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| 1 | Near-infrared photoimmunotherapy of pancreatic cancer using an indocyanine green-labeled anti-tissue factor antibody显示文摘AIM To investigate near-infrared photoimmunotherapeutic effect mediated by an anti-tissue factor(TF) antibody conjugated to indocyanine green(ICG) in a pancreatic cancer model.METHODS Near-infrared photoimmunotherapy(NIR-PIT) is a highly selective tumor treatment that utilizes an antibody-photosensitizer conjugate administration, followed by NIR light exposure. Anti-TF antibody 1849-ICG conjugate was synthesized by labeling of rat IgG2 b anti-TF monoclonal antibody 1849(anti-TF 1849) to a NIR photosensitizer,ICG. The expression levels of TF in two human pancreatic cancer cell lines were examined by western blotting. Specific binding of the 1849-ICG to TF-expressing BxPC-3 cells was examined by fluorescence microscopy. NIR-PITinduced cell death was determined by cell viability imaging assay. In vivo longitudinal fluorescence imaging was used to explore the accumulation of 1849-ICG conjugate in xenograft tumors. To examine the effect of NIRPIT, tumor-bearing mice were separated into 5 groups:(1) 100 μg of 1849-ICG i.v. administration followed by NIR light exposure(50 J/cm2) on two consecutive days(Days 1 and 2);(2) NIR light exposure(50 J/cm2) only on two consecutive days(Days 1 and 2);(3) 100 μg of 1849-ICG i.v. administration;(4) 100 μg of unlabeled antiTF 1849 i.v. administration; and(5) the untreated control. Semiweekly tumor volume measurements, accompanied with histological and immunohistochemical(IHC) analyses of tumors, were performed 3 d after the 2nd irradiation with NIR light to monitor the effect of treatments. RESULTS High TF expression in BxPC-3 cells was observed via western blot analysis, concordant with the observed preferential binding with intracellular localization of 1849-ICG via fluorescence microscopy. NIR-PIT-induced cell death was observed by performing cell viability imaging assay. In contrast to the other test groups, tumor growth was significantly inhibited by NIR-PIT with a statistically significant difference in relative tumor volumes for 27 d after the treatment start date [2.83 ± 0.38(NIR-PIT) vs 5.42 ± 1.61(Untreated), vs 4.90 ± 0.87(NIR), vs 4.28 ±1.87(1849-ICG), vs 4.35 ± 1.42(anti-TF 1849), at Day 27, P < 0.05]. Tumors that received NIR-PIT showed evidence of necrotic cell death-associated features upon hematoxylin-eosin staining accompanied by a decrease in Ki-67-positive cells(a cell proliferation marker) by IHC examination.CONCLUSION The TF-targeted NIR-PIT with the 1849-ICG conjugate can potentially open a new platform for treatment of TF-expressing pancreatic cancer. | Winn Aung Atsushi B Tsuji Aya Sugyo Hiroki Takashima Masahiro Yasunaga Yasuhiro Matsumura Tatsuya Higashi | 2018 | World Journal of Gastroenterology2018，24，48： | 7 |
| 2 | Gene expression of bone morphogenic protein 8B in the primary site,peripheral blood and bone marrow of patients with gastric cancer显示文摘 | Kosuke Mima Takeo Fukagawa Junji Kurashige Yuki Takano Ryutaro Uchi Hiroki Ueo Tae Matsumura Masahisa Ishibashi Genta Sawada Yusuke Takahashi Sayuri Akiyoshi Hidetoshi Eguchi Tomoya Sudo Keishi Sugimachi Masayuki Watanabe Hideshi Ishii Masaki Mori Hideo B | 2013 | Oncology Letters2013，，2： | 1 |
| 3 | Synthetic studies on pterin glycosides:the first synthesis of 2'-O-(α-D-glucopyranosyl)biopterin显示文摘 | TADASHI H HIROKI B HIROKI T | 2009 | Tetrahedron2009，65，38： | 1 |
| 4 | Protective effect pretreatment with cilostazol on cytotoxicity of cadmium and arsenic in cultured vascular endothelial cells显示文摘 | Yasuyuki F Hiroki B Yasuhiro S | 2011 | Toxicol Sci2011，36，： | 1 |
| 5 | Impact of various characteristics of electricity and heat demand on the optimal configuration of a microgrid显示文摘 | SHIGERU B HIROKI W HIROSHI A et aI | 2009 | Electrical Engineering in Japan2009，169，2： | 1 |
| 6 | Development of a centrifugal compressor equipped with magnetic beatings显示文摘 | HIROKI S YOSHITAKA B TOSHIKAZU M | 1999 | Research and Development Kobe Steel Engineering Reports1999，49，1： | 1 |
| 7 | Involvement of p38 MAPK in regulation of MMP13 mRNA in chondrocytes in re-sponse to surviving stress to endoplasmic reticulum显示文摘 | Kazunori H Goldring M B Hiroki Y | | 0，，03： | 1 |
| 8 | Persistent Nuclear Factor-kB Activation in Ucp2-- Mice Leads to Enhanced Nitric Oxide and Inflammatory Cytokine Production显示文摘 | Yushi B Hiroki O Xu B | 2005 | J Biol Chem2005，，19： | 1 |
| 9 | Impact of various characteristics of electricity and heat demand on the optimal configuration of a microgrid 显示文摘 | SHIGERU B HIROKI W HIROSHI A | 2009 | Elec- trical Engineering in Japan2009，169，2： | 1 |
| 10 | Human IgG1 antibodies suppress angiogenesis in a target-independent manner显示文摘Aberrant angiogenesis is implicated in diseases affecting nearly 10%of the world’s population.The most widely used antiangiogenic drug is bevacizumab,a humanized IgG1 monoclonal antibody that targets human VEGFA.Although bevacizumab does not recognize mouse Vegfa,it inhibits angiogenesis in mice.Here we show bevacizumab suppressed angiogenesis in three mouse models not via Vegfa blockade but rather Fc-mediated signaling through FcγRI(CD64)and c-Cbl,impairing macrophage migration.Other approved humanized or human IgG1 antibodies without mouse targets(adalimumab,alemtuzumab,ofatumumab,omalizumab,palivizumab and tocilizumab),mouse IgG2a,and overexpression of human IgG1-Fc or mouse IgG2a-Fc,also inhibited angiogenesis in wild-type and FcγR humanized mice.This anti-angiogenic effect was abolished by Fcgr1 ablation or knockdown,Fc cleavage,IgG-Fc inhibition,disruption of Fc-FcγR interaction,or elimination of FcRγ-initated signaling.Furthermore,bevacizumab’s Fc region potentiated its anti-angiogenic activity in humanized VEGFA mice.Finally,mice deficient in FcγRI exhibited increased developmental and pathological angiogenesis.These findings reveal an unexpected anti-angiogenic function for FcγRI and a potentially concerning off-target effect of hIgG1 therapies. | Sasha Bogdanovich Younghee Kim Takeshi Mizutani Reo Yasuma Laura Tudisco Valeria Cicatiello Ana Bastos-Carvalho Nagaraj Kerur Yoshio Hirano Judit Z Baffi Valeria Tarallo Shengjian Li Tetsuhiro Yasuma Parthasarathy Arpitha Benjamin J Fowler Charles B Wright Ivana Apicella Adelaide Greco Arturo Brunetti Menotti Ruvo Annamaria Sandomenico Miho Nozaki Ryo Ijima Hiroki Kaneko Yuichiro Ogura Hiroko Terasaki Balamurali K Ambati Jeanette HW Leusen Wallace Y Langdon Michael R Clark Kathryn L Armour Pierre Bruhns J Sjef Verbeek Bradley D Gelfand Sandro De Falco Jayakrishna Ambati | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 0 |
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