahiro Abe : Novel antimyeloma therapeutic option with inhibition of the HDAC1-IRF4 axis and PIM kinase, Blood Advances, Vol.7, No.6, 1019-1032, 2023. (Summary) Multiple myeloma (MM) preferentially expands and acquires drug resistance in the bone marrow (BM). We herein examined the role of histone deacetylase 1 (HDAC1) in the constitutive activation of the master transcription factor IRF4 and the prosurvival mediator PIM2 kinase in MM cells. The knockdown or inhibition of HDAC1 by the class I HDAC inhibitor MS-275 reduced the basal expression of IRF4 and PIM2 in MM cells. Mechanistically, the inhibition of HDAC1 decreased IRF4 transcription through histone hyperacetylation and inhibiting the recruitment of RNA polymerase II at the IRF4 locus, thereby reducing IRF4-targeting genes, including PIM2. In addition to the transcriptional regulation of PIM2 by the HDAC1-IRF4 axis, PIM2 was markedly upregulated by external stimuli from BM stromal cells and interleukin-6 (IL-6). Upregulated PIM2 contributed to the attenuation of the cytotoxic effects of MS-275. Class I HDAC and PIM kinase inhibitors cooperatively suppressed MM cell growth in the presence of IL-6 and in vivo. Therefore, the present results demonstrate the potential of the simultaneous targeting of the intrinsic HDAC1-IRF4 axis plus externally activated PIM2 as an efficient therapeutic option for MM fostered in the BM. (Keyword) Histone Deacetylase 1 / Interleukin-6 / Benzamides / Pyridines (Tokushima University Institutional Repository) ● Metadata: 118211 (Link to Publication Site) ● Publication site (DOI): 10.1182/bloodadvances.2022007155 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36129197 ● Search Scopus @ Elsevier (PMID): 36129197 ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2022007155 (Tokushima University Institutional Repository: 118211, DOI: 10.1182/bloodadvances.2022007155, PubMed: 36129197)
7.	Kimiko Nakano, Shiroh Fujii, Reiko Yamahana and Chiemi Onishi : Motivation for physical activity before and after allogeneic hematopoietic stem cell transplantation., Blood Cell Therapy, Vol.6, No.1, 11-17, 2023. (Summary) This study aimed to identify patient motivation for physical activity before and after allogeneic hematopoietic stem cell transplantation (HSCT). We conducted 14 semi-structured interviews of seven patients (two of each patient): one before starting a conditioning regimen and one after leaving the protected environment. All interviews were recorded and analyzed using the inductive content analysis method. The data collection period was May to December 2018. The participants comprised three men and four women aged 40-70 years. The patients underwent bone marrow, umbilical cord blood, or peripheral HSCT. The patients' motivation for physical activity before and after HSCT was classified into six categories and categorized into five themes including "to overcome HSCT," "to look after myself," "to respond to the donor," "the existence of supporters," and "encouragement from supporters." The categories and themes developed here based on patient responses provide an important perspective that should be promoted among healthcare providers who care for patients undergoing HSCT. (Link to Publication Site) ● Publication site (DOI): 10.31547/bct-2022-016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37324566 ● Search Scopus @ Elsevier (PMID): 37324566 ● Search Scopus @ Elsevier (DOI): 10.31547/bct-2022-016 (DOI: 10.31547/bct-2022-016, PubMed: 37324566)
8.	高原由実子, Hirokazu Miki, Shingen Nakamura, 林成樹, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 富永誠記, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, 大坂朱美, Takeshi Harada, Shiroh Fujii, Toshiyuki Suge, Keiko Aota, Shuji Ozaki and Masahiro Abe : 徳島県におけるHIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題, Shikoku Acta Medica, Vol.78, No.5-6, 193-198, 2022. (Summary) 【Introduction】The survival rate in patients with HIV infection and acquired immunodeficiency syndrome (AIDS) has been improved dramatically due to the advances in anti-HIV drug therapy, while aging-associated complications become a critical issue. The incidence of sudden occurrence of AIDS without prior detection of HIV infection, so called ``Ikinari AIDS'', still remains high. 【Objective】We retrospectively analyzed the incidence and clinical characteristics of HIV/AIDS patients in both Tokushima University Hospital and Tokushima Prefectural Central Hospital. 【Results】Eighty four patients (74 males and 10 females) with a median age of 39 years old (range 16 - 85) were enrolled. Thirty-four patients (40.5%) were diagnosed with ``Ikinari AIDS'' from 2001 to 2020. All 4 patients were diagnosed with ``Ikinari AIDS'' after 2020. AIDS-defining illnesses were diagnosed as follows ; pneumocystis pneumonia in 21 cases, CMV infection in 8 cases and candidiasis in 6 cases. All patients over 60 years old were suffered from AIDS. Other complications included syphilis in 17 cases, hepatitis B infection in 12 and herpes zoster in 7. 【Discussion/Conclusion】In Tokushima, the incidence rate of ``Ikinari AIDS'' appeared to be higher than that of national average. COVID - 19 pandemic hampered the public health care services of awareness-raising activity for HIV infection and telephone consultations about HIV, which may become more lease asymptomatic HIV patients without diagnosis. For early diagnosis of HIV/AIDS, it is becoming more important to share information to make early screening of HIV infection among medical staffs, such as medical doctors, dentists, nurses, pharmacists and MSWs. (Keyword) HIV / AIDS / Ikinari AIDS (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520013962706680448 (CiNii: 1520013962706680448)
9.	Naoto Okada, Akikazu Murakami, Masami Satou, Shingen Nakamura, Shiroh Fujii, Kimiko Sogabe, Mamiko Takahashi, Asami Okada, Akane Abe, Hideki Fujii, Masahiro Abe, Momoyo Azuma and Keisuke Ishizawa : First reported case of Lachnoanaerobaculum gingivalis bacteremia in an acute myeloid leukemia patient with oral mucositis during high dose chemotherapy., Anaerobe, Vol.76, 2022. (Summary) During chemotherapy in patients with oral mucositis, we should consider the possibility of L. gingivalis bacteremia. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.anaerobe.2022.102610 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35811059 ● Search Scopus @ Elsevier (PMID): 35811059 ● Search Scopus @ Elsevier (DOI): 10.1016/j.anaerobe.2022.102610 (DOI: 10.1016/j.anaerobe.2022.102610, PubMed: 35811059)
10.	Hiroki Yamada, Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : A machine learning model using SNPs obtained from a genome-wide association study predicts the onset of vincristine-induced peripheral neuropathy, The Pharmacogenomics Journal, 2022. (Summary) Vincristine treatment may cause peripheral neuropathy. In this study, we identified the genes associated with the development of peripheral neuropathy due to vincristine therapy using a genome-wide association study (GWAS) and constructed a predictive model for the development of peripheral neuropathy using genetic information-based machine learning. The study included 72 patients admitted to the Department of Hematology, Tokushima University Hospital, who received vincristine. Of these, 56 were genotyped using the Illumina Asian Screening Array-24 Kit, and a GWAS for the onset of peripheral neuropathy caused by vincristine was conducted. Using Sanger sequencing for 16 validation samples, the top three single nucleotide polymorphisms (SNPs) associated with the onset of peripheral neuropathy were determined. Machine learning was performed using the statistical software R package "caret". The 56 GWAS and 16 validation samples were used as the training and test sets, respectively. Predictive models were constructed using random forest, support vector machine, naive Bayes, and neural network algorithms. According to the GWAS, rs2110179, rs7126100, and rs2076549 were associated with the development of peripheral neuropathy on vincristine administration. Machine learning was performed using these three SNPs to construct a prediction model. A high accuracy of 93.8% was obtained with the support vector machine and neural network using rs2110179 and rs2076549. Thus, peripheral neuropathy development due to vincristine therapy can be effectively predicted by a machine learning prediction model using SNPs associated with it. (Tokushima University Institutional Repository) ● Metadata: 117583 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41397-022-00282-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35752658 ● Search Scopus @ Elsevier (PMID): 35752658 ● Search Scopus @ Elsevier (DOI): 10.1038/s41397-022-00282-8 (Tokushima University Institutional Repository: 117583, DOI: 10.1038/s41397-022-00282-8, PubMed: 35752658)
11.	Shin Kondo, Tatsuro Inoue, Takashi Saito, Yuka Kawamura, Ayane Katayama, Masafumi Nakamura, Ryohei Sumitani, Mamiko Takahashi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh : Allogeneic haematopoietic stem cell transplantation and patient falls: impact of lower extremity muscle strength., BMJ Supportive & Palliative Care, 2022. (Summary) Pretransplant LEMS was a significant predictor of post-transplant falls. The results of this study may help to prevent falls in patients undergoing allo-HSCT. (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjspcare-2022-003582 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35534187 ● Search Scopus @ Elsevier (PMID): 35534187 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2022-003582 (DOI: 10.1136/bmjspcare-2022-003582, PubMed: 35534187)
12.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : A genome-wide association study predicts the onset of dysgeusia due to anti-cancer drug treatment, Biological & Pharmaceutical Bulletin, Vol.45, No.1, 114-117, 2022. (Summary) Dysgeusia is a major side effect of anti-cancer drug treatment. Since dysgeusia significantly lowers the patient's QOL, predicting and avoiding its onset in advance is desirable. Accordingly, aims of the present study were to use a genome-wide association study (GWAS) to identify genes associated with the development of dysgeusia in patients taking anti-cancer drugs and to predict the development of dysgeusia using associated single nucleotide polymorphisms (SNPs). GWAS was conducted on 76 patients admitted to the Department of Hematology, Tokushima University Hospital. Using Sanger sequencing for 23 separately collected validation samples, the top two SNPs associated with the development of dysgeusia were determined. GWAS identified rs73049478 and rs41396146 SNPs on the retinoic acid receptor beta (RARB) gene associated with dysgeusia development due to the administration of anti-cancer drugs. Evaluation of the two SNPs using 23 validation samples indicated that the accuracy rate of rs73049478 was relatively high (87.0%). Thus, the findings of the present study suggest that the rs73049478 SNP of RARB can be used to predict the onset of dysgeusia caused by the administration of anti-cancer drugs. (Keyword) Antineoplastic Agents / Dysgeusia / Genetic Predisposition to Disease / Genome-Wide Association Study / Humans / Pharmaceutical Preparations / Polymorphism, Single Nucleotide / Quality of Life (Tokushima University Institutional Repository) ● Metadata: 117584 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b21-00745 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34657909 ● CiNii @ National Institute of Informatics (CRID): 1390290617368322560 ● Summary page in Scopus @ Elsevier: 2-s2.0-85123201593 (Tokushima University Institutional Repository: 117584, DOI: 10.1248/bpb.b21-00745, PubMed: 34657909, CiNii: 1390290617368322560, Elsevier: Scopus)
13.	Shin Kondo, Kumiko Kagawa, Takashi Saito, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh : Allogeneic haematopoietic stem cell transplantation-clinical outcomes: impact of leg muscle strength., BMJ Supportive & Palliative Care, 2021. (Summary) Pre-transplant LEMS was a significant factor in predicting OS and NRM. (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjspcare-2021-003256 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34949601 ● Search Scopus @ Elsevier (PMID): 34949601 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2021-003256 (DOI: 10.1136/bmjspcare-2021-003256, PubMed: 34949601)
14.	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)
15.	Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis., Internal Medicine, Vol.60, No.11, 1753-1757, 2021. (Summary) A 33-year-old man was admitted to our hospital for fever and abdominal pain. A blood analysis revealed pancytopenia and increased serum pancreatic enzymes with disseminated intravascular coagulation. A detailed examination revealed acute pancreatitis, with diffuse swelling of the pancreas and diffuse beaded dilatation of the main pancreatic duct, which mimicked autoimmune pancreatitis complicated by acute myeloid leukemia. Systemic cytotoxic chemotherapy led to the remission of leukemia and pancreatitis. We hypothesized that the etiology of acute pancreatitis was invasion of leukemia cells. Acute pancreatitis is rare as a symptom of leukemia; however, we should consider the possibility of leukemia during the differential diagnosis of acute pancreatitis. (Keyword) Acute Disease / Adult / Autoimmune Diseases / Autoimmune Pancreatitis / Humans / Leukemia, Myeloid, Acute / Male / Pancreatitis (Tokushima University Institutional Repository) ● Metadata: 116536 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.4916-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33456032 ● Search Scopus @ Elsevier (PMID): 33456032 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.4916-20 (Tokushima University Institutional Repository: 116536, DOI: 10.2169/internalmedicine.4916-20, PubMed: 33456032)
16.	Tashima Hozumi, Endo Yuka, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : Association analysis between adverse drug reactions to cytarabine therapy and single nucleotide polymorphisms in cytarabine metabolic genes in patients with hematopoietic tumor, Personalized Medicine Universe, Vol.10, 1-6, 2021. (Tokushima University Institutional Repository) ● Metadata: 117585 (Link to Publication Site) ● Publication site (DOI): 10.46459/pmu.2021002 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.46459/pmu.2021002 (Tokushima University Institutional Repository: 117585, DOI: 10.46459/pmu.2021002)
17.	Mamiko Takahashi, Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Intravenous busulfan-based conditioning with autologous stem cell transplantation for refractory B-cell lymphoma with central nervous system involvement., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 196-201, 2021. (Summary) The prognosis of relapsed or refractory lymphoma with central nervous system (CNS) involvement remains poor because of the lack of anticancer drugs with sufficient CNS penetration. [Case 1] A 65-year-old man was diagnosed with Stage IV mantle cell lymphoma. After two courses of chemotherapy and autologous hematopoietic stem cell (HSC) collection, urinary retention with fever developed. Cerebrospinal fluid analysis revealed leptomeningeal involvement, which was refractory to high-dose methotrexate therapy. Autologous peripheral blood stem cell transplantation (ASCT) was performed, followed by intravenous busulfan (ivBU), cyclophosphamide, and etoposide ; thereafter, no relapse has been detected for over six years. [Case 2] A 40-year-old woman with right lower hemiplegia was diagnosed with primary CNS lymphoma. Although four courses of high-dose methotrexate therapy were administered, the cerebral tumor increased in size. HSCs were collected after methotrexate therapy, and ASCT was performed in addition to conditioning using ivBU, cyclophosphamide, and etoposide, followed by whole-brain and local boost irradiation. She achieved complete remission, but relapsed two years after ASCT. High-dose ivBU-containing conditioning regimens with ASCT may be useful for refractory B-cell lymphoma with CNS involvement. J. Med. Invest. 68 : 196-201, February, 2021. (Tokushima University Institutional Repository) ● Metadata: 116021 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.196 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994471 ● Search Scopus @ Elsevier (PMID): 33994471 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.196 (Tokushima University Institutional Repository: 116021, DOI: 10.2152/jmi.68.196, PubMed: 33994471)
18.	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)
19.	Kengo Udaka, Shingen Nakamura, Shiroh Fujii, Ryosuke Miyamoto, Naoko Matsui, Shiyori Kawata, Taiki Hori, Junpei Murai, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Kumiko Kagawa, Yuishin Izumi, Masahiro Abe and Hirokazu Miki : Successful treatment of progressive multifocal leukoencephalopathy with mirtazapine and mefloquine in refractory myeloma, International Journal of Myeloma, Vol.10, No.1, 8-12, 2020.
20.	Shuji Ozaki, Takeshi Harada, Hikaru Yagi, Etsuko Sekimoto, Hironobu Shibata, Toshio Shigekiyo, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : Polyclonal Immunoglobulin Recovery after Autologous Stem Cell Transplantation Is an Independent Prognostic Factor for Survival Outcome in Patients with Multiple Myeloma, Cancers, Vol.12, No.1, 12, 2019. (Summary) We retrospectively analyzed multiple myeloma (MM) patients who underwent autologous stem cell transplantation (ASCT) without maintenance therapy to assess the impact of recovery of normal immunoglobulin (Ig) on clinical outcomes. The recovery of polyclonal Ig was defined as normalization of all values of serum IgG, IgA, and IgM 1 year after ASCT. Among 50 patients, 26 patients showed polyclonal Ig recovery; 14 patients were in ≥complete response (CR) and 12 remained in non-CR after ASCT. The patients with Ig recovery exhibited a significantly better progression-free survival (PFS, median, 46.8 vs 26.7 months, = 0.0071) and overall survival (OS, median, not reached vs 65.3 months, < 0.00001) compared with those without Ig recovery. The survival benefits of Ig recovery were similarly observed in ≥CR patients (median OS, not reached vs 80.5 months, = 0.061) and non-CR patients (median OS, not reached vs 53.2 months, = 0.00016). Multivariate analysis revealed that non-CR and not all Ig recovery were independent prognostic factors for PFS (HR, 4.284, 95%CI (1.868-9.826), = 0.00059; and HR, 2.804, 95%CI (1.334-5.896), = 0.0065, respectively) and also for OS (HR, 8.245, 95%CI (1.528-44.47), = 0.014; and HR, 36.55, 95%CI (3.942-338.8), = 0.0015, respectively). Therefore, in addition to the depth of response, the recovery of polyclonal Ig after ASCT is a useful indicator especially for long-term outcome and might be considered to prevent overtreatment with maintenance therapy in transplanted patients with MM. (Tokushima University Institutional Repository) ● Metadata: 115047 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers12010012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31861479 ● Summary page in Scopus @ Elsevier: 2-s2.0-85077198248 (Tokushima University Institutional Repository: 115047, DOI: 10.3390/cancers12010012, PubMed: 31861479, Elsevier: Scopus)
21.	井上雄介, Akishige Ikegame, 徳永尚樹, 千尋井上, Takayuki Nakao, Kojiro Nagai, 高橋真美子, Shiroh Fujii, Shingen Nakamura and Masahiro Abe : 芽球様の形態を示した肝脾型T細胞リンパ腫の一症例, 日本検査血液学会雑誌, Vol.20, No.2, 231-237, 2019.
22.	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)
23.	Yuko Miyakami, Shingen Nakamura, Masahiro Oura, Yasunobu Okamoto, 高橋真美子, Kimiko Sogabe, 岩佐昌美, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Hisanori Uehara and Masahiro Abe : De novo CD 20-negative diffuse large B-cell lymphoma developed with sustained fever and markedly high C-reactive protein level, Shikoku Acta Medica, Vol.74, No.5-6, 193-200, 2018. (Summary) A 68-year-old woman presented with sustained fever for more than 1 month and admitted due to hematemesis and systemic edema. Computed tomography scan revealed swelling of the cervical, paraaortic lymph nodes. Blood test results showed severe anemia, elevation of white blood cell count, elevation of liver enzyme and coagulopathy with high C-reactive protein. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells with necrosis and hemorrhage, which are positive for CD79α, CD30, MUM-1, and bcl-6 and negative for CD20, CD5, CD10, ALK, CD38, CD138, and EBER. Gene rearrangement of immunoglobulin heavy chain was detected in tumor cells. Bone marrow aspiration showed tumor involvement. The patient was diagnosed with de novo CD20-negative diffuse large B-cell lymphoma(DLBCL)stage IV B. Reduced CHOP therapy was performed under artificial respiration due to pulmonary edema and takotsubo cardiomyopathy. Although her general condition and high CRP levels temporarily improved, she died 47 days after admission due to rapid relapse. De novo CD20-negative DLBCL was rare and presented with high CRP levels and rapid progression, and was thought to be clinically different from the existing DLBCL. It is imperative to elucidate molecular pathophysiology and establish new treatment strategy for de novo CD20-negative DLBCL. (Keyword) CD20 / fever of unknown origin / diffuse large B-cell lymphoma / CRP (Tokushima University Institutional Repository) ● Metadata: 112987 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050583647829887360 (Tokushima University Institutional Repository: 112987, CiNii: 1050583647829887360)
24.	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)
25.	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)
26.	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)
27.	山口純代, Shingen Nakamura, 住田智志, 前田悠作, Masahiro Oura, 高橋真美子, 岩佐昌美, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Jun Kishi and Masahiro Abe : Development of adult T-cell leukemia/lymphoma during immunosuppressive Therapy for human T-cell leukemia virus type 1 associated arthropathy, Shikoku Acta Medica, Vol.73, No.5,6, 301-308, 2017. (Summary) A 64-year-old woman presented with lower leg edema, fever, and bilateral joint pain, involving the wrists, fingers, and knees, in April 201X. Serological test results were negative for rheumatoid factor, antinuclear antibody, and anti-cyclic citrullinated peptide antibody. A diagnosis of remitting seronegative symmetrical synovitis with pitting edema syndrome, a type of seronegative rheumatoid arthritis, was made and prednisolone was administered. The joint pain was refractory to prednisolone therapy. In February, 201X+2, the patient presented with right cervical lymphadenopathy. The CT scan revealed swelling of the cervical, axillary, and inguinal lymph nodes bilaterally and rapidly enlarged. In April, 18F-fluorodeoxyglucose PET/CT scan showed an abnormal collection in the enlarged lymph nodes. The patient subsequently developed hoarseness with dyspnea and attended our department. Blood test results showed high levels of lactate dehydrogenase (547U/L) and soluble interleukin‐2 receptor (34200 IU/L) and were positive for anti-human T-cell leukemia virus type1 (HTLV‐1) antibody. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells positive for CD3, CD4, and CD25 and negative for CD7. Monoclonal integration of HTLV‐1 proviral DNA was detected in the lymph node. A diagnosis of adult T-cell leukemia/lymphoma (ATLL), lymphoma type was made. The pain involving multiple joints was attributed to HTLV‐1associated arthropathy. Immunosuppressive therapy for HTLV‐1 carrier status may have played a role in the development of ATLL. (Keyword) Adult T-cell leukemia/lymphoma / HTLV-1 / rheumatoid arthritis / immunosuppressive therapy (Tokushima University Institutional Repository) ● Metadata: 112059 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050020697876757248 (Tokushima University Institutional Repository: 112059, CiNii: 1050020697876757248)
28.	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)
29.	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)
30.	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)
31.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Shingen Nakamura, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masami Iwasa, Itsuro Endo, Takeshi Kondo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Yoshiaki Kuroda, Hideaki Horikawa, Eiji Tanaka, Masahiro Abe and Toshio Matsumoto : A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration., Oncotarget, Vol.7, No.43, 70447-70461, 2016. (Summary) Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. (Tokushima University Institutional Repository) ● Metadata: 113048 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.11927 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27626482 ● Search Scopus @ Elsevier (PMID): 27626482 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.11927 (Tokushima University Institutional Repository: 113048, DOI: 10.18632/oncotarget.11927, PubMed: 27626482)
32.	Takeshi Harada, Hirokazu Miki, Q Cui, A Oda, Ryota Amachi, Jumpei Teramachi, A Bat-Erdene, K Sogabe, M Iwasa, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Sumiko Yoshida, I Endo, Ken-ichi Aihara, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Expansion of Th1-like V9V2T cells by new-generation IMiDs, lenalidomide and pomalidomide, in combination with zoledronic acid., Leukemia, Vol.31, No.1, 258-262, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2016.273 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27698446 ● Search Scopus @ Elsevier (PMID): 27698446 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2016.273 (DOI: 10.1038/leu.2016.273, PubMed: 27698446)
33.	Michiko Yamashita, Yoshiyuki Fujii, Keiji Ozaki, Yoshio Urano, Masami Iwasa, Shingen Nakamura, Shiroh Fujii, Masahiro Abe, Yasuharu Sato and Tadashi Yoshino : Human immunodeficiency virus-positive secondary syphilis mimicking cutaneous T-cell lymphoma., Diagnostic Pathology, Vol.10, 185, 2015. (Summary) Malignant syphilis or lues maligna is a severe form of secondary syphilis that was commonly reported in the pre-antibiotic era, and has now reemerged with the advent of the human immunodeficiency virus (HIV) epidemic. However, the characteristic histopathological findings of malignant syphilis remain controversial. The aim of this case report was to clarify the clinical and histopathological findings of HIV-positive malignant secondary syphilis. A Japanese man in his forties complained of fever, skin lesions, headache, and myalgia without lymphadenopathy during the previous 4 weeks. The skin lesions manifested as erythematous, nonhealing, ulcerated papules scattered on his trunk, extremities, palm, and face. Although the skin lesions were suspected to be cutaneous T-cell lymphomas on histological analyses, they lacked T-cell receptor Jγ rearrangement; moreover, immunohistochemical analyses confirmed the presence of spirochetes. The patient was administered antibiotics and anti-retroviral therapy, which dramatically improved the symptoms. On the basis of these observations of the skin lesions, we finally diagnosed the patient with HIV-associated secondary syphilis that mimicked cutaneous T-cell lymphoma. The patient's systemic CD4+ lymphocyte count was very low, and the infiltrate was almost exclusively composed of CD8+ atypical lymphocytes; therefore, the condition was easily misdiagnosed as cutaneous lymphoma. Although the abundance of plasma cells is a good indicator of malignant syphilis on skin histological analyses, in some cases, the plasma cell count may be very low. Therefore, a diagnosis of malignant secondary syphilis should be considered before making a diagnosis of primary cutaneous peripheral T-cell lymphoma or lymphoma associated with HIV infection. (Keyword) AIDS-Related Opportunistic Infections / Anti-Bacterial Agents / Anti-HIV Agents / Biopsy / Coinfection / Diagnosis, Differential / HIV Infections / Humans / immunohistochemistry / Lymphoma, T-Cell, Cutaneous / male / Predictive Value of Tests / skin / Skin Neoplasms / Syphilis / Syphilis, Cutaneous / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1186/s13000-015-0419-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26449225 ● Summary page in Scopus @ Elsevier: 2-s2.0-84943540407 (DOI: 10.1186/s13000-015-0419-5, PubMed: 26449225, Elsevier: Scopus)
34.	Shingen Nakamura, Hirokazu Miki, Asuka Oda, Ryota Amachi, Jumpei Teramachi, Kimiko Sogabe, Hikaru Fujino, Tomoko Maruhashi, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe : Susceptibility to bendamustine considerably varies among myeloma cells, but is enhanced in acidic conditions, International Journal of Myeloma, Vol.6, No.1, 7-11, 2015.
35.	Hirokazu Miki, Shingen Nakamura, A Oda, R Amachi, Keiichiro Watanabe, D Hanson, Jumpei Teramachi, Masahiro Hiasa, H Yagi, K Sogabe, M Takahashi, T Maruhashi, K Udaka, T Harada, Shiroh Fujii, A Nakano, Kumiko Kagawa, M Ri, S Iida, Shuji Ozaki, T Matsumoto and Masahiro Abe : Induction of endoplasmic reticulum stress by bortezomib sensitizes myeloma cells to DR5-mediated cell death, International Journal of Myeloma, Vol.5, No.1, 1-7, 2015. (Summary) <p>TNF-related apoptosis-including ligand/Apo2 (TRAIL)-mediated immunotherapy is an attractive anti-tumor modality with high tumor specificity. In order to improve its therapeutic efficacy, we further need to implement a novel maneuver for sensitization of malignant cells to TRAIL. Bortezomib (BTZ), a novel anti-myeloma (MM) agent, potently induces endoplasmic reticulum (ER) stress to cause apoptosis. Here, we explored the roles of BTZ in the cytotoxicity of anti-TRAIL receptor agonistic antibodies against MM cells with special reference to ER stress. BTZ enhanced the expression of death receptor 5 (DR5) but not DR4 in MM cells at surface protein as well as mRNA levels. However, the DR5 expression was not affected by BTZ without ER stress induction in MM cells with a point mutation in a BTZ-binding proteasome β<sub>5</sub> subunit. Tunicamycin, an ER stress inducer, was able to enhance the DR5 expression even in the BTZ-resistant MM cells, suggesting the role of ER stress in up-regulation of DR5 expression. Interestingly, BTZ facilitated extrinsic caspase-mediated apoptosis by anti-DR5 agonistic antibody in MM cells along with reducing c-FLICE-like interleukin protein, a caspase 8 inhibitor. These results suggest that BTZ enhances DR5 expression and its downstream apoptotic signaling through ER stress to sensitize MM cells to TRAIL-mediated immunotherapy.</p> (Keyword) multiple myeloma / bortezomib / TRAIL / DR5 / ER stress (Link to Publication Site) ● Publication site (DOI): 10.57352/ijm.5.1_1 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390292815284471040 ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.5.1_1 (DOI: 10.57352/ijm.5.1_1, CiNii: 1390292815284471040)
36.	Kumiko Kagawa, Shingen Nakamura, 八木ひかる, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 宇髙憲吾, Shiroh Fujii, Hirokazu Miki and Masahiro Abe : Successful treatment of refractory severe aplastic anemia with bone marrow transplantation from a genetically identical twin, Shikoku Acta Medica, Vol.70, No.3,4, 77-80, 2014. (Summary) Aplastic anemia is a bone marrow failure caused by severely curtailed hematopoietic stem cells (HSCs) and dysregulation of ambient immune cells. Immumo-suppressive conditioning followed by allogeneic HSC transplantation is currently a mainstay in treatment for patients at a younger age or those refractory to conventional immunosuppressive remedies. Syngeneic HSC transplantation appears to be promising, but has been very rarely performed ; therefore, its impact on a long-term outcome as well as the best preparative measures for HSC engraftment and immune amelioration are still largely unknown. Here, we reported a successful and beneficial syngeneic HSC transplantation for a refractory case with very severe aplastic anemia. A 30-year-old female presented high fever after tooth extraction, and was diagnosed with very severe aplastic anemia. Cyclosporine and anti-thymocyte globulin were initiated, but showed no hematological effects. After obtaining an informed consent, she underwent bone marrow transplantation from a genetically identical twin following an non-myeloablative conditioning regimen consisted of cyclophosphamide (750mg/m2, 4 days), fludarabine phosphate (25mg/m2, 4 days). Cyclosporine was given for acute GvHD prophylaxis. Her neutrophils recovered over 500/μl on 12 days after the transplantation, and her blood counts have been maintained in a normal range over 7 years thereafter. Although a fate of HSCs from a genetically identical twin and an immune response of ambient cells in the bone marrow in recipients remains largely unknown, from the present case and previously reported cases, we dare to recommend immunoablative conditioning and acute GvHD prophylaxis in syngeneic HSC transplantation for a refractory case with aplastic anemia for better engraftment and sustained onward recovery of hematopoiesis. (Keyword) aplastic anemia / genetically identical twin / syngeneic hematopoietic stem cell transplantation (Tokushima University Institutional Repository) ● Metadata: 109757 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172854348416 (Tokushima University Institutional Repository: 109757, CiNii: 1050302172854348416)
37.	Masahiro Hiasa, Jumpei Teramachi, A Oda, Ryota Amachi, T Harada, Shingen Nakamura, Hirokazu Miki, Shiroh Fujii, Kumiko Kagawa, Keiichiro Watanabe, Itsuro Endo, Y Kuroda, T Yoneda, Daisuke Tsuji, Michiyasu Nakao, Eiji Tanaka, Kenichi Hamada, Shigeki Sano, Kouji Itou, Toshio Matsumoto and Masahiro Abe : Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma., Leukemia, 2014. (Summary) Pim-2 kinase is overexpressed in multiple myeloma (MM) cells to enhance their growth and survival, and regarded as a novel therapeutic target in MM. However, the impact of Pim-2 inhibition on bone disease in MM remains unknown. We demonstrated here that Pim-2 expression was also upregulated in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells in the presence of cytokines known as the inhibitors of osteoblastogenesis in MM, including interleukin-3 (IL-3), IL-7, tumor necrosis factor-, transforming growth factor- (TGF-) and activin A, as well as MM cell conditioned media. The enforced expression of Pim-2 abrogated in vitro osteoblastogenesis by BMP-2, which suggested Pim-2 as a negative regulator for osteoblastogenesis. Treatment with Pim-2 short-interference RNA as well as the Pim inhibitor SMI-16a successfully restored osteoblastogenesis suppressed by all the above inhibitory factors and MM cells. The SMI-16a treatment potentiated BMP-2-mediated anabolic signaling while suppressing TGF- signaling. Furthermore, treatment with the newly synthesized thiazolidine-2,4-dione congener, 12a-OH, as well as its prototypic SMI-16a effectively prevented bone destruction while suppressing MM tumor growth in MM animal models. Thus, Pim-2 may have a pivotal role in tumor progression and bone loss in MM, and Pim-2 inhibition may become an important therapeutic strategy to target the MM cell-bone marrow interaction.Leukemia advance online publication, 30 May 2014; doi:10.1038/leu.2014.147. (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2014.147 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24787487 ● Search Scopus @ Elsevier (PMID): 24787487 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2014.147 (DOI: 10.1038/leu.2014.147, PubMed: 24787487)
38.	Takeshi Harada, Shuji Ozaki, Asuka Oda, Daisuke Tsuji, Akishige Ikegame, Masami Iwasa, Kengo Udaka, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Yoshiaki Kuroda, Shigeto Kawai, Kouji Itou, Hisafumi Yamada-Okabe, Toshio Matsumoto and Masahiro Abe : Combination with a Defucosylated Anti-HM1.24 Monoclonal Antibody plus Lenalidomide Induces Marked ADCC against Myeloma Cells and Their Progenitors, PLoS ONE, Vol.8, No.12, e83905, 2013. (Summary) The immunomodulatory drug lenalidomide (Len) has drawn attention to potentiate antibody-dependent cellular cytotoxicity (ADCC)-mediated immunotherapies. We developed the defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317) overexpressed in multiple myeloma (MM) cells. In this study, we evaluated ADCC by YB-AHM and Len in combination against MM cells and their progenitors. YB-AHM was able to selectively kill via ADCC MM cells in bone marrow samples from patients with MM with low effector/target ratios, which was further enhanced by treatment with Len. Interestingly, Len also up-regulated HM1.24 expression on MM cells in an effector-dependent manner. HM1.24 was found to be highly expressed in a drug-resistant clonogenic "side population" in MM cells; and this combinatory treatment successfully reduced SP fractions in RPMI 8226 and KMS-11 cells in the presence of effector cells, and suppressed a clonogenic potential of MM cells in colony-forming assays. Collectively, the present study suggests that YB-AHM and Len in combination may become an effective therapeutic strategy in MM, warranting further study to target drug-resistant MM clonogenic cells. (Keyword) Aged / Aged, 80 and over / Antibodies, Monoclonal, Humanized / Antibody-Dependent Cell Cytotoxicity / Antigens, CD / Antineoplastic Combined Chemotherapy Protocols / Cell Line, Tumor / Drug Synergism / Female / GPI-Linked Proteins / Glycosylation / Humans / immunotherapy / Lenalidomide / Male / Middle Aged / Multiple Myeloma / Neoplastic Stem Cells / Side-Population Cells / Thalidomide / Up-Regulation (Tokushima University Institutional Repository) ● Metadata: 106068 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0083905 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24386306 ● Summary page in Scopus @ Elsevier: 2-s2.0-84891280322 (Tokushima University Institutional Repository: 106068, DOI: 10.1371/journal.pone.0083905, PubMed: 24386306, Elsevier: Scopus)
39.	Shingen Nakamura, Hirokazu Miki, Shinsuke Kido, Ayako Nakano, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Keiichiro Watanabe, Takeshi Harada, Shiroh Fujii, Kyoko Takeuchi, Kumiko Kagawa, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Activating transcription factor 4, an ER stress mediator, is required for, but exce ssive ER stress suppresses osteoblastogenesis by bortezomib., International Journal of Hematology, Vol.98, No.1, 66-73, 2013. (Summary) Endoplasmic reticulum (ER) stress is induced in matrix-producing osteoblasts and plays an essential role in osteoblastogenesis. Although the bone anabolic activity of proteasome inhibitors has been demonstrated, the roles of ER stress induced by proteasome inhibition in osteoblastogenesis remain largely unknown. Here we show that bortezomib translationally increases protein levels of activating transcription factor 4 (ATF4), a downstream mediator of ER stress, in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells. The suppression of ATF4 expression by siRNA abrogated osteocalcin expression and mineralized nodule formation by MC3T3-E1 cells induced by bortezomib, indicating a critical role for ATF4 in bortezomib-mediated osteoblastogenesis. However, bortezomib at 20 nM or higher abolished the mineralized nodule formation along with reductions in the expression of osteoblastogenesis mediators β-catenin and Osterix. Furthermore, at 50 nM, bortezomib induced the expression of C/EBP homologous protein (CHOP), suggesting activation of the ATF4-CHOP pro-apoptotic pathway. These results suggest that a low dose of bortezomib induces osteogenic activity, but that, in contrast, excessive ER stress caused by bortezomib at higher doses hampers osteoblastogenesis. Therefore, dosing schedules for proteasome inhibitors warrant further study to maximize anabolic actions without compromising anti-MM activity in patients with multiple myeloma (MM). (Keyword) 3T3 Cells / Activating Transcription Factor 4 / Animals / Antineoplastic Agents / Biological Markers / Bone Marrow Cells / Boronic Acids / Calcification, Physiologic / Cells, Cultured / Endoplasmic Reticulum Stress / Gene Expression Regulation / Gene Silencing / Humans / Mice / Multiple Myeloma / Neoplasm Proteins / Osteoblasts / Osteocalcin / Osteogenesis / Proteasome Inhibitors / Pyrazines / RNA, Small Interfering / Stromal Cells (Tokushima University Institutional Repository) ● Metadata: 105938 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-013-1367-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23708974 ● Summary page in Scopus @ Elsevier: 2-s2.0-84880304849 (Tokushima University Institutional Repository: 105938, DOI: 10.1007/s12185-013-1367-z, PubMed: 23708974, Elsevier: Scopus)
40.	Keisuke Fujioka, Atsuro Saijo, Yuko Toyoda, Souji Kakiuchi, Masaki Hanibuchi, Masahiko Azuma, Kyoko Takeuchi, Shiroh Fujii, Shingen Nakamura, Kengo Utaka, Kumiko Kagawa, Masahiro Abe, Tomoya Mizutani and Yasuhiko Nishioka : 皮膚ランダム生検が診断に有用であった血管内リンパ腫の一例, Shikoku Acta Medica, Vol.67, No.5,6, 257-262, 2011. (Summary) A62‐year‐old woman was referred to our hospital for further examination of fever of unknownorigin, splenomegaly and pancytopenia. On admission, she had persistent fever and psychologicalsymptoms. Blood examination showed pancytopenia and elevated level of LDH, soluble IL‐2receptorand ferritin. Computed tomography showed multiple low density areas in the spleen, but no systemiclymphadenopathy. In magnetic resonance imaging of the pons, a low and high intensity area onT1‐and T2‐weighted image, respectively, was detected. Taken together these findings, she wassuspected to have hepatosplentic T-cell lymphoma or intravascular large B-cell lymphoma. To makea definite diagnosis, random skin biopsy was performed. Immunohistochemical stainings revealedthe massive infiltration of CD20‐and CD79α‐positive large lymphoid cells inside the vessels, whichyielded the diagnosis of intravascular large B-cell lymphoma. (Keyword) fever of unknown origin / intravascular large B-cell lymphoma / random skin biopsy (Tokushima University Institutional Repository) ● Metadata: 97858 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050020697877915520 (Tokushima University Institutional Repository: 97858, CiNii: 1050020697877915520)
41.	Hirokazu Miki, Shingen Nakamura, Shuji Ozaki, A Oda, H Amou, Akishige Ikegame, Keiichiro Watanabe, Masahiro Hiasa, Q Cui, T Harada, Shiroh Fujii, A Nakano, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, A Sakai, Masahiro Abe and Toshio Matsumoto : KRN5500, a spicamycin derivative, exerts anti-myeloma effects through impairing both myeloma cells and osteoclasts., British Journal of Haematology, Vol.155, No.3, 328-339, 2011. (Summary) The spicamycin analogue KRN5500 alters glycoprotein processing and induces damage in the endoplasmic reticulum (ER)-Golgi apparatus in cancer cells. In the present study, we explored the cytotoxic effects of KRN5500 on multiple myeloma (MM) cells and the bone marrow microenvironment with special reference to ER stress. Cell proliferation assay showed that KRN5500 induced G1 arrest and apoptosis in MM cells in a time- and dose-dependent manner. KRN5500 enhanced ER stress independently of caspase activation in MM cells. This cell death was observed even in the presence of bone marrow stroma cells or osteoclasts. Notably, KRN5500 induced cell death also in osteoclasts. In vivo effects of KRN5500 were evaluated using two xenograft models established in severe combined immunodeficient (SCID) mice by either subcutaneous injection of RPMI 8226 cells or intra-bone injection of INA-6 cells to subcutaneously implanted rabbit bones (SCID-rab model). KRN5500 significantly inhibited tumour growth in both animal models, and decreased the number of osteoclasts, which resulted in prevention of bone destruction in the SCID-rab model. These results suggest that KRN5500 exerts anti-MM effects through impairing both MM cells and osteoclasts. Therefore, this unique mechanism of KRN5500 might be a useful therapeutic option in patients with MM. (Keyword) Animals / Apoptosis / Bone Marrow Cells / Caspases / Cell Line, Tumor / Cell Proliferation / Dose-Response Relationship, Drug / Female / G1 Phase / Humans / Mice / Mice, SCID / Multiple Myeloma / Osteoclasts / Purine Nucleosides / Rabbits / Random Allocation / Stromal Cells / Tumor Microenvironment / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2141.2011.08844.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21902681 ● Search Scopus @ Elsevier (PMID): 21902681 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2141.2011.08844.x (DOI: 10.1111/j.1365-2141.2011.08844.x, PubMed: 21902681)
42.	Qu Cui, Hironobu Shibata, Asuka Oda, Hiroe Amou, Ayako Nakano, Kenichiro Yata, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Targeting myeloma-osteoclast interaction with V9V2 T cells., International Journal of Hematology, Vol.94, No.1, 63-70, 2011. (Summary) Multiple myeloma (MM) cells stimulate osteoclastogenesis, and osteoclasts (OCs) in turn enhance MM growth and drug resistance, resulting in a vicious cycle. V9V2 T cells exert potent anti-tumor effects, making T cell-based immunotherapies using these cells attractive candidates for currently incurable malignancies, such as MM. However, the impact of such treatments on the MM-OC interaction is largely unknown. We demonstrate here that V9V2 T cells expanded by zoledronic acid and IL-2 exerted potent cytotoxic effects on both MM cells and OCs, even in coculture settings, but showed no such effect on bone marrow stromal cells. V9V2 T cells marginally affected colony formation from normal hematopoietic progenitors, and furthermore migrated toward osteopontin and MIP-1, factors produced by the MM-OC interaction. These results suggest that V9V2 T cells expanded by zoledronic acid and IL-2 are able to migrate to MM bone lesions and preferentially target OCs as well as MM cells, thereby inhibiting both tumor expansion and bone destruction. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-011-0885-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21698356 ● Search Scopus @ Elsevier (PMID): 21698356 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0885-9 (DOI: 10.1007/s12185-011-0885-9, PubMed: 21698356)
43.	J Asano, A Nakano, A Oda, H Amou, Masahiro Hiasa, Kyoko Takeuchi, H Miki, S Nakamura, T Harada, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Ken-ichiro Yata, A Sakai, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : The serine/threonine kinase Pim-2 is a novel anti-apoptotic mediator in myeloma cells., Leukemia, 2011. (Summary) Bone marrow stromal cells (BMSCs) and osteoclasts (OCs) confer multiple myeloma (MM) cell survival through elaborating factors. We demonstrate herein that IL-6 and TNF family cytokines, TNF, BAFF and APRIL, but not IGF-1 cooperatively enhance the expression of the serine/threonine kinase Pim-2 in MM cells. BMSCs and OCs upregulate Pim-2 expression in MM cells largely via the IL-6/STAT3 and NF-B pathway, respectively. Pim-2 short interfering RNA reduces MM cell viability in cocultures with BMSCs or OCs. Thus, upregulation of Pim-2 appears to be a novel anti-apoptotic mechanism for MM cell survival. Interestingly, the mammalian target of rapamycin inhibitor rapamycin further suppresses the MM cell viability in combination with the Pim-2 silencing. The Pim inhibitor (Z)-5-(4-propoxybenzylidene) thiazolidine-2, 4-dione and the PI3K inhibitor LY294002 cooperatively enhance MM cell death. The Pim inhibitor suppresses 4E-BP1 phosphorylation along with the reduction of Mcl-1 and c-Myc. Pim-2 may therefore become a new target for MM treatment.Leukemia advance online publication, 8 April 2011; doi:10.1038/leu.2011.60. (Tokushima University Institutional Repository) ● Metadata: 106134 (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2011.60 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21475253 ● Search Scopus @ Elsevier (PMID): 21475253 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2011.60 (Tokushima University Institutional Repository: 106134, DOI: 10.1038/leu.2011.60, PubMed: 21475253)

Academic Letter:

1.	Yusaku Maeda, Shoichiro Takao, Shiori Morita, Shin Kondo, Michiko Yamashita, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Hirokazu Miki, Masahiro Abe and Shingen Nakamura : Quality of skeletal muscles during allogeneic stem-cell transplantation: a pilot study, BMJ Supportive & Palliative Care, 2024. (Link to Publication Site) ● Publication site (DOI): 10.1136/spcare-2024-005070 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-005070 (DOI: 10.1136/spcare-2024-005070)

Proceeding of International Conference:

1.	Takeshi Harada, Asuka Oda, Yosuke Matsushita, Ryohei Sumitani, Yusuke Inoue, Tomoyo Hara, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Kiyoe Kurahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, Toyomasa Katagiri and Masahiro Abe : ADAR1-dsRNA metabolism in myeloma cells with 1q amplification: a novel therapeutic target, 19th International Myeloma Society Annual Meeting, Aug. 2022.
2.	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.
3.	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.
4.	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)
5.	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.
6.	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.
7.	Takeshi Harada, Asuka Oda, Yohann Grondin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masami Iwasa, Masahiro Oura, Shingen Nakamura, Kumiko Kagawa, Yasunobu Okamoto, Kimiko Sogabe, Shiroh Fujii, Hirokazu Miki, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe : The critical role of the HDAC1-IRF4-Pim-2 axis in myeloma cell growth and survival: therapeutic impacts of targeting the HDAC1-IRF4-Pim-2 axis, 60th ASH Annual Meeting & Exposition, San Diego, Dec. 2018.
8.	Shingen Nakamura, Hirokazu Miki, Ariunzaya Bat-Erdene, Yasunobu Okamoto, Kimiko Sogabe, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe : Alteration of muscle mass after chemotherapy in patients with newly diagnosed multiple myeloma., Esmo asia 2018, Nov. 2018.
9.	Takeshi Harada, Oda Asuka, Jumpei Teramachi, Bat-Erdene Ariunzaya, Iwasa Masami, Oura Masahiro, Shingen Nakamura, Kumiko Kagawa, Okamoto Yasunobu, Kimiko Sogabe, Shiroh Fujii, Hirokazu Miki, Hideshima Teru, Anderson C. Kenneth and Masahiro Abe : Selective inhibition of class-I HDAC induces myeloma cell death through targeting IRF4-Pim-2 axis, The 9th JSH International Symposium 2018 in Kyoto, Jul. 2018. (Keyword) Multiple myeloma / Class-I HDAC / IRF4 / Pim2
10.	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.
11.	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.
12.	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.
13.	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.
14.	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)
15.	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)
16.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kumiko Kagawa, Hirokazu Miki, Shiroh Fujii, Keiichiro Watanabe, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Critical role of Pim-2 in NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis: Therapeutic impact of Pim inhibition on myeloma bone disease., 2014 ASBMR Annual Meeting, Houston, Sep. 2014.
17.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, H Mori, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto : Induction of bone formation in myeloma osteolytic lesions by cathepsinK inhibition, Kyoto, Apr. 2013.
18.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, Hirokazu Miki, Shingen Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acidic milieu suppersses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression., Kyoto, Apr. 2013.
19.	Harada Takeshi, Ozaki Shuji, Oda Asuka, Iwasa Masami, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Shibata Hironobu, Akishige Ikegame, Daisuke Tsuji, Ito Kohji, Ri Masaki, Iida Shinsuke, Shiotsu Yukimasa, Kawai Shigeto, Yamada-Okabe Hisafumi and Toshio Matsumoto : Combination therapy of a defucosylated anti-HM1.24 monoclonal antibody plus Ienalidomide induces marked antibody-dependent cellular cytotoxicity and inhibits the clonogenic potential of myeloma cancer stem-like cells. Atlanta, Dec. 2012., The 54th Annual Meeting of the American Society of Hamatology, Dec. 2012.
20.	T Harada, Shuji Ozaki, A Oda, M Iwasa, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Hirofumi Shibata, Akishige Ikegame, Daisuke Tsuji, Kouji Itou, M Ri, S Iida, Y Shiotsu, S Kawai, H Yamada-Okabe and Toshio Matsumoto : Combination Therapy of a Defucosylated Anti-HM1.24 Monoclonal Antibody Plus Lenalidomide Induces Marked Antibody-Dependent Cellular Cytotoxicity and Inhibits the Clonogenic Potential of Myeloma Cancer Stem-Like Cells., 54th ASH Annual Meeting and Exposition, USA, Atlanta, Dec. 2012.
21.	Keiichiro Watanabe, Masahiro Abe, M Kawatani, Masahiro Hiasa, A Kawano, T Jinno, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, H Osada and Toshio Matsumoto : Aggravation of myeloma growth and drug resistance by an acidic created in myeloma-osteoclast interaction., ASBMR 2011 Annual Meeting, San Diego, Sep. 2011.
22.	Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition., ASBMR 2011 Annual Meeting, San Diego, Sep. 2011.
23.	Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Dual effects of Pim inhibition on myeloma: induction of bone formation and tumor suppression., IOF-ANZBMS 2011 Annual Meeting, Gold Coast, Sep. 2011.
24.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : An Acidic Mileu Created In Myeloma-Osteoclast Interaction Enhances Tumor Growth, but Triggers Anti-Myeloma Activity of Reveromycin A, a Novel Anti-Resorptive Agent, 52th American Society of Hematology, Orlando, Dec. 2010.
25.	Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Lenalidomide In Combination with Zoledronic Acid Restores the Activation and Anti-Myeloma Effects of γδT Cells Attenuated by the Bone Marrow Microenvironment, 52th American Society of Hematology, Orlando, Dec. 2010.
26.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : A Novel Anti-resorptive Agent, Reveromycin A, Ameliorates Bone Destruction and Tumor Growth in Myeloma, ASBMR 2010 Annual Meeting, Toronto, Oct. 2010.
27.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : The novel anti-resorptive agent reveromycin A ameliorates bone destruction and tumor growth in myeloma, 10th International Conference Cancer-induced Bone Disease, Sheffield (United Kingdom), Sep. 2010.

Proceeding of Domestic Conference:

1.	住谷龍平, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Shiroh Fujii, Takeshi Harada, Hirokazu Miki and 安倍正博 : 周期的な発熱，血小板減少，高LDH血症で発症したびまん性大細胞型B細胞リンパ腫の1例, 第128回日本内科学会四国地方会,
2.	Yusaku Maeda, Shingen Nakamura, Saki Saijo, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Shiroh Fujii, Takeshi Harada and Hirokazu Miki : 多職種による集学的ケアを行ったインヒビター保有重症先天性血友病Aの1例, 第129回内科学会四国地方会,
3.	阪本朋香, Yoshie Imai, 三木こずえ, Shiroh Fujii, Hirokazu Miki, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, 八木ひかる, 高橋真美子, Takeshi Harada, 前田悠作, Shingen Nakamura and Ken-ichi Matsuoka : 治療過程にある多発性骨髄腫患者が治療を続ける意味, 第39回日本がん看護学会学術集会, Feb. 2025.
4.	明石和子, Yoshie Imai, Shingen Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 初回再発した老年期の造血器腫瘍患者が捉える化学療法への構え, 第9回日本がんサポーティブケア学会学術集会, May 2024.
5.	Ryohei Sumitani, Hirokazu Miki, Kazumi Okamura, 前田悠作, Masahiro Oura, Kimiko Sogabe, 八木ひかる, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Takeshi Oya, Masahiro Abe and 佐藤亜紀 : KRAS変異を認めた治療抵抗性Rosai-Dorfman病の1例, 臨床血液, Vol.65, No.5, 473, May 2024.
6.	HIRAOKA Junichiro, Yuta Arai, Seiji Iwamoto, 岡田直子, MATSUSHITA Tomoki, Yuka Hiroshima, Takayoshi Shinya, Masafumi Harada, Kei Daizumoto, Yoshito Kusuhara, Kimiko Sogabe and Shiroh Fujii : 後天性von Willebrand病により術後止血に難渋した1例, 第268回徳島医学会学術集会, Mar. 2024.
7.	明石和子, Yoshie Imai, Shingen Nakamura, 西條早希, 前田悠作, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 初回再発した成人期の造血器腫瘍患者が捉える化学療法への構え, 第21回日本臨床腫瘍学会学術集, Feb. 2024.
8.	HIRAOKA Junichiro, Yuta Arai, Seiji Iwamoto, 岡田直子, MATSUSHITA Tomoki, HIROSHIMA Yuka, Takayoshi Shinya, Masafumi Harada, Kei Daizumoto, Yoshito Kusuhara, Kimiko Sogabe and Shiroh Fujii : von Willebrand病により術後止血に難渋した1例, Dec. 2023.
9.	明石和子, Yoshie Imai, Shingen Nakamura, 西條早希, 前田悠作, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 再発・難治性造血器腫瘍患者が捉えるアドバンス・ケア・プランニング, 第61回日本癌治療学会学術集会, Oct. 2023.
10.	Ryohei Sumitani, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Shiroh Fujii, Takeshi Harada, Hirokazu Miki and Masahiro Abe : 周期的な発熱，血小板減少，高LDH血症で発症したびまん性大細胞型B細胞リンパ腫の1例, 第128回日本内科学会四国地方会, Jul. 2023.
11.	佃恵里加, 李悦子, 瀧本朋美, 小田直輝, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki and Masahiro Abe : ダラツムマブ投与患者における間接抗グロブリン試験干渉期間の検討, Japanese Journal of Transfusion and Cell Therapy, Vol.68, No.6, 582-583, Dec. 2022.
12.	Mamiko Takahashi, Shingen Nakamura, Shin Kondo, Masafuumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki and Masahiro Abe : Importance of skeletal muscle mass during chemotherapies in patients with hematological malignancies, JSH2022, Oct. 2022.
13.	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.
14.	新居寛子, 髙橋真美子, Shiroh Fujii, Kimiko Sogabe, 林成樹, Ryohei Sumitani, Masahiro Oura, Takeshi Harada, Shingen Nakamura, 安積麻衣, 湊将典, Hirokazu Miki and Masahiro Abe : ループス腎炎に対してミコフェノール酸モフェチル投与中に発症した他の医原性免疫不全関連リンパ増殖性疾患の1例, 第265回徳島医学会学術集会, Jul. 2022.
15.	Ryohei Sumitani, Makiko Mizuguchi, Masahiro Oura, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Toshihiro Hashimoto, Takeshi Harada and Masahiro Abe : 126, 第126回日本内科学会四国地方会, Jun. 2022.
16.	中村昌史, Hirokazu Miki, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, 西尾進, Tetsu Tomonari and Masahiro Abe : ALアミロイドーシスの肝病変の評価における超音波エラストグラフィの有用性, The Japanese Journal of Clinical Hematology, Vol.63, No.6, 685-686, Jun. 2022. (Keyword) 肝臓疾患(超音波診断,薬物療法) 組織弾性イメージング *アミロイドーシス-免疫グロブリン軽鎖(超音波診断,薬物療法) ヒト中年(45∼64) 男女
17.	Shingen Nakamura, HORI Taiki, Masafumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada and Masahiro Abe : Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia, The 47th annual meeting of Japanese Society of Myeloma, May 2022.
18.	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.
19.	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.
20.	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.
21.	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.
22.	丸橋朋子, Hirokazu Miki, Kimiko Sogabe, Takeshi Harada, 小田明日香, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, 高橋真美子, Shiroh Fujii and Masahiro Abe : 骨髄腫細胞のプロテアソーム阻害薬への抵抗性の機序と温熱療法によるその克服の可能性, 第47回日本骨髄腫学会学術集会, May 2022.
23.	Shingen Nakamura, 堀太貴, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 髙橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada and Masahiro Abe : 形質細胞疾患における新型コロナワクチンの有効性, 第47回日本骨髄腫学会学術集会, May 2022.
24.	Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, 西尾進, 友成哲 and Masahiro Abe : 肝臓アミロイドーシスに対する超音波エラストグラフィを用いた非侵襲的診断法の有用性, 第47回日本骨髄腫学会学術集会, May 2022.
25.	Shingen Nakamura, 堀太貴, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada, Ken-ichi Aihara and Masahiro Abe : 形質細胞異常症患者におけるSARS-CoV-2に対するmRNAワクチンの液性免疫応答の評価(Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia), International Journal of Myeloma, Vol.12, No.3, 199, May 2022. (Keyword) 予防接種単クローン性免疫グロブリン血症-良性(免疫学) 液性免疫アミロイドーシス-免疫グロブリン軽鎖(免疫学) *COVID-19ワクチン(治療的利用,薬理学)
26.	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
27.	高原由実子, Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Masahiro Abe, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 青田桂子 and Shuji Ozaki : HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題, Shikoku Acta Medica, Vol.78, No.1-2, 89, Apr. 2022.
28.	Ryohei Sumitani, Takeshi Harada, 中村昌史, 水口槙子, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 髙橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Mio Yada, Yoshihiro Matsudate, Hisanori Uehara and Masahiro Abe : 少量methotrexate療法が有効であった進行期原発性皮膚未分化大細胞型リンパ腫., The Japanese Journal of Clinical Hematology, Vol.63, No.6, 536-543, Mar. 2022. (Summary) 進行期の原発性皮膚未分化大細胞リンパ腫(pcALCL)に対する標準治療は定まっていない．症例は71歳,男性．多発性の皮膚紅斑と結節病変を認め,左耳介後部からの生検でリンパ腫性丘疹症(LyP)と診断された．局所電子線照射にて全ての病変は消退したが,5ヵ月後に両内眼角に結節病変が出現し,同部位の生検ではCD30陽性大型細胞が大部分を占めpcALCLと診断された．PET/CTにて右口蓋扁桃腫大,頸部,鼠径部の表在リンパ節腫大およびFDG集積を認め,TNM分類T3bN3M0であった．慢性閉塞性肺疾患による呼吸機能低下と肺炎を反復していたため,多剤併用化学療法ではなくmethotrexate(MTX)15mg/週の内服療法を選択した．皮膚,リンパ節病変は縮小し,副作用なく長期間病勢コントロールが可能であった．pcALCLの標準治療は確立されていないが様々な治療法が開発されてきており,少量MTX療法は呼吸器感染症を繰り返すフレイルな患者に有用であった．LyPにpcALCLが続発する機序や本疾患群に対する少量MTX療法の作用機序の解明が望まれる．(著者抄録) (Keyword) Etoposid / Methotrexate / 顔面腫瘍 / lung disease / 皮膚疾患-顔面 / 皮膚腫瘍 / 扁桃腫瘍 / 放射線療法 / Folic Acid / リンパ腫-未分化大細胞 / 心筋症-たこつぼ型 / PET-CT検査 / フレイル / Homo sapiens / 高齢者 (Link to Publication Site) ● Publication site (DOI): 10.11406/rinketsu.63.536 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.63.536 (DOI: 10.11406/rinketsu.63.536)
29.	高原由実子, Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, Takeshi Harada, Shiroh Fujii, Keiko Aota, Shuji Ozaki and Masahiro Abe : HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題., --- 264 ( 3 ) ---, 第264回徳島医学会学術集会(令和3年度冬期), 2022年2月20日(Web開催), Feb. 2022.
30.	Hiroki Yamada, Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析によるビンクリスチン副作用発現関連遺伝子の同定と機械学習を用いた副作用発現予測モデルの構築, 第60回日本薬学会中国四国支部学術大会, Nov. 2021.
31.	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.
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 : 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.
33.	Shingen Nakamura, 上野宜久, Sumiko Yoshida, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, 広津崇亮 and Masahiro Abe : 血液がんにおける線虫がん検査 N-NOSEの検討(Detection of hematological malignancies using N-NOSE(Nematode-NOSE)), 日本血液学会学術集会, OS1-11B-2, Sep. 2021. (Keyword) 検尿走化性 Caenorhabditis elegans 造血器腫瘍(診断) ヒト男女
34.	Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Kumiko Kagawa, Nishio Susumu, Tetsu Tomonari and Masahiro Abe : 肝臓アミロイドーシスに対する超音波エラストグラフィの診断的有用性., 第83回日本血液学会学術集会, OS1-8D-2, Sep. 2021.
35.	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.
36.	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.
37.	Hirokazu Miki, Shingen Nakamura, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Masateru Kondo, Naoto Okada, Yoshimi Bando, Itsuro Endo and Masahiro Abe : The importance of retaining physical functions to prevent SRE in multiple myeloma., 第46回日本骨髄腫学会学術集会, May 2021.
38.	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
39.	石田卓也, Hirokazu Miki, 髙橋真美子, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, Tetsu Tomonari, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Keiko Aota, Hiroyoshi Watanabe and Masahiro Abe : HIV感染血友病患者における臨床的特徴と今後の課題, 第262回徳島医学会学術集会, Mar. 2021.
40.	Maruhashi Tomoko, Shiroh Fujii, Kumiko Kagawa, Nakamura Masafumi, Shiyori Kawata, Makiko Mizuguchi, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Takahashi Mamiko, Takeshi Harada, Shingen Nakamura, Hirokazu Miki and Masahiro Abe : 造血幹細胞移植(allo-SCT)が奏効したMLL遺伝子変異合併CML急性転化(CML-BP)の2例, 第43回日本造血細胞移植学会総会, Mar. 2021.
41.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習による遺伝情報を用いた抗がん剤投与の味覚障害発現予測モデルの構築, 第59回中国四国支部学術大会, Dec. 2020.
42.	Yuka Endoh, Hozumi Tashima, 岡田直人, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノム情報を用いた機械学習によるシタラビン投与後の副作用発現予測モデルの構築, 第59回中国四国支部学術大会, Dec. 2020.
43.	清重尚希, Ryohei Sumitani, 水口槙子, 中村昌史, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, 賀川久美子, Masahiro Abe, Shingen Nakamura, Hirokazu Miki, 曽賀愛未, 一宮由貴 and Yuri Yamamoto : 急性転化をきたしたAYA世代慢性骨髄性白血病の1例, Shikoku Acta Medica, Vol.76, No.5-6, 354-355, Dec. 2020. (Keyword) 同種移植抗腫瘍剤(治療的利用) *白血病-BCR-ABL陽性慢性骨髄性(診断,治療,薬物療法) 急性転化(白血病) 障害者の子供造血幹細胞移植家族介護者ヒト青年期(13~18) 女
44.	Hirokazu Miki, 悦子李, 佃恵里加, 小田直輝, 瀧本朋美, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Daratumumab投与による輸血関連検査への影響とその対策, Shikoku Acta Medica, Vol.76, No.5-6, 341, Dec. 2020. (Keyword) Coombsテスト / 骨髄腫-多発性(診断,薬物療法) / Daratumumab(治療的利用) / ヒト / 中年(45~64) / 高齢者(65~79) / 高齢者(80~) / 男 / 女
45.	中村昌史, Shiroh Fujii, Hirokazu Miki, 細木美苗, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 大櫛祐一郎 and Masahiro Abe : ACE阻害薬による血管性浮腫が原因と考えられた喉頭浮腫の一例, 第123回日本内科学会四国地方会, Nov. 2020.
46.	丸橋朋子, Hirokazu Miki, 中村昌史, 高橋真美子, Shiroh Fujii, 中野綾子 and Masahiro Abe : Evans症候群に合併した自己免疫性骨髄線維症の1例, 第123回日本内科学会四国地方会, Nov. 2020.
47.	市原聖也, Ryohei Sumitani, 中村昌史, 水口槙子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : ウイルス関連血球貪食症候群が疑われたアグレッシブNK細胞白血病の1例, 第123回日本内科学会四国地方会, Nov. 2020.
48.	Akane Abe, Nobuhito Naito, Kenji Otsuka, Yukikiyo Kawakami, Shiroh Fujii, Seiji Iwamoto, Seidai Satou, Hiroshi Kawano, Hiroshi Nokihara and Yasuhiko Nishioka : 非小細胞肺癌に合併した後天性血友病Aの1例, 第123回日本内科学会四国地方会, Nov. 2020.
49.	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.
50.	Masahiro Ohhra, Takeshi Harada, 寺町順平, 小田明日香, Yusuke Inoue, Kimiko Sogabe, Ryohei Sumitani, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Hasegawa Hiroo, Fujiwara Hiroshi and Masahiro Abe : Critical roles of the TAK1-c-Myc loop as a novel therapeutic target for ATL, 第82回日本血液学会学術集会, Oct. 2020.
51.	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.
52.	Masahiro Oura, Shingen Nakamura, 堀太貴, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Tomoko Kobayashi, Takeshi Oya and Masahiro Abe : 結節性紅斑と悪性腫瘍関連血球貪食症候群を惹起した骨髄異形成症候群の1例, The Japanese Journal of Clinical Hematology, Vol.61, No.10, 1542, Oct. 2020. (Keyword) 骨髄異形成症候群(合併症) 紅斑-結節性(病因) *血球貪食性リンパ組織球症(病因) ヒト中年(45~64) 男
53.	中村昌史, Hirokazu Miki, Masahiro Oura, 川田知代, 堀太貴, 村井純平, Ryohei Sumitani, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, 菅崎幹樹, 徳永尚樹, Akishige Ikegame, 森下英理子 and Masahiro Abe : クロスミキシングテストの特徴的な所見が診断の契機となったプレカリクレイン欠乏症の1例, The Japanese Journal of Clinical Hematology, Vol.61, No.10, 1537-1538, Oct. 2020. (Keyword) Prekallikrein(欠損・欠乏) 血液凝固異常(診断) *血液凝固検査ヒト中年(45~64) 男
54.	村井純平, 堀太貴, 川田知代, Ryohei Sumitani, 宇高憲吾, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Masahiro Abe, Hirokazu Miki, 桝田志保, Itsuro Endo and Seiji Fukumoto : 高ビタミンD血症による高Ca血症を来したホジキンリンパ腫の一例, Shikoku Acta Medica, Vol.76, No.1-2, 124, Apr. 2020. (Keyword) Calcitriol(毒性・副作用,血液) / Hodgkin病(合併症,薬物療法) / Vitamin D(毒性・副作用,血液) / 高カルシウム血症(化学的誘発) / 腫瘍多剤併用療法 / ヒト / 高齢者(65~79) / 男
55.	Yuka Endoh, Hozumi Tashima, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築, 日本薬学会第140年会, Mar. 2020.
56.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 遺伝情報を用いた機械学習による抗がん剤投与の味覚障害発現予測モデルの構築, 日本薬学会第140年会, Mar. 2020.
57.	遠藤優香, 田島穂澄, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築, 日本薬学会年会要旨集, 26M-am07S, Mar. 2020. (Keyword) Cytarabine(毒性・副作用) / 皮膚疾患(化学的誘発) / リスク評価 / 機械学習 / ヒト
58.	安宅克博, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Yasuhiko Nishioka and Masahiro Abe : 長期にわたる血小板減少が先行した芽球性形質細胞様樹状細胞腫瘍の1例, 第120回日本内科学会四国地方会, May 2019.
59.	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
60.	Yuto Tanigaki, Yuta Yamaguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析を用いたテイコプラニン・バンコマイシン投与による皮疹発現および血中濃度関連遺伝子座の同定, 日本薬学会第139年会, Mar. 2019.
61.	Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析を用いたビンクリスチンによる末梢神経障害発現関連遺伝子の同定, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
62.	Yuta Yamaguchi, Yuto Tanigaki, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : CYP遺伝子多型とバンコマイシンの副作用発現及び血中濃度との関連解析, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
63.	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.
64.	Masami Iwasa, Takeshi Harada, Bat-Erdene Ariunzaya, 小田明日香, Kimiko Sogabe, Masahiro Oura, Jumpei Teramachi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : HDAC阻害による骨髄腫細胞のIFN-γ-STAT1- PD-L1経路の増強効果, 第80回日本血液学会学術集会, Oct. 2018. (Keyword) Multiple myeloma
65.	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.
66.	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.
67.	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.
68.	Masami Iwasa, Takeshi Harada, Bat-Erdene Ariunzaya, 小田明日香, 前田悠作, 高橋真美子, Masahiro Oura, Jumpei Teramachi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : Amplification of the IFN- γ -STAT1- PD-L1 pathway in myeloma cells by panobinostat, The 43rd Annual Meeting of the Japanese Society of Myeloma, May 2018. (Keyword) Multiple myeloma
69.	Takeshi Harada, Oda Asuka, Jumpei Teramachi, Bat-Erdene Ariunzaya, Iwasa Masami, Maeda Yusaku, Shingen Nakamura, Oura Masahiro, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Hideshima Teru, Anderson C. Kenneth and Masahiro Abe : HDAC1/3 inhibition disrupts the IRF4-Pim-2 pathway to induce effective myeloma cell death, The 43rd Annual Meeting of the Japanese Society of Myeloma, May 2018. (Keyword) Multiple myeloma / Class-I HDAC / IRF4 / Pim-2
70.	Yuto Tanigaki, Youichi Sato, Yuta Yamaguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : テイコプラニン投与による副作用発現および血中濃度とCYP遺伝子多型との関連解析, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
71.	Hozumi Tashima, Youichi Sato, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : シタラビン投与による副作用発現と代謝経路関連遺伝子多型の関連解析, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
72.	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.
73.	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.
74.	Rio Ohmori, Youichi Sato, Misaki Kiguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : ビンクリスチンによる副作用発現とMDR1遺伝子多型との関連性, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
75.	Yuta Yamaguchi, Youichi Sato, Yuto Tanigaki, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : バンコマイシン投与による副作用発現及び血中濃度とCYP遺伝子多型との関連解析, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
76.	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.
77.	岡本恵暢, Shingen Nakamura, 上村宗範, Ryohei Sumitani, 高橋真美子, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe and Hirokazu Miki : 発熱と下肢対麻痺で発症した血管内大細胞型B細胞性リンパ腫の2例, Shikoku Acta Medica, Vol.72, No.5-6, 236-237, Dec. 2016. (Keyword) 下肢 / 発熱(病因) / 対麻痺(病因) / リンパ腫 / びまん性大細胞型B細胞性(合併症,薬物療法,病理学) / 血管腫瘍(合併症,薬物療法,病理学) / 血管内(合併症,薬物療法,病理学) / Homo sapiens / 中年(45∼64) / 高齢者(65∼79) / female
78.	Jumpei Teramachi, Hiroshi Mori, Yasuo Ochi, Ryota Amachi, Asuka Oda, Masahiro Hiasa, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma., The 77th Annual Meeting of the Japanese Society of Hematology, Oct. 2016.
79.	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.
80.	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.
81.	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.
82.	Keiichiro Watanabe, Jumpei Teramachi, H Mori, Y Ochi, Ryota Amachi, A Oda, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma, 第77回日本血液学会学術集会, Oct. 2015.
83.	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.
84.	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.
85.	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.
86.	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.
87.	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.
88.	丸橋朋子, Shingen Nakamura, 曽我部公子, 八木ひかる, 高橋真美子, 宇高憲吾, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Atsuro Saijo, Mayuri Nakano, Momoyo Azuma, Yasuhiko Nishioka, 近藤憲保, 井内新, 藤田博己 and 馬原文彦 : 当院で経験した重症熱性血小板減少症候群の3例, 第250回徳島医学会学術集会, Feb. 2015.
89.	Jumpei Teramachi, Masahiro Hiasa, 原田武志, Ryota Amachi, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of Pim inhibition on myeloma bone disease: blockade of NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis, 日本血液学会, Oct. 2014.
90.	Keiichiro Watanabe, Masahiro Abe, H Mori, K Udaka, M Iwasa, D Hanson, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto : Bone restoration and tumor suppression in myeloma by cathepsin K inhibition with Bortezomib, 第75回日本血液学会学術集会, Oct. 2013.
91.	大黒由加里, Takeshi Kondo, Shiroh Fujii, Shingen Nakamura, 倉橋清衛, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 著名な汎血球減少と肝筋逸脱酵素高値を呈した神経性食欲不振症の一例, 第13回日本内分泌学会四国支部学術集会, Sep. 2013.
92.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acdic milieu confers the resistance to TRAIL in myeloma cells through the PI3K-Akt-mediated epigenetic down-regulation of the TRAIL receptor DR4, International Bone and Mineral Society 2013, May 2013.
93.	Keiichiro Watanabe, Masahiro Abe, H Mori, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : Induction of cathepsin K induce bone formation in myeloma osteolytic lesions, International Bone and Mineral Society 2013, May 2013.
94.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acdic milieu suppresses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression, 14th International Myeloma Workshop, Apr. 2013.
95.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : Induction of bone formation in myeloma osteolytic lesions by cathepsin K inhibition, 14th International Myeloma Workshop, Apr. 2013.
96.	Hirokazu Miki, Shingen Nakamura, 竹内恭子, 原田武志, 岩佐昌美, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe and Toshio Matsumoto : 赤芽球癆を合併した多中心性Castleman病の1例, 日本内科学会第107回四国地方会, Dec. 2012.
97.	Shiroh Fujii, Masahiro Abe, Ryota Amachi, Keiichiro Watanabe, Masahiro Hiasa, 竹内恭子, 岩佐昌美, 原田武志, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Toshio Matsumoto : Pim inhibition preferentially induces anti-myeloma activity in an acidic milien, 第74回日本血液学会学術集会, Oct. 2012.
98.	原田武志, Shuji Ozaki, 岩佐昌美, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, 柴田泰伸, 重清俊雄, 岡田直人, 長尾多美子, 鈴木麗子, Shoji Sakiyama, Masahiro Abe and Toshio Matsumoto : 徳島県のエイズ拠点病院におけるHIV感染症及び後天性免疫不全症候群の現状, 第245回徳島県医学会学術総会, Jul. 2012.
99.	大黒由加里, Shingen Nakamura, 岩佐昌美, 原田武志, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe, Toshio Matsumoto and Hirokazu Miki : 腰痛と副腎不全症状で発症した両側副腎原発DLBCLの1例, 日本内科学会第106回四国地方会, Jun. 2012.
100.	原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 中野綾子, Kumiko Kagawa, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 徳島県における多発性骨髄腫の治療成績の検討, 第109回日本内科学会総会・講演会, Apr. 2012.
101.	原田武志, Shuji Ozaki, 小田明日香, 天羽宏枝, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 中野綾子, Kumiko Kagawa, 竹内恭子, Masahiro Abe, 柴田泰伸 and Toshio Matsumoto : Lenalidomide 治療中の多発性骨髄腫患者におけるCRP上昇の検討, 第51回日本血液学会中国四国地方会, Mar. 2012.
102.	Kumiko Kagawa, 原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 遺伝子組み替えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例, 第34回日本造血細胞移植学会, Feb. 2012.
103.	Kumiko Kagawa, 原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 遺伝子組み換えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例, 第34回日本造血細胞移植学会, Feb. 2012.
104.	Keiichiro Watanabe, Masahiro Abe, Q Cui, Masahiro Hiasa, M Kawatani, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, A Nakano, K Kagawa, K Takeuchi, H Osada, Eiji Tanaka and Toshio Matsumoto : Targeting an acidic microenvironment by reveromycin A to overcome drug resistance to myeloma cells and ameliorate bone disease., 第36回日本骨髄腫研究会総会, Nov. 2011.
105.	Keisuke Fujioka, Atsuro Saijo, Yuko Toyoda, Souji Kakiuchi, Masaki Hanibuchi, Masahiko Azuma, Yasuhiko Nishioka, Kyoko Takeuchi, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Masahiro Abe and Tomoya Mizutani : 不明熱で発症し皮膚生検が診断に有効であった血管内リンパ腫の1例, 第243回徳島医学会学術集会, Jul. 2011.
106.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : Reveromycin A prevents bone destruction and suppresses tumor growth in myeloma, 第72回日本血液学会, Dec. 2010.
107.	宇高憲吾, Naoko Matsui, 宮本亮介, Yuka Terasawa, Kenta Sato, Koutaro Asanuma, Yuishin Izumi, Ryuji Kaji, Shiroh Fujii, Kyoko Takeuchi, Masahiro Abe and Masafumi Harada : 多発性骨髄腫の経過中に進行性多巣性白質脳症をきたした一例, Shikoku Acta Medica, Vol.66, No.5-6, 198, Dec. 2010. (Keyword) Cytarabine(治療的利用); Prednisolone(治療的利用); 自家移植; 骨髄腫-多発性(合併症,治療); 白質脳症-進行性多巣性(合併症,画像診断,薬物療法); Mirtazapine(治療的利用); FLAIR法; 末梢血幹細胞移植 / ヒト; 中年(45∼64); 男
108.	Kumiko Kagawa, Jinno Tasashi, Harada Kakeshi, Cui Qu, Keiichiro Watanabe, Masahiro Hiasa, Oda Asuka, Amo Hiroe, Akishige Ikegame, Miki Hirokazu, Shiroh Fujii, Nakano Ayako, Kyoko Takeuchi, Shuji Ozaki, Masahiro Abe and Toshio Matsumoto : Sensitization of hematopietic malignant cells to TRAIL with bortezomib and a TACE inhibitor, 第72回日本血液学会, Sep. 2010.
109.	Shingen Nakamura, Masahiro Abe, Cui Qu, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Miki Hirokazu, Nakano Ayako, Oda Asuka, Amo Hiroe, Jinno Tasashi, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Bortezomib-induced osteoblast differentiation is hampered by excessive ER stress, 第72回日本血液学会, Sep. 2010.
110.	Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Jinnno Tadashi, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Bone marrow stromal cells attenuate gama delta T, 第72回日本血液学会, Sep. 2010.
111.	Shingen Nakamura, Masahiro Abe, Cui Qu, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, 三木浩和, 中野綾子, 小田明日香, 天羽宏枝, 神野雅, 原田武志, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : ボルテゾミブによる骨芽細胞分化の促進は過剰な小胞体ストレスによって抑制される, 第28回日本骨代謝学会, Jul. 2010.

Et cetera, Workshop:

1.	相原弘幸, BANDO Ryo, Ryota Matsumoto, Kimiko Sogabe, Zengu Robahto, TOMONORI Takahashi, Yoshihito Saijyo, Tomoya Hara, Muneyuki Kadota, Yutaka Kawabata, Rie Ueno, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shiroh Fujii, Hiroki Hata and Masataka Sata : 学生・研修医セッション1(冠動脈)血友病A患者における重症三枝病変に対する冠動脈バイパス術の一例, 第125回日本循環器学会四国地方会, Dec. 2024.
2.	梶田敬介, Shingen Nakamura, 曽我部公子, 藤野ひかる, 丸橋朋子, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Hiroaki Toba and 阿部正博 : 胸腺腫瘍に合併した赤芽球癆の二例-病態解明へのアプローチ-, 第252回徳島医学会学術集会, Feb. 2016.
3.	Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Kumiko Kagawa, Shiroh Fujii, 原田武志, Hirokazu Miki, Keiichiro Watanabe, 小野明日香, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : 骨髄腫の酸性環境はTRAIL受容体発現をエピジェネティックに抑制し，TRAIL抵抗性をもたらす, 第20回徳島骨代謝研究会, Nov. 2013.
4.	Masahiro Hiasa, Masahiro Abe, 中野綾子, Keiichiro Watanabe, Kyoko Takeuchi, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, 原田武志, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Pimキナーゼの阻害による骨髄腫の進展抑制, 癌と骨病変研究会, Nov. 2011.

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

Suppression of tumor progression in multiple myeloma by osteogenic microenvironment: Elucidation of the molecular pathogenesis of tumor suppressing niche (Project/Area Number: 21K16244 )
Elucidation of acidic metabolism in multiple myeloma and the development of novel therapies targeting its acidic microenvironment. (Project/Area Number: 19K17858 )
Search by Researcher Number (00618473)

Associate Professor : Fujii, Shiroh

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