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 β5 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.
","ja":"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 β5 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.
"},"publication_date":"2015-01","publication_name":{"en":"International Journal of Myeloma","ja":"International Journal of Myeloma"},"volume":"Vol.5","number":"No.1","starting_page":"1","ending_page":"7","languages":["eng"],"referee":true,"identifiers":{"doi":["10.57352/ijm.5.1_1"],"issn":["2187-3143"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:49, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167269"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/109757","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/109757","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050001337464993408/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=303542","label":"url"}],"paper_title":{"en":"Successful treatment of refractory severe aplastic anemia with bone marrow transplantation from a genetically identical twin","ja":"同系骨髄移植が著効した最重症再生不良性貧血の1例"},"authors":{"en":[{"name":"Kagawa Kumiko"},{"name":"Nakamura Shingen"},{"name":"八木 ひかる"},{"name":"Sogabe Kimiko"},{"name":"髙橋 真美子"},{"name":"丸橋 朋子"},{"name":"宇髙 憲吾"},{"name":"Fujii Shiroh"},{"name":"Miki Hirokazu"},{"name":"Abe Masahiro"}],"ja":[{"name":"賀川 久美子"},{"name":"中村 信元"},{"name":"八木 ひかる"},{"name":"曽我部 公子"},{"name":"髙橋 真美子"},{"name":"丸橋 朋子"},{"name":"宇髙 憲吾"},{"name":"藤井 志朗"},{"name":"三木 浩和"},{"name":"安倍 正博"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2014-06","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.70","number":"No.3,4","starting_page":"77","ending_page":"80","languages":["jpn"],"referee":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:50, {"insert":{"user_id":"B000341201","type":"published_papers","id":"25911417"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24787487","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=283755","label":"url"}],"paper_title":{"en":"Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma.","ja":"Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma."},"authors":{"en":[{"name":"Hiasa Masahiro"},{"name":"Teramachi Jumpei"},{"name":"Oda A"},{"name":"Amachi Ryota"},{"name":"Harada T"},{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Fujii Shiroh"},{"name":"Kagawa Kumiko"},{"name":"Watanabe Keiichiro"},{"name":"Endo Itsuro"},{"name":"Kuroda Y"},{"name":"Yoneda T"},{"name":"Tsuji Daisuke"},{"name":"Nakao Michiyasu"},{"name":"Tanaka Eiji"},{"name":"Hamada Kenichi"},{"name":"Sano Shigeki"},{"name":"Itou Kouji"},{"name":"Matsumoto Toshio"},{"name":"Abe Masahiro"}],"ja":[{"name":"日浅 雅博"},{"name":"寺町 順平"},{"name":"Oda A"},{"name":"天知 良太"},{"name":"Harada T"},{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"藤井 志朗"},{"name":"賀川 久美子"},{"name":"渡邉 佳一郎"},{"name":"遠藤 逸朗"},{"name":"Kuroda Y"},{"name":"Yoneda T"},{"name":"辻 大輔"},{"name":"中尾 允泰"},{"name":"田中 栄二"},{"name":"浜田 賢一"},{"name":"佐野 茂樹"},{"name":"伊藤 孝司"},{"name":"松本 俊夫"},{"name":"安倍 正博"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2014-05-02","publication_name":{"en":"Leukemia","ja":"Leukemia"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/leu.2014.147"],"issn":["1476-5551"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:51, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167271"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/106068","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24386306","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84891280322&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=349631","label":"url"}],"paper_title":{"en":"Combination with a Defucosylated Anti-HM1.24 Monoclonal Antibody plus Lenalidomide Induces Marked ADCC against Myeloma Cells and Their Progenitors","ja":"Combination with a Defucosylated Anti-HM1.24 Monoclonal Antibody plus Lenalidomide Induces Marked ADCC against Myeloma Cells and Their Progenitors"},"authors":{"en":[{"name":"Harada Takeshi"},{"name":"Ozaki Shuji"},{"name":"Oda Asuka"},{"name":"Tsuji Daisuke"},{"name":"Ikegame Akishige"},{"name":"Iwasa Masami"},{"name":"Udaka Kengo"},{"name":"Fujii Shiroh"},{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Kagawa Kumiko"},{"name":"Kuroda Yoshiaki"},{"name":"Kawai Shigeto"},{"name":"Itou Kouji"},{"name":"Yamada-Okabe Hisafumi"},{"name":"Matsumoto Toshio"},{"name":"Abe Masahiro"}],"ja":[{"name":"原田 武志"},{"name":"尾崎 修治"},{"name":"小田 明日香"},{"name":"辻 大輔"},{"name":"池亀 彰茂"},{"name":"岩佐 昌美"},{"name":"宇髙 憲吾"},{"name":"藤井 志朗"},{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"賀川 久美子"},{"name":"黒田 芳明"},{"name":"川合 重人"},{"name":"伊藤 孝司"},{"name":"岡部 尚文"},{"name":"松本 俊夫"},{"name":"安倍 正博"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2013-12-26","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.8","number":"No.12","starting_page":"e83905","ending_page":"e83905","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0083905"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:52, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167272"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/105938","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23708974","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84880304849&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=284313","label":"url"}],"paper_title":{"en":"Activating transcription factor 4, an ER stress mediator, is required for, but exce ssive ER stress suppresses osteoblastogenesis by bortezomib.","ja":"Activating transcription factor 4, an ER stress mediator, is required for, but exce ssive ER stress suppresses osteoblastogenesis by bortezomib."},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Kido Shinsuke"},{"name":"Nakano Ayako"},{"name":"Hiasa Masahiro"},{"name":"Oda Asuka"},{"name":"Amou Hiroe"},{"name":"Watanabe Keiichiro"},{"name":"Harada Takeshi"},{"name":"Fujii Shiroh"},{"name":"Takeuchi Kyoko"},{"name":"Kagawa Kumiko"},{"name":"Ozaki Shuji"},{"name":"Matsumoto Toshio"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"Kido Shinsuke"},{"name":"Nakano Ayako"},{"name":"日浅 雅博"},{"name":"Oda Asuka"},{"name":"Amou Hiroe"},{"name":"渡邉 佳一郎"},{"name":"Harada Takeshi"},{"name":"藤井 志朗"},{"name":"Takeuchi Kyoko"},{"name":"賀川 久美子"},{"name":"Ozaki Shuji"},{"name":"松本 俊夫"},{"name":"安倍 正博"}]},"description":{"en":"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).","ja":"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)."},"publication_date":"2013-05-25","publication_name":{"en":"International Journal of Hematology","ja":"International Journal of Hematology"},"volume":"Vol.98","number":"No.1","starting_page":"66","ending_page":"73","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s12185-013-1367-z"],"issn":["1865-3774"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:53, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167273"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40019180117/","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/97858","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050001337463886208/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=253199","label":"url"}],"paper_title":{"en":"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","ja":"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"},"authors":{"en":[{"name":"Fujioka Keisuke"},{"name":"Saijo Atsuro"},{"name":"Toyoda Yuko"},{"name":"Kakiuchi Souji"},{"name":"Hanibuchi Masaki"},{"name":"Azuma Masahiko"},{"name":"Takeuchi Kyoko"},{"name":"Fujii Shiroh"},{"name":"Nakamura Shingen"},{"name":"Utaka Kengo"},{"name":"Kagawa Kumiko"},{"name":"Abe Masahiro"},{"name":"Mizutani Tomoya"},{"name":"Nishioka Yasuhiko"}],"ja":[{"name":"藤岡 啓介"},{"name":"西條 敦郎"},{"name":"豊田 優子"},{"name":"柿内 聡司"},{"name":"埴淵 昌毅"},{"name":"吾妻 雅彦"},{"name":"竹内 恭子"},{"name":"藤井 志朗"},{"name":"中村 信元"},{"name":"宇高 憲吾"},{"name":"賀川 久美子"},{"name":"安倍 正博"},{"name":"水谷 友哉"},{"name":"西岡 安彦"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2011-12-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.67","number":"No.5,6","starting_page":"257","ending_page":"262","languages":["jpn"],"referee":true,"invited":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:54, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167274"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21902681","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=248823","label":"url"}],"paper_title":{"en":"KRN5500, a spicamycin derivative, exerts anti-myeloma effects through impairing both myeloma cells and osteoclasts.","ja":"KRN5500, a spicamycin derivative, exerts anti-myeloma effects through impairing both myeloma cells and osteoclasts."},"authors":{"en":[{"name":"Miki Hirokazu"},{"name":"Nakamura Shingen"},{"name":"Ozaki Shuji"},{"name":"Oda A"},{"name":"Amou H"},{"name":"Ikegame Akishige"},{"name":"Watanabe Keiichiro"},{"name":"Hiasa Masahiro"},{"name":"Cui Q"},{"name":"Harada T"},{"name":"Fujii Shiroh"},{"name":"Nakano A"},{"name":"Kagawa Kumiko"},{"name":"Takeuchi Kyoko"},{"name":"Yata Ken-ichiro"},{"name":"Sakai A"},{"name":"Abe Masahiro"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"三木 浩和"},{"name":"中村 信元"},{"name":"尾崎 修治"},{"name":"Oda A"},{"name":"Amou H"},{"name":"池亀 彰茂"},{"name":"渡邉 佳一郎"},{"name":"日浅 雅博"},{"name":"Cui Q"},{"name":"Harada T"},{"name":"藤井 志朗"},{"name":"Nakano A"},{"name":"賀川 久美子"},{"name":"竹内 恭子"},{"name":"矢田 健一郎"},{"name":"Sakai A"},{"name":"安倍 正博"},{"name":"松本 俊夫"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2011-11","publication_name":{"en":"British Journal of Haematology","ja":"British Journal of Haematology"},"volume":"Vol.155","number":"No.3","starting_page":"328","ending_page":"339","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/j.1365-2141.2011.08844.x"],"issn":["1365-2141"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:55, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167275"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21698356","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=231221","label":"url"}],"paper_title":{"en":"Targeting myeloma-osteoclast interaction with V9V2 T cells.","ja":"Targeting myeloma-osteoclast interaction with V9V2 T cells."},"authors":{"en":[{"name":"Cui Qu"},{"name":"Shibata Hironobu"},{"name":"Oda Asuka"},{"name":"Amou Hiroe"},{"name":"Nakano Ayako"},{"name":"Yata Kenichiro"},{"name":"Hiasa Masahiro"},{"name":"Watanabe Keiichiro"},{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Harada Takeshi"},{"name":"Fujii Shiroh"},{"name":"Kagawa Kumiko"},{"name":"Takeuchi Kyoko"},{"name":"Ozaki Shuji"},{"name":"Matsumoto Toshio"},{"name":"Abe Masahiro"}],"ja":[{"name":"Cui Qu"},{"name":"Shibata Hironobu"},{"name":"Oda Asuka"},{"name":"Amou Hiroe"},{"name":"Nakano Ayako"},{"name":"Yata Kenichiro"},{"name":"日浅 雅博"},{"name":"渡邉 佳一郎"},{"name":"中村 信元"},{"name":"Miki Hirokazu"},{"name":"Harada Takeshi"},{"name":"藤井 志朗"},{"name":"賀川 久美子"},{"name":"竹内 恭子"},{"name":"尾崎 修治"},{"name":"松本 俊夫"},{"name":"安倍 正博"}]},"description":{"en":"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.","ja":"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."},"publication_date":"2011-06-23","publication_name":{"en":"International Journal of Hematology","ja":"International Journal of Hematology"},"volume":"Vol.94","number":"No.1","starting_page":"63","ending_page":"70","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s12185-011-0885-9"],"issn":["1865-3774"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:56, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167276"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/130004501433/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20805677","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001205037088512/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-78349258607&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=303541","label":"url"}],"paper_title":{"en":"Multiple myeloma complicated with disseminated zygomycosis after bortezomib therapy","ja":"ボルテゾミブ療法後に播種性接合菌症を合併した多発性骨髄腫"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"YATA Kenichiro"},{"name":"JINNO Tadashi"},{"name":"HARADA Takeshi"},{"name":"FUJII Shiro"},{"name":"MIKI Hirokazu"},{"name":"NAKANO Ayako"},{"name":"KAGAWA Kumiko"},{"name":"TAKEUCHI Kyoko"},{"name":"OZAKI Shuji"},{"name":"Abe Masahiro"},{"name":"MATSUMOTO Toshio"}],"ja":[{"name":"中村 信元"},{"name":"矢田 健一郎"},{"name":"神野 雅"},{"name":"原田 武志"},{"name":"藤井 志朗"},{"name":"三木 浩和"},{"name":"中野 綾子"},{"name":"賀川 久美子"},{"name":"竹内 恭子"},{"name":"尾崎 修治"},{"name":"安倍 正博"},{"name":"松本 俊夫"}]},"description":{"en":"A 67-year-old man was diagnosed with multiple myeloma IgA-lambda type, Durie-Salmon classification stage IIIA in October 2001. He received five courses of induction chemotherapy consisting of vincristine, doxorubicin and dexamethasone and then underwent high dose chemotherapy followed by autologous stem cell transplantation in March 2003. He achieved partial response, but then relapsed after treatment with thalidomide and was admitted to our hospital in June 2007. The patient was complicated by tumor lysis syndrome (TLS) after receiving bortezomib therapy twice. Computed tomography after bortezomib therapy showed the rapid appearance of tumors in the right upper lobe of the lung, tail of the pancreas and the spleen. Though he was treated with antifungal agents, micafungin and voriconazole, he died eighty-five days after admission. Autopsy specimen showed fungal clumps and hemorrhagic infarction in the lung and spleen, and vegetation at the mitral valve was the same fungus as found in the lung. We diagnosed disseminated zygomycosis based on the pathological fungal morphology. This case suggested that metabolic acidosis was caused by TLS, while poorly controlled diabetes, secondary hemochromatosis due to transfusion, and breakthrough zygomycosis during antifungal therapy were thought to be factors contributing to the development of zygomycosis.","ja":"67歳男性，背部痛を契機に2001年10月に多発性骨髄腫IgA-λ stage IIIAと診断された．VAD療法5コース後の2003年3月に自家末梢血幹細胞移植併用大量化学療法を行うも再発した．以後，サリドマイド療法などを行うも再燃し，2007年6月入院した．入院後のボルテゾミブ(Bor)療法で，2度の腫瘍崩壊症候群をきたした．その後のCTで右肺上葉，膵尾部，脾臓の腫瘤が急速に出現し，ミカファンギンやボリコナゾールを投与するも，入院85日後に死亡した．剖検で，肺，脾臓に多発性の真菌塊と出血性梗塞が認められ，僧帽弁には真菌塊の疣贅を認め，組織学的に播種性接合菌症と診断した．Bor療法後の腫瘍崩壊によるアシドーシスや，コントロール不良の糖尿病，輸血による鉄過剰，抗真菌薬投与中のブレークスルー感染症などが発症の誘因と考えられた．"},"publication_date":"2010-08","publication_name":{"en":"The Japanese Journal of Clinical Hematology","ja":"臨床血液"},"volume":"Vol.51","number":"No.8","starting_page":"690","ending_page":"695","languages":["jpn"],"referee":true,"identifiers":{"doi":["10.11406/rinketsu.51.690"],"issn":["0485-1439"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:57, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167277"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19098416","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=250561","label":"url"}],"paper_title":{"en":"[A case of peritonitis carcinomatosa from goblet cell carcinoid of the appendix treated by intraperitoneal paclitaxel and systemic S-1 chemotherapy].","ja":"[A case of peritonitis carcinomatosa from goblet cell carcinoid of the appendix treated by intraperitoneal paclitaxel and systemic S-1 chemotherapy]."},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Kimura Shigeaki"},{"name":"Kashima Masahiro"},{"name":"Shichijo Kana"},{"name":"Yoshida Sumiko"},{"name":"Harada Eiji"},{"name":"Matsushita Takaya"},{"name":"Tamaki Yasutami"},{"name":"Horiuchi Noriaki"},{"name":"Takeichi Toshiaki"},{"name":"Fujimoto Hiroshi"},{"name":"Masuda Kazuhiko"},{"name":"Iwasaka Naohito"},{"name":"Shinomiya Sadao"}],"ja":[{"name":"中村 信元"},{"name":"Kimura Shigeaki"},{"name":"Kashima Masahiro"},{"name":"Shichijo Kana"},{"name":"吉田 守美子"},{"name":"Harada Eiji"},{"name":"松下 隆哉"},{"name":"Tamaki Yasutami"},{"name":"Horiuchi Noriaki"},{"name":"Takeichi Toshiaki"},{"name":"Fujimoto Hiroshi"},{"name":"Masuda Kazuhiko"},{"name":"Iwasaka Naohito"},{"name":"Shinomiya Sadao"}]},"description":{"en":"Goblet cell carcinoid of the appendix is a rare neoplasm and clinically tends to take a malignant course. Most cases are young and early stage, and the surgical strategy is available. But appropriate chemotherapy for inoperable cases with peritoneal dissemination is not established. A 77-year-old woman with a past history of appendectomy was admitted to our hospital complaining of abdominal fullness. Abdominal computed tomography showed massive ascites and slight contrast enhancement of appendix. A tumor was found by colonoscopic examination at the orifice of vermiform and was diagnosed pathologically as goblet cell carcinoid of the appendix. Laparoscopy showed multiple peritoneal dissemination. We performed intraperitoneal paclitaxel(PTX)administration at 70 mg/m(2) week without any resection of the tumor. Ascites were reduced immediately, but drug-induced interstitial pneumonia occurred due to PTX. After steroid therapy, we switched to systemic S-1 therapy. For about one year, her tumor was controlled but became worse thirteen months after diagnosis and died. It is thought that intraabdominal paclitaxel administration and systemic S-1 therapy can be one of appropriate forms of chemotherapy for inoperable peritoneal carcinomatosis from goblet cell carcinoid of appendix.","ja":"Goblet cell carcinoid of the appendix is a rare neoplasm and clinically tends to take a malignant course. Most cases are young and early stage, and the surgical strategy is available. But appropriate chemotherapy for inoperable cases with peritoneal dissemination is not established. A 77-year-old woman with a past history of appendectomy was admitted to our hospital complaining of abdominal fullness. Abdominal computed tomography showed massive ascites and slight contrast enhancement of appendix. A tumor was found by colonoscopic examination at the orifice of vermiform and was diagnosed pathologically as goblet cell carcinoid of the appendix. Laparoscopy showed multiple peritoneal dissemination. We performed intraperitoneal paclitaxel(PTX)administration at 70 mg/m(2) week without any resection of the tumor. Ascites were reduced immediately, but drug-induced interstitial pneumonia occurred due to PTX. After steroid therapy, we switched to systemic S-1 therapy. For about one year, her tumor was controlled but became worse thirteen months after diagnosis and died. It is thought that intraabdominal paclitaxel administration and systemic S-1 therapy can be one of appropriate forms of chemotherapy for inoperable peritoneal carcinomatosis from goblet cell carcinoid of appendix."},"publication_date":"2008-12","publication_name":{"en":"Japanese Journal of Cancer and Chemotherapy","ja":"癌と化学療法"},"volume":"Vol.35","number":"No.13","starting_page":"2425","ending_page":"2428","languages":["jpn"],"referee":true,"identifiers":{"issn":["0385-0684"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:58, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167278"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18633226","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-48249146275&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=250562","label":"url"}],"paper_title":{"en":"[A long-surviving patient with lung pleomorphic carcinoma treated with postoperative carboplatin and paclitaxel combination chemotherapy].","ja":"[A long-surviving patient with lung pleomorphic carcinoma treated with postoperative carboplatin and paclitaxel combination chemotherapy]."},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Horiuchi Noriaki"},{"name":"Katsura Daisuke"},{"name":"Shichijo Kana"},{"name":"Yoshida Sumiko"},{"name":"Harada Eiji"},{"name":"Matsushita Takaya"},{"name":"Matsuzaki Yasuyuki"},{"name":"Tamaki Yasutami"},{"name":"Kimura Shigeaki"},{"name":"Takeichi Toshiaki"},{"name":"Fujimoto Hiroshi"},{"name":"Masuda Kazuhiko"},{"name":"Iwasaka Naohito"},{"name":"Shinomiya Sadao"}],"ja":[{"name":"中村 信元"},{"name":"Horiuchi Noriaki"},{"name":"Katsura Daisuke"},{"name":"Shichijo Kana"},{"name":"吉田 守美子"},{"name":"Harada Eiji"},{"name":"松下 隆哉"},{"name":"Matsuzaki Yasuyuki"},{"name":"Tamaki Yasutami"},{"name":"Kimura Shigeaki"},{"name":"Takeichi Toshiaki"},{"name":"Fujimoto Hiroshi"},{"name":"Masuda Kazuhiko"},{"name":"Iwasaka Naohito"},{"name":"Shinomiya Sadao"}]},"description":{"en":"We presented the case of a 46-year-old man with no medical or family history but with a history of smoking 3 packs of cigarettes per day for the past 25 years. He was admitted to our hospital due to hemoptysis. Chest computed tomography revealed a tumor of right upper lung and interstitial pneumonia in the surrounding lung parenchyma. He was operated upon and diagnosed with stage IIB pleomorphic carcinoma of the lung with invasion of the chest wall. He underwent three courses of postoperative carboplatin (CBDCA) (area under the curve 5 on day 1, every 3 weeks and paclitaxel(PTX) (200 mg/m(2); day 1, every 3 weeks) combination chemotherapy. No recurrence was observed for a period of 760 days after the operation. According to previous reports, lung pleomorphic carcinoma is aggressive and has a poor prognosis. Further, the significance of chemotherapy in the management of this disease has not been established. Postoperative combination chemotherapy of CBDCA and PTX may result in a good prognosis for this disease.","ja":"We presented the case of a 46-year-old man with no medical or family history but with a history of smoking 3 packs of cigarettes per day for the past 25 years. He was admitted to our hospital due to hemoptysis. Chest computed tomography revealed a tumor of right upper lung and interstitial pneumonia in the surrounding lung parenchyma. He was operated upon and diagnosed with stage IIB pleomorphic carcinoma of the lung with invasion of the chest wall. He underwent three courses of postoperative carboplatin (CBDCA) (area under the curve 5 on day 1, every 3 weeks and paclitaxel(PTX) (200 mg/m(2); day 1, every 3 weeks) combination chemotherapy. No recurrence was observed for a period of 760 days after the operation. According to previous reports, lung pleomorphic carcinoma is aggressive and has a poor prognosis. Further, the significance of chemotherapy in the management of this disease has not been established. Postoperative combination chemotherapy of CBDCA and PTX may result in a good prognosis for this disease."},"publication_date":"2008-06","publication_name":{"en":"Japanese Journal of Cancer and Chemotherapy","ja":"癌と化学療法"},"volume":"Vol.35","number":"No.6","starting_page":"965","ending_page":"968","languages":["jpn"],"referee":true,"identifiers":{"issn":["0385-0684"]},"published_paper_type":"scientific_journal"},"priority":"input_data"} line:59, {"insert":{"user_id":"B000341201","type":"published_papers","id":"15167279"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=269878","label":"url"}],"paper_title":{"en":"Part7. 2. 新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に). がん骨転移治療 ビスフォスフォネート治療によるBone Management","ja":"Part7. 2. 新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に). がん骨転移治療 ビスフォスフォネート治療によるBone Management"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Abe Masahiro"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"中村 信元"},{"name":"安倍 正博"},{"name":"松本 俊夫"}]},"publication_date":"2012","publication_name":{"en":"先端医学者 高橋俊二 編集","ja":"先端医学者 高橋俊二 編集"},"starting_page":"206","ending_page":"214","languages":["jpn"],"published_paper_type":"research_institution"},"priority":"input_data"} ==== end registerFile(/WWW/pub2/data/ERD/person/229265/researchmap/published_papers.jsonl, 2LoJ844B7kacV6CWoi8l) ==== ==== begin registerFile(/WWW/pub2/data/ERD/person/229265/researchmap/misc.jsonl) ==== line:1, {"insert":{"user_id":"B000341201","type":"misc","id":"43514557"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=402668","label":"url"}],"paper_title":{"en":"【最新の骨粗鬆症学(第2版)-骨粗鬆症学の最新知見-】続発性骨粗鬆症の診断と治療 抗悪性腫瘍薬に伴う骨粗鬆症(解説)","ja":"【最新の骨粗鬆症学(第2版)-骨粗鬆症学の最新知見-】続発性骨粗鬆症の診断と治療 抗悪性腫瘍薬に伴う骨粗鬆症(解説)"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"安倍 正博"}]},"publication_date":"2023","publication_name":{"en":"日本臨床(0047-1852)81巻増刊1 最新の骨粗鬆症学 Page580-584(2023.01)","ja":"日本臨床(0047-1852)81巻増刊1 最新の骨粗鬆症学 Page580-584(2023.01)"},"languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:2, {"insert":{"user_id":"B000341201","type":"misc","id":"41593237"},"force":{"see_also":[{"@id":"https://search.jamas.or.jp/link/ui/2023027045","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390293412208923264/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394190","label":"url"}],"paper_title":{"en":"【骨髄腫と類縁疾患-全身をみわたす診断・治療】Overview 多発性骨髄腫の発症・進展機序","ja":"【骨髄腫と類縁疾患-全身をみわたす診断・治療】Overview 多発性骨髄腫の発症・進展機序"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"安倍 正博"}]},"description":{"en":"<文献概要>▼多発性骨髄腫(MM)はゲノム不安定性や遺伝子プロモーターのメチル化などのepigeneticな制御の異常に加え多段階の分子遺伝学的異常により,意義不明の単クローン性ガンマグロブリン血症(MGUS)を経て発症・進展する.▼MMの発症原因は不明であるが,疫学調査により性差,地域差,人種差,遺伝学的要因,被曝歴,年齢との関連が示唆されている.▼全ゲノム解析やマウスモデル,腸内細菌叢の解析などからMMのさまざまな発症機序が推測されている.","ja":"<文献概要>▼多発性骨髄腫(MM)はゲノム不安定性や遺伝子プロモーターのメチル化などのepigeneticな制御の異常に加え多段階の分子遺伝学的異常により,意義不明の単クローン性ガンマグロブリン血症(MGUS)を経て発症・進展する.▼MMの発症原因は不明であるが,疫学調査により性差,地域差,人種差,遺伝学的要因,被曝歴,年齢との関連が示唆されている.▼全ゲノム解析やマウスモデル,腸内細菌叢の解析などからMMのさまざまな発症機序が推測されている."},"publication_date":"2022-10-01","publication_name":{"en":"Internal Medicine","ja":"臨床雑誌 内科"},"volume":"Vol.130","number":"No.4","starting_page":"691","ending_page":"694","languages":["jpn"],"identifiers":{"doi":["10.15106/j_naika130_691"],"issn":["0022-1961"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:3, {"insert":{"user_id":"B000341201","type":"misc","id":"41593236"},"force":{"see_also":[{"@id":"https://search.jamas.or.jp/link/ui/WB16080025","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394191","label":"url"}],"paper_title":{"en":"【腎臓症候群(第3版)-その他の腎臓疾患を含めて-】各種病態にみられる腎障害 造血器疾患 多発性骨髄腫","ja":"【腎臓症候群(第3版)-その他の腎臓疾患を含めて-】各種病態にみられる腎障害 造血器疾患 多発性骨髄腫"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"安倍 正博"}]},"publication_date":"2022-10","publication_name":{"en":"Nihon Rinsho. Japanese Journal of Clinical Medicine","ja":"日本臨牀"},"starting_page":"124","ending_page":"130","languages":["jpn"],"identifiers":{"issn":["0047-1852"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:4, {"insert":{"user_id":"B000341201","type":"misc","id":"33352909"},"force":{"see_also":[{"@id":"http://search.jamas.or.jp/link/ui/2021054713","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=379414","label":"url"}],"paper_title":{"en":"【骨粗鬆症 最新の知見に基づいた治療薬の考え方・使い方】薬剤性骨粗鬆症に対するマネジメントの勘所 がん治療に伴う骨粗鬆症","ja":"【骨粗鬆症 最新の知見に基づいた治療薬の考え方・使い方】薬剤性骨粗鬆症に対するマネジメントの勘所 がん治療に伴う骨粗鬆症"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"安倍 正博"}]},"description":{"en":"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.
","ja":"ALアミロイドーシスは，多発性骨髄腫やMGUS(monoclonal gammopathy of undetermined significance)などのモノクローナルな形質細胞が産生する免疫グロブリン軽鎖および重鎖が，アミロイド線維として組織に沈着し，臓器障害を惹起する難治性疾患である．なかでも心アミロイドーシス(以下CA)は，心不全症状が出現してからは，無治療の場合極めて予後不良であるため，その管理・治療が重要である1)．ALアミロイドーシスに対しては，自家末梢血幹細胞移植併用メルファラン大量療法(以下ASCT)の有効性が報告されているが，CAにおいては治療関連毒性が強く，その適応を慎重に検討する必要がある2, 3)．近年，多発性骨髄腫において，ボルテゾミブ(Bor)や，免疫調節薬であるサリドマイド(Thal)やレナリドミド(Len)などの新規薬を用いた治療により，治療成績が向上している．ALアミロイドーシス症例においてもこれらの新規薬の有効性が示され，CAに対しても，重篤な有害事象の発生率が低く，有効であったとの報告がある4∼6)．しかしながら，その長期の治療成績や予後については，十分な情報がない．そこで我々は，当科において治療し，長期生存が得られた心不全合併CA例について，後方視的に検討した．
"}},"priority":"input_data"} line:2, {"insert":{"user_id":"B000341201","type":"books_etc","id":"32804638"},"force":{"see_also":[{"@id":"https://ci.nii.ac.jp/naid/130005096286/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001205035009152/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=318297","label":"url"}],"book_title":{"en":"Management of bone disease in myeloma patients: zoledronic acid or denosumab?","ja":"「骨髄腫∼いつ治療するのか?∼初発，再発，そして早期介入」骨髄腫骨病変の管理:ゾレドロン酸かデノスマブか"},"authors":{"en":[{"name":"Abe Masahiro"},{"name":"Miki Hirokazu"},{"name":"Nakamura Shingen"}],"ja":[{"name":"安倍 正博"},{"name":"三木 浩和"},{"name":"中村 信元"}]},"publisher":{"en":"The Japanese Society of Hematology","ja":"臨床血液"},"publication_date":"2015","languages":["jpn"],"description":{"en":"With improvement of survival owing to the recent implementation of new anti-myeloma (MM) agents, bone management will become more important for maintaining the quality of life (QoL) of patients. Bisphosphonates are currently the standard of care for MM-related bone disease. Zoledronic acid is recommended for newly diagnosed MM patients receiving front-line anti-MM treatment regardless of existing detectable bone lesions. Intriguingly, an overall survival benefit has been observed with zoledronic acid in patients on anti-MM treatment with documented bone disease at baseline. Denosumab, a human monoclonal antibody against RANKL, has been demonstrated to reduce bone-related events in patients with MM as effectively as zoledronic acid. Hypocalcemia is generally accepted as occurring more frequently and more severely with denosumab than with zoledronic acid, especially in patients with renal insufficiency. Bisphosphonates but not denosumab deposit in bone with a long half-life, which may make a difference in long-term efficacy as well as adverse effects. Clinical benefits of long-term anti-resorptive therapies after achieving a good response should be clarified, in order to avoid the emergence of severe complications. Impacts of new agents in combination with these anti-resorptive agents on bone metabolism have yet to be studied.","ja":"新規薬が臨床応用され骨髄腫の治療成績が向上しているが，骨破壊病変は依然として生活の質(QoL)の低下の最も多い原因である．初回化学療法を受ける症候性骨髄腫患者すべてに骨病変の有無にかかわらずゾレドロン酸の点滴静注を反復することが骨病変の進行防止と予後の改善の点から推奨されている．デノスマブはゾレドロン酸と同等の治療効果を発揮する．デノスマブは即効性で皮下投与という利便性があり，腎機能にも影響を与えにくいが，低カルシウム血症を来しやすく，ゾレドロン酸と同程度に顎骨壊死の発生がみられる．ゾレドロン酸は骨に長期間蓄積するが，デノスマブは骨への蓄積性がない．したがって，長期投与後の骨質への影響などに両者の違いがある可能性がある．また，治療奏効後の強力な骨吸収抑制薬継続投与の有用性および新規薬との併用下での骨病変治療薬の至適な投与開始時期，投与方法や投与期間，予後に及ぼす影響が今後の検討課題である．"}},"priority":"input_data"} line:3, {"insert":{"user_id":"B000341201","type":"books_etc","id":"12940224"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=300218","label":"url"}],"book_title":{"en":"臓器移植．ALアミロイドーシス，多発性骨髄腫の類縁疾患","ja":"臓器移植．ALアミロイドーシス，多発性骨髄腫の類縁疾患"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"安倍 正博"}]},"publisher":{"en":"Iyaku Journal Co., Ltd.","ja":"医薬ジャーナル社"},"publication_date":"2014-08-12","languages":["jpn"]},"priority":"input_data"} line:4, {"insert":{"user_id":"B000341201","type":"books_etc","id":"12940225"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=300217","label":"url"}],"book_title":{"en":"アミロイドーシス効果判定基準 効果判定基準 2005コンセンサスクライテリア，2011新基準．ALアミロイドーシス，多発性骨髄腫の類縁疾患","ja":"アミロイドーシス効果判定基準 効果判定基準 2005コンセンサスクライテリア，2011新基準．ALアミロイドーシス，多発性骨髄腫の類縁疾患"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Abe Masahiro"}],"ja":[{"name":"中村 信元"},{"name":"安倍 正博"}]},"publisher":{"en":"Iyaku Journal Co., Ltd.","ja":"医薬ジャーナル社"},"publication_date":"2014-08-12","languages":["jpn"]},"priority":"input_data"} line:5, {"insert":{"user_id":"B000341201","type":"books_etc","id":"12940226"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=303540","label":"url"}],"book_title":{"en":"(chapter6)","ja":"(chapter6)"},"authors":{"en":[{"name":"Nakamura Shingen"}],"ja":[{"name":"中村 信元"}]},"publication_date":"2014-01","languages":["jpn"]},"priority":"input_data"} line:6, {"insert":{"user_id":"B000341201","type":"books_etc","id":"12940227"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=268244","label":"url"}],"book_title":{"en":"新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に)","ja":"新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に)"},"authors":{"en":[{"name":"Nakamura Shingen"},{"name":"Abe Masahiro"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"中村 信元"},{"name":"安倍 正博"},{"name":"松本 俊夫"}]},"publication_date":"2012-03-30","languages":["jpn"]},"priority":"input_data"} ==== end registerFile(/WWW/pub2/data/ERD/person/229265/researchmap/books_etc.jsonl, 4boJ844B7kacV6CWpS-j) ==== ==== begin registerFile(/WWW/pub2/data/ERD/person/229265/researchmap/awards.jsonl) ==== line:1, 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栄二"},{"name":"松本 俊夫"}]},"award_title":{"en":"The novel anti-resorptive agent reveromycin A ameliorates bone destruction and tumor growth in myeloma","ja":"The novel anti-resorptive agent reveromycin A ameliorates bone destruction and tumor growth in myeloma"},"association":{"en":"10th International Conference Cancer-Induced Bone Disease","ja":"10th International Conference Cancer-Induced Bone Disease"},"award_date":"2010-09-22"},"priority":"input_data"} line:2, {"insert":{"user_id":"B000341201","type":"awards","id":"32804645"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=238356","label":"url"}],"award_name":{"en":"52nd ASH Travel Award","ja":"52nd ASH Travel Award"},"winners":{"en":[{"name":"Watanabe Keiichiro"},{"name":"Abe Masahiro"},{"name":"Cui Qu"},{"name":"Kawatani Makoto"},{"name":"Hiasa Masahiro"},{"name":"Nakano Ayako"},{"name":"Jinno Tadashi"},{"name":"Fujii Shiroh"},{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Kagawa Kumiko"},{"name":"Takeuchi Kyoko"},{"name":"Ozaki Shuji"},{"name":"Tanaka Eiji"},{"name":"Osada Hiroyuki"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"渡邉 佳一郎"},{"name":"安倍 正博"},{"name":"Cui Qu"},{"name":"Kawatani Makoto"},{"name":"日浅 雅博"},{"name":"Nakano Ayako"},{"name":"Jinno Tadashi"},{"name":"藤井 志朗"},{"name":"中村 信元"},{"name":"Miki Hirokazu"},{"name":"賀川 久美子"},{"name":"竹内 恭子"},{"name":"尾崎 修治"},{"name":"田中 栄二"},{"name":"Osada Hiroyuki"},{"name":"松本 俊夫"}]},"award_title":{"en":"An acidic milieu created in myeloma-osteoclast interaction enhances tumor growth, but triggers anti-myeloma activity of Reveromycin A, a novel anti-resorptive agent","ja":"An acidic milieu created in myeloma-osteoclast interaction enhances tumor growth, but triggers anti-myeloma activity of Reveromycin A, a novel anti-resorptive agent"},"association":{"en":"52nd ASH","ja":"52nd ASH"},"award_date":"2010-12-06"},"priority":"input_data"} line:3, 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