Yuansong Bai
University of Tokyo
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Publication
Featured researches published by Yuansong Bai.
Gene Therapy | 2003
Yuansong Bai; Yasushi Soda; Kiyoko Izawa; Tsuyoshi Tanabe; X Kang; Arinobu Tojo; H Hoshino; Hiroyuki Miyoshi; Shigetaka Asano; Kenzaburo Tani
Difficulty in gene transduction of human blood cells, including hematopoietic stem cells, has hampered the development of gene therapy applications for hematological disorders, encouraging the development and use of new gene delivery systems. In this study, we used a third-generation self-inactivating (SIN) lentiviral vector system based on human immunodeficiency virus type 1 (HIV-1) to improve transduction efficiency and prevent vector-related toxicity. The transduction efficiency of the HIV-1-based vector was compared directly with the Moloney murine leukemia virus (MLV) SIN vector in human leukemia cell lines. Initial transduction efficiencies were almost 100% for the HIV and less than 50% for the MLV vectors. Similar results were observed in 11 types of primary cells obtained from leukemia or myeloma patients. Transgene expression persisted for 8 weeks in cells transduced with the HIV vector, but declined with the MLV vector. In addition, resting peripheral blood lymphocytes and CD34+ hematopoietic cells were transduced successfully with the HIV vector, but not with the MLV vector. Finally, we confirmed vector gene integration in almost all colony-forming cells transduced with the HIV vector, but not with the MLV vector. In conclusion, this lentiviral vector is an excellent gene transduction system for human blood cells because of its high gene transduction and host chromosome integration efficiency.
Cancer Gene Therapy | 2006
X Kang; X Xiao; Masamitsu Harata; Yuansong Bai; Yukoh Nakazaki; Yasushi Soda; Ryo Kurita; Takehiko Tanaka; F Komine; Kiyoko Izawa; Reiko Kunisaki; Misao Setoyama; H Nishimori; A Natsume; Makoto Sunamura; L Lozonshi; I. Saitoh; T Tokino; Shigetaka Asano; Yusuke Nakamura; Kenzaburo Tani
Glioblastomas are the most common primary brain tumors in adults. These tumors exhibit a high degree of vascularization, and malignant progression from astrocytoma to glioblastoma is often accompanied by increased angiogenesis and the upregulation of vascular endothelial growth factor and its receptors. In this study, we investigated the in vivo antiangiogenic and antitumor effects of brain-specific angiogenesis inhibitor 1 (BAI1) using human glioblastoma cell lines. Glioblastoma cells were transduced with an adenoviral vector encoding BAI1 (AdBAI1), and Northern and Western blot analyses, respectively, demonstrated BAI1 mRNA and protein expression in the transduced tumor cells. Using an in vivo neovascularization assay, we found that angiogenesis surrounding AdBAI1-transduced glioblastoma cells transplanted into transparent skinfold chambers of SCID mice was significantly impaired compared to control treated cells. Additionally, in vivo inoculation with AdBAI1 of established subcutaneous or intracerebral transplanted tumors significantly impaired tumor growth and promoted increased mouse survival. Morphologically, the tumors exhibited signs of impaired angiogenesis, such as extensive necrosis and reduced intratumoral vascular density. Taken together, these data strongly indicate that BAI1 may be an excellent gene therapy candidate for the treatment of brain tumors, especially human glioblastomas.
Molecular Therapy | 2004
Yuansong Bai; Yasushi Soda; Minghan Chen; Kiyoko Izawa; Seiichiro Kobayashi; Akira Tomonari; Jun Ooi; Fumitaka Nagamura; Satoshi Takahashi; Kaoru Uchimaru; Tohru Iseki; Hiroyuki Miyoshi; Tsuneo A. Takahashi; Kenzaburo Tani; Arinobu Tojo; Shigetaka Asano
Inactivation of the INK4A/ARF locus has been implicated in tumorigenesis, particularly in leukemogenesis. It has been found in 25–60% cases of acute leukemia and 20–50% cases of lymphoma. Although deletion of the INK4A/ARF locus is uncommon in AML, mRNA expression is likely to be disrupted, resulting from hypermethylation or mutation in the promoter region. There is some evidence that restoration of p16INK4a into p16-deficient leukemia cell lines suppresses their proliferation in suspension culture or their clonogenic growth in semisolid culture. However, previous studies were conducted by retrovirus or plasmid-mediated gene transfer under drug selection, suggesting low efficiency of transduction which appears disadvantageous to interpret the results of the growth inhibitory gene. Here we constructed a lentiviral vector expressing either p16ink4a or p14arf respectively, and validated its effect on leukemia cells, especially in combination with anti-leukemia agents including imatinib, ATRA and TNF-α. The p16, p14, hrGFP or mock lentiviral transfer vector was introduced into 293T cells along with packaging plasmids (pMDLg/p.RRE and pMD.G) and pRSV-Rev. The resulting VSV-G-pseudotyped lentivirus supernatant was concentrated by ultracentrifugation for high-titer virus stock. K562, NB4 and IMS-M2 cells were infected with those prepared viruses at the multiplicity of infection (moi) of 20–50, which allowed almost 100% of infection efficiency based on hrGFP fluorescence. The former two cell lines were deficient in p16 and p14 transcripts and had mutated p53 but intact pRb, while the latter one expressed both transcripts and had mutated p53 but intact pRb. Overexpression of p16 induced leukemia cells to accumulate in the G1 phase, followed by partial (IMS-M2) or complete (K562 and NB4) inhibition of cell growth. In addition, overexpression of p14 resulted in partial (IMS-M2) or substantial (K562 and NB4) apoptotic cell death, suggesting the presence of p53-independent pathway of apoptosis through p14. Next, we transduced p16 and p14 in primary blast cells from CML-BC or AML patients, resulting in their growth inhibition and apoptosis with a patient to patient variation. On the other hand, clonal growth and differentiation of cord blood progenitor cells was not affected by enforced expression of either p16 or p14 at the same moi. Next, not only imatinib and TNF-α-induced apoptosis of K562 and IMS-M2 cells but also ATRA-induced apoptosis of NB4 cells were markedly enhanced by transduction of p14 at a low moi less than 2.5. These results suggest that INK4A/ARF protein-mimetic agents may be promising options for leukemia in combination with the present anti-leukemia agents since these diseases are relatively resistant to a single agent.
Blood | 2004
Masamitsu Harata; Yasushi Soda; Kenzaburo Tani; Jun Ooi; Tomoko Takizawa; Minghan Chen; Yuansong Bai; Kiyoko Izawa; Seiichiro Kobayashi; Akira Tomonari; Fumitaka Nagamura; Satoshi Takahashi; Kaoru Uchimaru; Tohru Iseki; Takashi Tsuji; Tsuneo A. Takahashi; Kanji Sugita; Shinpei Nakazawa; Arinobu Tojo; Kazuo Maruyama; Shigetaka Asano
Biochemical and Biophysical Research Communications | 2006
Xiaohong Zhang; Yasushi Soda; Kenji Takahashi; Yuansong Bai; Ayako Mitsuru; Koichi Igura; Hitoshi Satoh; Satoru Yamaguchi; Kenzaburo Tani; Arinobu Tojo; Tsuneo A. Takahashi
Blood | 2004
Yasushi Soda; Kenzaburo Tani; Yuansong Bai; Minoru Saiki; Minghan Chen; Kiyoko Izawa; Seiichiro Kobayashi; Satoshi Takahashi; Kaoru Uchimaru; Tomoko Kuwabara; Masaaki Warashina; Tsuyoshi Tanabe; Hiroyuki Miyoshi; Kanji Sugita; Shinpei Nakazawa; Arinobu Tojo; Kazunari Taira; Shigetaka Asano
Haematologica | 2008
Seiichiro Kobayashi; Yasushi Soda; Yuansong Bai; Arinobu Tojo
Archive | 2013
Shigetaka Asano; Hiroyuki Miyoshi; Kanji Sugita; Shinpei Nakazawa; Arinobu Tojo; Kazunari Taira; Satoshi Takahashi; Kaoru Uchimaru; Tomoko Kuwabara; Masaaki Warashina; Kenzaburo Tani; Yuansong Bai; Minoru Saiki; Minghan Chen; Kiyoko Izawa
Open Journal of Blood Diseases | 2012
Yan Dong; Seiichiro Kobayashi; Yamin Tian; Manabu Ozawa; Takafumi Hiramoto; Kiyoko Izawa; Yuansong Bai; Yasushi Soda; Erika Sasaki; Toshio Itoh; Yoshiro Maru; Satoshi Takahashi; Kaoru Uchimaru; Naoki Oyaizu; Arinobu Tojo; Chieko Kai; Kenzaburo Tani
Blood | 2010
Yamin Tian; Yan Dong; Seiichiro Kobayashi; Manabu Ozawa; Kiyoko Izawa; Yuansong Bai; Yasushi Soda; Erika Sasaki; Toshio Itoh; Naoki Oyaizu; Satoshi Takahashi; Arinobu Tojo; Chieko Kai; Kenzaburo Tani