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| 1 | Serum vascular endothelial growth factor as a predictor of response and survival in patients with advanced hepatocellular carcinoma undergoing hepatic arterial infusion chemotherapy显示文摘 | Takashi Niizeki Shuji Sumie Takuji Torimura Junichi Kurogi Ryoko Kuromatsu Hideki Iwamoto Hajime Aino Masahito Nakano Atsushi Kawaguchi Tatsuyuki Kakuma Michio Sata | 2012 | Journal of Gastroenterology2012，，6： | 2 |
| 2 | Knockout of exogenous EGFP gene in porcine somatic cells using zinc-finger nucleases显示文摘 | Masahito Watanabe Kazuhiro Umeyama Hitomi Matsunari Shuko Takayanagi Erika Haruyama Kazuaki Nakano Tsukasa Fujiwara Yuka Ikezawa Hiromitsu Nakauchi Hiroshi Nagashima | 2010 | Biochemical and Biophysical Research Communications2010，，1： | 1 |
| 3 | Feasibility of large experimental animal models in testing novel therapeutic strategies for diabetes显示文摘Diabetes is among the top 10 causes of death in adults and caused approximately four million deaths worldwide in 2017.The incidence and prevalence of diabetes is predicted to increase.To alleviate this potentially severe situation,safer and more effective therapeutics are urgently required.Mice have long been the mainstay as preclinical models for basic research on diabetes,although they are not ideally suited for translating basic knowledge into clinical applications.To validate and optimize novel therapeutics for safe application in humans,an appropriate large animal model is needed.Large animals,especially pigs, are well suited for biomedical research and share many similarities with humans,including body size,anatomical features,physiology,and pathophysiology.Moreover,pigs already play an important role in translational studies,including clinical trials for xenotransplantation.Progress in genetic engineering over the past few decades has facilitated the development of transgenic animals,including porcine models of diabetes.This article discusses features that attest to the attractiveness of genetically modified porcine models of diabetes for testing novel treatment strategies using recent technical advances. | Masaki Nagaya Koki Hasegawa Ayuko Uchikura Kazuaki Nakano Masahito Watanabe Kazuhiro Umeyama Hitomi Matsunari Kenji Osafune Eiji Kobayashi Hiromitsu Nakauchi Hiroshi Nagashima | 2021 | World Journal of Diabetes2021，12，4： | 1 |
| 4 | Tumor-derived insulin-like growth factor-binding protein-1 contributes to resistance of hepatocellular carcinoma to tyrosine kinase inhibitors显示文摘Background:Antiangiogenic tyrosine kinase inhibitors(TKIs)provide one of the few therapeutic options for effective treatment of hepatocellular carcinoma(HCC).However,patients with HCC often develop resistance toward antiangiogenic TKIs,and the underlying mechanisms are not understood.The aim of this study was to determine the mechanisms underlying antiangiogenic TKI resistance in HCC.Methods:We used an unbiased proteomic approach to define proteins that were responsible for the resistance to antiangiogenic TKIs in HCC patients.We evaluated the prognosis,therapeutic response,and serum insulin-like growth factor-binding protein-1(IGFBP-1)levels of 31 lenvatinib-treated HCC patients.Based on the array of results,a retrospective clinical study and preclinical experiments using mouse and human hepatoma cells were conducted.Additionally,in vivo genetic and pharmacological gain-and loss-of-function experiments were performed.Results:In the patient cohort,IGFBP-1 was identified as the signaling molecule with the highest expression that was inversely associated with overall survival.Mechanistically,antiangiogenic TKI treatment markedly elevated tumor IGFBP-1 levels via the hypoxia-hypoxia inducible factor signaling.IGFBP-1 stimulated angiogenesis through activation of the integrinα5β1-focal adhesion kinase pathway.Consequently,loss of IGFBP-1 and integrinα5β1 by genetic and pharmacological approaches re-sensitized HCC to lenvatinib treatment.Conclusions:Together,our data shed light onmechanisms underlying acquired resistance of HCC to antiangiogenic TKIs.Antiangiogenic TKIs induced an increase of tumor IGFBP-1,which promoted angiogenesis through activating the IGFBP-1-integrinα5β1 pathway.These data bolster the application of a new therapeutic concept by combining antiangiogenic TKIs with IGFBP-1 inhibitors. | Hiroyuki Suzuki Hideki Iwamoto Takahiro Seki Toru Nakamura Atsutaka Masuda Takahiko Sakaue Toshimitsu Tanaka Yasuko Imamura Takashi Niizeki Masahito Nakano Shigeo Shimose Tomotake Shirono Yu Noda Naoki Kamachi Miwa Sakai Kazutoyo Morita Masamichi Nakayama Tomoharu Yoshizumi Ryoko Kuromatsu Hirohisa Yano Yihai Cao Hironori Koga Takuji Torimura | 2023 | Cancer Communications2023，43，4： | 0 |
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