start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue=2 article-no= start-page=335 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200202 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Sensitive Photodynamic Detection of Adult T-cell Leukemia/Lymphoma and Specific Leukemic Cell Death Induced by Photodynamic Therapy: Current Status in Hematopoietic Malignancies en-subtitle= kn-subtitle= en-abstract= kn-abstract=Adult T-cell leukemia/lymphoma (ATL), an aggressive type of T-cell malignancy, is caused by the human T-cell leukemia virus type I (HTLV-1) infections. The outcomes, following therapeutic interventions for ATL, have not been satisfactory. Photodynamic therapy (PDT) exerts selective cytotoxic activity against malignant cells, as it is considered a minimally invasive therapeutic procedure. In PDT, photosensitizing agent administration is followed by irradiation at an absorbance wavelength of the sensitizer in the presence of oxygen, with ultimate direct tumor cell death, microvasculature injury, and induced local inflammatory reaction. This review provides an overview of the present status and state-of-the-art ATL treatments. It also focuses on the photodynamic detection (PDD) of hematopoietic malignancies and the recent progress of 5-Aminolevulinic acid (ALA)-PDT/PDD, which can efficiently induce ATL leukemic cell-specific death with minor influence on normal lymphocytes. Further consideration of the ALA-PDT/PDD system along with the circulatory system regarding the clinical application in ATL and others will be discussed. ALA-PDT/PDD can be promising as a novel treatment modality that overcomes unmet medical needs with the optimization of PDT parameters to increase the effectiveness of the tumor-killing activity and enhance the innate and adaptive anti-tumor immune responses by the optimized immunogenic cell death. en-copyright= kn-copyright= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuokaKen-Ichi en-aut-sei=Matsuoka en-aut-mei=Ken-Ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UtsunomiyaAtae en-aut-sei=Utsunomiya en-aut-mei=Atae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil=Department of Hematology, Oncology & Respiratory Med., Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Hematology, Oncology & Respiratory Med., Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Hematology, Imamura General Hospital kn-affil= en-keyword=ATL kn-keyword=ATL en-keyword=HTLV-1 kn-keyword=HTLV-1 en-keyword=PDT kn-keyword=PDT en-keyword=PDD kn-keyword=PDD en-keyword=chemotherapy kn-keyword=chemotherapy en-keyword=allogeneic hematopoietic cell transplantation kn-keyword=allogeneic hematopoietic cell transplantation en-keyword=immunotherapy kn-keyword=immunotherapy en-keyword=GVHD kn-keyword=GVHD en-keyword=ALA-PDT/PDD kn-keyword=ALA-PDT/PDD END start-ver=1.4 cd-journal=joma no-vol=125 cd-vols= no-issue=2 article-no= start-page=103 end-page=107 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Duodenal follicular lymphoma lacks AID but expresses BACH2 and has memory B cell characteristics kn-title=十二指腸濾胞性リンパ腫はAIDの発現を欠くがBACH2の発現を有しmemoryB細胞としての性質を有する en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name=高田尚良 kn-aut-sei=高田 kn-aut-mei=尚良 aut-affil-num=1 ORCID= en-aut-name=SatoYasuharu en-aut-sei=Sato en-aut-mei=Yasuharu kn-aut-name=佐藤康晴 kn-aut-sei=佐藤 kn-aut-mei=康晴 aut-affil-num=2 ORCID= en-aut-name=NakamuraNaoya en-aut-sei=Nakamura en-aut-mei=Naoya kn-aut-name=中村直哉 kn-aut-sei=中村 kn-aut-mei=直哉 aut-affil-num=3 ORCID= en-aut-name=TokunakaMami en-aut-sei=Tokunaka en-aut-mei=Mami kn-aut-name=徳中摩美 kn-aut-sei=徳中 kn-aut-mei=摩美 aut-affil-num=4 ORCID= en-aut-name=MikiYukari en-aut-sei=Miki en-aut-mei=Yukari kn-aut-name=三木由香里 kn-aut-sei=三木 kn-aut-mei=由香里 aut-affil-num=5 ORCID= en-aut-name=KikutiYara Yukie en-aut-sei=Kikuti en-aut-mei=Yara Yukie kn-aut-name=菊池イアーラ幸江 kn-aut-sei=菊池 kn-aut-mei=イアーラ幸江 aut-affil-num=6 ORCID= en-aut-name=IgarashiKazuhiko en-aut-sei=Igarashi en-aut-mei=Kazuhiko kn-aut-name=五十嵐和彦 kn-aut-sei=五十嵐 kn-aut-mei=和彦 aut-affil-num=7 ORCID= en-aut-name=ItoEtsuro en-aut-sei=Ito en-aut-mei=Etsuro kn-aut-name=伊藤悦郎 kn-aut-sei=伊藤 kn-aut-mei=悦郎 aut-affil-num=8 ORCID= en-aut-name=HarigaeHideo en-aut-sei=Harigae en-aut-mei=Hideo kn-aut-name=張替秀雄 kn-aut-sei=張替 kn-aut-mei=秀雄 aut-affil-num=9 ORCID= en-aut-name=KatoSeiichi en-aut-sei=Kato en-aut-mei=Seiichi kn-aut-name=加藤省一 kn-aut-sei=加藤 kn-aut-mei=省一 aut-affil-num=10 ORCID= en-aut-name=HayashiEiko en-aut-sei=Hayashi en-aut-mei=Eiko kn-aut-name=林詠子 kn-aut-sei=林 kn-aut-mei=詠子 aut-affil-num=11 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name=岡剛史 kn-aut-sei=岡 kn-aut-mei=剛史 aut-affil-num=12 ORCID= en-aut-name=HoshiiYoshinobu en-aut-sei=Hoshii en-aut-mei=Yoshinobu kn-aut-name=星井嘉信 kn-aut-sei=星井 kn-aut-mei=嘉信 aut-affil-num=13 ORCID= en-aut-name=TariAkira en-aut-sei=Tari en-aut-mei=Akira kn-aut-name=田利晶 kn-aut-sei=田利 kn-aut-mei=晶 aut-affil-num=14 ORCID= en-aut-name=OkadaHiroyuki en-aut-sei=Okada en-aut-mei=Hiroyuki kn-aut-name=岡田裕之 kn-aut-sei=岡田 kn-aut-mei=裕之 aut-affil-num=15 ORCID= en-aut-name=MohamadoABD Alkader Lamia en-aut-sei=Mohamado en-aut-mei=ABD Alkader Lamia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=17 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=18 ORCID= en-aut-name=KinoshitaTomohiro en-aut-sei=Kinoshita en-aut-mei=Tomohiro kn-aut-name=木下朝博 kn-aut-sei=木下 kn-aut-mei=朝博 aut-affil-num=19 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name=吉野正 kn-aut-sei=吉野 kn-aut-mei=正 aut-affil-num=20 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科病理学（腫瘍病理） affil-num=3 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=4 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=5 en-affil= kn-affil=香川保健医療短期大学 affil-num=6 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=7 en-affil= kn-affil=東北大学大学院医学系研究科 生物化学分野 affil-num=8 en-affil= kn-affil=弘前大学医学部　小児科学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・免疫病学分野 affil-num=10 en-affil= kn-affil=名古屋大学病院　病理部 affil-num=11 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=12 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=13 en-affil= kn-affil=山口大学医学部　病理学 affil-num=14 en-affil= kn-affil=広島赤十字・原爆病院　消化器内科 affil-num=15 en-affil= kn-affil=岡山大学病院　光学診療部 affil-num=16 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=17 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科血液・腫瘍・呼吸器内科学 affil-num=18 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科血液・腫瘍・呼吸器内科学 affil-num=19 en-affil= kn-affil=愛知がんセンター　血液細胞療法部 affil-num=20 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） en-keyword=follicular lymphoma kn-keyword=follicular lymphoma en-keyword=gastrointestinal tract kn-keyword=gastrointestinal tract en-keyword=BACH2 kn-keyword=BACH2 en-keyword=memory B cell kn-keyword=memory B cell END start-ver=1.4 cd-journal=joma no-vol=463 cd-vols= no-issue=5 article-no= start-page=697 end-page=711 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201311 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=In aggressive variants of non-Hodgkin lymphomas, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Polycomb group (PcG) proteins are important for the regulation of hematopoiesis by regulating chromatin compaction and silencing genes related to differentiation and cell cycle. Overexpression of enhancer of zeste homologue 2 (Ezh2) and Bmi-1/PCGF4 has been implicated in solid organ cancers, while Mel-18/PCGF2 has been reported as a tumor suppressor. Detailed expression profiles of PcG proteins and their diagnostic significance in malignant lymphomas are still unknown. In this study, we analyzed the expression levels of Ezh2, Bmi-1, Mel-18, and Ki67 in 197 Hodgkin's and non-Hodgkin's lymphoma patient samples and in lymphoma cell lines using immunohistochemistry, fluorescent immunocytochemistry, and Western blotting. Immunohistochemical staining showed that Ezh2 expression was significantly increased in aggressive compared to indolent subtypes of B cell neoplasms (P = 0.000-0.030), while no significant differences in Bmi-1 expression were found between these subtypes. Compared to the normal counterpart, T cell lymphomas showed significant overexpression of Bmi-1 (P = 0.011) and Ezh2 (P = 0.000). The Ki67 labeling index showed a positive correlation with Ezh2 expression in B cell lymphomas (correlation coefficient (Co) = 0.983, P = 0.000) and T/NK cell lymphomas (Co = 0.629, P = 0.000). Fluorescent immunohistochemical staining showed coexpression of Ezh2 and Ki67 in the same tumor cells, indicating that Ezh2 expression correlates with cell proliferation. Both B and T/NK cell neoplasms showed low expression of Mel-18 and high expression of both Bmi-1 and Ezh2. In conclusion, in aggressive lymphoma variants, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2. Coexpression of Bmi-1 and Ezh2 is a characteristic of aggressive lymphomas. Ezh2 correlates with the proliferation and aggressive nature of non-Hodgkin's lymphomas. en-copyright= kn-copyright= en-aut-name=Abd Al KaderLamia en-aut-sei=Abd Al Kader en-aut-mei=Lamia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SunXu en-aut-sei=Sun en-aut-mei=Xu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SatoHiaki en-aut-sei=Sato en-aut-mei=Hiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MurakamiIchiro en-aut-sei=Murakami en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TojiTomohiro en-aut-sei=Toji en-aut-mei=Tomohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=ManabeAkihiro en-aut-sei=Manabe en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KimuraHiroshi en-aut-sei=Kimura en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Dalian Med Univ, Dept Pathol, Affiliated Hosp 1 affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Med Technol, Grad Sch Hlth Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Osaka Univ, Grad Sch Frontier Sci affil-num=10 en-affil=D kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci en-keyword=Ezh2 kn-keyword=Ezh2 en-keyword=Bmi-1 kn-keyword=Bmi-1 en-keyword=Mel-18 kn-keyword=Mel-18 en-keyword=Malignant lymphoma kn-keyword=Malignant lymphoma en-keyword=PRC1.2 kn-keyword=PRC1.2 en-keyword=PRC1.4 kn-keyword=PRC1.4 END start-ver=1.4 cd-journal=joma no-vol=10 cd-vols= no-issue=1 article-no= start-page=17237 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201014 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=5-aminolevulinic acid-mediated photodynamic therapy can target aggressive adult T cell leukemia/lymphoma resistant to conventional chemotherapy en-subtitle= kn-subtitle= en-abstract= kn-abstract=Photodynamic therapy (PDT) is an emerging treatment for various solid cancers. We recently reported that tumor cell lines and patient specimens from adult T cell leukemia/lymphoma (ATL) are susceptible to specific cell death by visible light exposure after a short-term culture with 5-aminolevulinic acid, indicating that extracorporeal photopheresis could eradicate hematological tumor cells circulating in peripheral blood. As a bridge from basic research to clinical trial of PDT for hematological malignancies, we here examined the efficacy of ALA-PDT on various lymphoid malignancies with circulating tumor cells in peripheral blood. We also examined the effects of ALA-PDT on tumor cells before and after conventional chemotherapy. With 16 primary blood samples from 13 patients, we demonstrated that PDT efficiently killed tumor cells without influencing normal lymphocytes in aggressive diseases such as acute ATL. Importantly, PDT could eradicate acute ATL cells remaining after standard chemotherapy or anti-CCR4 antibody, suggesting that PDT could work together with other conventional therapies in a complementary manner. The responses of PDT on indolent tumor cells were various but were clearly depending on accumulation of protoporphyrin IX, which indicates the possibility of biomarker-guided application of PDT. These findings provide important information for developing novel therapeutic strategy for hematological malignancies. en-copyright= kn-copyright= en-aut-name=SandoYasuhisa en-aut-sei=Sando en-aut-mei=Yasuhisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuokaKen-Ichi en-aut-sei=Matsuoka en-aut-mei=Ken-Ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SumiiYuichi en-aut-sei=Sumii en-aut-mei=Yuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KondoTakumi en-aut-sei=Kondo en-aut-mei=Takumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IkegawaShuntaro en-aut-sei=Ikegawa en-aut-mei=Shuntaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SugiuraHiroyuki en-aut-sei=Sugiura en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NakamuraMakoto en-aut-sei=Nakamura en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IwamotoMiki en-aut-sei=Iwamoto en-aut-mei=Miki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MeguriYusuke en-aut-sei=Meguri en-aut-mei=Yusuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=AsadaNoboru en-aut-sei=Asada en-aut-mei=Noboru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=EnnishiDaisuke en-aut-sei=Ennishi en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=FujiiKeiko en-aut-sei=Fujii en-aut-mei=Keiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=UtsunomiyaAtae en-aut-sei=Utsunomiya en-aut-mei=Atae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= affil-num=1 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=12 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=13 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=14 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=15 en-affil=Department of Hematology, Imamura General Hospital kn-affil= affil-num=16 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=17 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=T-cell lymphoma kn-keyword=T-cell lymphoma en-keyword=Targeted therapies kn-keyword=Targeted therapies END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=207 end-page=212 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Analysis of the genome of an Epstein-Barr-virus (EBV)-related herpesvirus in a cynomolgus monkey cell line (Si-IIA) en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A simian cell line, Si-IIA, harboring Epstein-Barr-virus (EBV) -related herpesvirus (Si-IIA-EBV), produces malignant lymphoma in rabbits when administered by intravenous inoculation. In this study, we analyzed the Si-IIA-EBV genome and compared it with human EBV and herpesvirus macaca fascicularis 1 (HVMF 1 ), which is associated with B-cell lymphoma developing in SIV-infected immunosuppressed monkeys. DNA from Si-IIA-EBV was amplified by the polymerase chain reaction using three different primer pairs complementary to human EBV (B95-8) DNA; two of the primer pairs covered part of the long internal repeat 1 region (IR 1) and the third covered part of the BRRF 1 region. Direct sequencing of the three PCR products revealed that Si-IIA-EBV DNA had about 82% nucleotide homology to the human EBV DNA in all three regions and 92.4% homology to HVMF1 in the IR1 region. The blotting pattern by Southern blot analysis was different between Si-IIA-EBV and human EBV.

en-copyright= kn-copyright= en-aut-name=InoHideo en-aut-sei=Ino en-aut-mei=Hideo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YanaiHiroyuki en-aut-sei=Yanai en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TeramotoNorihiro en-aut-sei=Teramoto en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KoiralaTirtha Raj en-aut-sei=Koirala en-aut-mei=Tirtha Raj kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChenHong-Li en-aut-sei=Chen en-aut-mei=Hong-Li kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TakahashiKiyoshi en-aut-sei=Takahashi en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=AkagiTadaastu en-aut-sei=Akagi en-aut-mei=Tadaastu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University en-keyword=Epstein-Barr virus kn-keyword=Epstein-Barr virus en-keyword=HVMF 1 kn-keyword=HVMF 1 en-keyword=lymphoma kn-keyword=lymphoma en-keyword=?monkey cell line kn-keyword=?monkey cell line en-keyword=PCR kn-keyword=PCR END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=3 article-no= start-page=143 end-page=151 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198906 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Immortalization of rat spleen and thymus T cells by human T-cell leukemia virus type I. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Co-cultivation of thymus and spleen cells of Fisher and Lewis rats with lethally irradiated MT-2 cells harboring human T-cell leukemia virus type I (HTLV-I) resulted in the establishment of lymphoid cell lines, FIRT-1, FIRS-1, LERT-1, and LERS-1, respectively. Cells of these cell lines had rat T-cell characters as demonstrated by the positive reaction to monoclonal antibodies (MAbs) to rat T cell antigens (Thy 1 and pan T). They lacked surface immunoglobulins and strongly expressed rat interleukin-2 receptor antigen (Tac) and Ia antigen. Karyotypic analysis revealed that they had the normal rat karyotype in early cultures, but showed marked aneuploidy after long cultivation. None of them expressed HTLV gag proteins (p19 and p24) or virus particles, but they contained HTLV-I proviral DNA monoclonally and weakly expressed pX gene products (p40x). They were not transplantable into syngeneic newborn rats.

en-copyright= kn-copyright= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakataHiroshi en-aut-sei=Takata en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TeramotoNorihiro en-aut-sei=Teramoto en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YanoShoki en-aut-sei=Yano en-aut-mei=Shoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Kochi Medical School affil-num=6 en-affil= kn-affil=Kochi Medical School en-keyword=human T-cell leukemia virus kn-keyword=human T-cell leukemia virus en-keyword=rat T cell kn-keyword=rat T cell en-keyword=immortalization kn-keyword=immortalization END start-ver=1.4 cd-journal=joma no-vol=55 cd-vols= no-issue=6 article-no= start-page=319 end-page=328 dt-received= dt-revised= dt-accepted= dt-pub-year=2001 dt-pub=200112 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Recent advances in DNA microarrays. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The structure of the human genome is almost completely elucidated and the life sciences will now aim for a general and integrated study of gene expressions and the functional elucidation of proteins. In such a study, various new techniques have been developed, and DNA microarray technology is the most representative one. As for the DNA microarray techniques, several thousands to tens of thousands of gene segments are immobilized on a glass slide at high density, and cDNA probes prepared from specific cells or tissues are hybridized on the slides from which gene expression profiles are obtained at one sweep in a short time. The present development of this technique and its possible application to medicine-related fields are described.</P>

en-copyright= kn-copyright= en-aut-name=NakanishiTohru en-aut-sei=Nakanishi en-aut-mei=Tohru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=DNA microarray kn-keyword=DNA microarray en-keyword=DNA chip kn-keyword=DNA chip en-keyword=human genome kn-keyword=human genome en-keyword=embryonic stem(ES)cell kn-keyword=embryonic stem(ES)cell en-keyword= single nucleotide polymorphism(SNP) kn-keyword= single nucleotide polymorphism(SNP) END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=2 article-no= start-page=67 end-page=74 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Induction and prevention of virus-associated malignant lymphoma by serial transmission of EBV-related virus from cynomolgus by blood transfusion in rabbits. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Epstein-Barr virus (EBV)-related herpesvirus (Si-IIA-EBV) was serially transmitted for 3 passages from rabbit to rabbit of the opposite sex by blood transfusion, which subsequently induced virus-associated rabbit lymphomas. The virus could be transmitted by transfusion with 15-20 ml of whole blood (7/7) or irradiated blood (1/6) from the EBV-related virus-infected rabbits, but there was no transmission with transfusion of cell-free plasma (0/6) from the infected rabbits. Passive anti-EBV-VCA IgG (x 20 approximately x 10) titers decreased during the first 1-2 weeks in the transfused rabbits. The virus-transmitted rabbits showed a gradual increase in antibody titers ranging from peak titers of x 640 to x 2560 after 3 weeks of transfusion. The recipient origin of malignant lymphoma that developed in the first rabbit transfused by infected blood was confirmed by chromosomal analysis. This rabbit model thus shows that EBV-related herpesvirus is serially transmissible by blood transfusion and that transmission can not be completely prevented by irradiation of blood, but removal of blood cells is the best way to prevent transmission of EBV-related virus. Therefore, this animal model provides a convenient in vivo system for studies of the prevention and therapy of transfusion-related transmission of EBV and EBV-associated lymphoproliferative diseases in immunocompromised human beings.

en-copyright= kn-copyright= en-aut-name=KoiralaTirtha Raj en-aut-sei=Koirala en-aut-mei=Tirtha Raj kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=JinZaishun en-aut-sei=Jin en-aut-mei=Zaishun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OnodaSachiyo en-aut-sei=Onoda en-aut-mei=Sachiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OdaWakako en-aut-sei=Oda en-aut-mei=Wakako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IchimuraKoichi en-aut-sei=Ichimura en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OharaNobuya en-aut-sei=Ohara en-aut-mei=Nobuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Tottori University, Tottori affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University affil-num=11 en-affil=Okayama University kn-affil= en-keyword=?Epstein-Barr virus(EBV) kn-keyword=?Epstein-Barr virus(EBV) en-keyword=rabbit kn-keyword=rabbit en-keyword=lymphoproliferative diseases kn-keyword=lymphoproliferative diseases en-keyword=blood transfusion kn-keyword=blood transfusion END start-ver=1.4 cd-journal=joma no-vol=54 cd-vols= no-issue=5 article-no= start-page=193 end-page=200 dt-received= dt-revised= dt-accepted= dt-pub-year=2000 dt-pub=200010 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Characterization of epstein-barr virus-infected mantle cell lymphoma lines. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

It has been reported that Epstein-Barr virus (EBV) resides in resting B cells in vivo. However, an ideal in vitro system for studying EBV latent infection in vivo has not yet been established. In this study, a mantle cell lymphoma line, SP53, was successfully infected with a recombinant EBV containing a neomycin-resistant gene. The EBV-carrying SP53 cells were obtained by selection using G418. They expressed EBER-1, EBNAs, and LMP1; this expression pattern of the EBV genes was similar to that in a lymphoblastoid cell line (LCL). However, proliferation assay showed that the EBV-carrying SP53 cells have a doubling time of 73 h, compared with 57 h of SP53 cells. Transplantation of 10(8) SP53 cells to nude mice formed tumors in 4 of 10 mice inoculated, but the EBV-carrying SP53 cells did not. Unexpectedly, EBV infection reduced the proliferation and tumorigenicity of SP53 cells. However, the EBV-carrying SP53 cells showed higher resistance to apoptosis induced by serum starvation than did the SP53 cells. The inhibition of proliferation and the resistance to apoptosis induced in SP53 cells by EBV infection indicate that this cell line might to some extent provide a model of in vivo EBV reservoir cells.

en-copyright= kn-copyright= en-aut-name=JinZaishun en-aut-sei=Jin en-aut-mei=Zaishun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TeramotoNorihiro en-aut-sei=Teramoto en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakadaKenzo en-aut-sei=Takada en-aut-mei=Kenzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Hokkaido University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University en-keyword=Epstein-Barr virus kn-keyword=Epstein-Barr virus en-keyword=mantle cell lymphoma kn-keyword=mantle cell lymphoma en-keyword=latent infection kn-keyword=latent infection en-keyword=in vivo reservoir kn-keyword=in vivo reservoir en-keyword=SP53 line kn-keyword=SP53 line END