研究者詳細 - 藤原　俊義

MISC - 藤原　俊義

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大学発ベンチャーの研究開発-悪性腫瘍に対するウイルス製剤Telomelysinの臨床開発-

藤原俊義, 田中紀章, 浦田泰生

Biotherapy 20,3,310-317 2006年

大学発ベンチャーの研究開発：悪性腫瘍に対するウイルス製剤Telomelysinの臨床開発.

藤原俊義, 田中紀章, 浦田泰生

Biotherapy 20: 310-317 2006年

主要癌の遺伝子治療研究の現況-肺癌-

藤原俊義, 田中紀章

Biotherapy 20,3,270-279 2006年

主要癌の遺伝子治療研究の現況：肺癌.

藤原俊義, 田中紀章

Biotherapy 20: 270-279 2006年

ZD1839 (Gefitinib, 'Iressa'), an epidermal growth factor receptor-tyrosine kinase inhibitor, enhances the anti-cancer effects of TRAIL in human esophageal squamous cell carcinoma

F Teralshi, S Kagawa, T Watanabe, Y Tango, T Kawashima, T Umeoka, M Nisizaki, N Tanaka, T Fujiwara

FEBS LETTERS 579 ( 19 ) 4069 - 4075 2005年8月

記述言語：英語出版者・発行元：ELSEVIER SCIENCE BV

The EGF (epidermal growth factor) receptor-tyrosine kinase inhibitor ZD1839 (Getitinib, 'Iressa') blocks the cell signaling pathways involved in cell proliferation, survival, and angiogenesis in various cancer cells. TNF-related death apoptosis inducing ligand (TRAIL) acts as an anticancer agent. We investigated the antitumor effects of ZD-1839 alone or in combination with TRAIL against human esophageal squamous cell cancer (ESCC) lines. Although all ESCC cells expressed EGF receptor at a protein level, the effect of ZD1839 on cell growth did not correlate with the level of EGFR expression and phosphorylation of EGF receptor protein in ESCC lines. ZD1839 caused a dose-dependent growth arrest at GO-G, phase associated with increased p27 expression. As TE8 cells are resistant to TRAIL, we tested whether ZD1839 combined with TRAIL induced apoptosis of TE8 cells via the inhibition of EGF receptor signaling by ZD1839. ZD1839 inhibited the phosphorylation of Akt, and enhanced TRAIL-induced apoptosis via activation of caspase-3 and caspase-9, and inactivation of Bcl-xL. Our results indicated that ZD1839 has anti-cancer properties against human esophageal cancer cells. ZD1839 also augmented the anti-cancer activity of TRAIL, even in TRAIL-resistant tumors. These results suggest that treatment with ZD1839 and TRAIL may have potential in the treatment of ESCC patients. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

DOI： 10.1016/j.febslet.2005.06.031

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Alport 症候に合併した食道び漫性平滑筋腫の1例(食道・胃・十二指腸18, 第60回日本消化器外科学会総会)

西江学, 猶本良夫, 山辻知樹, 白川靖博, 浅海信也, 藤原俊義, 松原長秀, 岩垣博巳, 磯崎博司, 田中紀章

日本消化器外科学会雑誌 38 ( 7 ) 1209 - 1209 2005年7月

Transcriptional blockade induces p53-dependent apoptosis associated with translocation of p53 to mitochondria

Y Arima, M Nitta, S Kuninaka, DW Zhang, T Fujiwara, Y Taya, M Nakao, H Saya

JOURNAL OF BIOLOGICAL CHEMISTRY 280 ( 19 ) 19166 - 19176 2005年5月

記述言語：英語出版者・発行元：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

The tumor suppressor p53 functions as a transcriptional activator to induce cell cycle arrest and apoptosis in response to DNA damage. Although p53 was also shown to mediate apoptosis in a manner independent of its transactivation activity, the mechanism and conditions that trigger such cell death have remained largely unknown. We have now shown that inhibition of RNA polymerase II-mediated transcription by α-amanitin or RNA interference induced p53-dependent apoptosis. Inhibition of pol II-mediated transcription resulted in down-regulation of p21(Cip1), which was caused by both transcriptional suppression and protein degradation, despite eliciting p53 accumulation, allowing the cells to progress into S phase and then to undergo apoptosis. This cell death did not require the transcription of p53 target genes and was preceded by translocation of the accumulated p53 to mitochondria. Our data thus suggested that blockade of pol II-mediated transcription induced p53 accumulation in mitochondria and was the critical factor for eliciting p53-dependent but transcription-independent apoptosis.

DOI： 10.1074/jbc.M410691200

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Enhanced oncolysis by a tropism-modified telomerase-specific replication-selective adenoviral agent OBP-405 ('Telomelysin-RGD)

M Taki, S Kagawa, M Nishizaki, H Mizuguchi, T Hayakawa, S Kyo, K Nagai, Y Urata, N Tanaka, T Fujiwara

ONCOGENE 24 ( 19 ) 3130 - 3140 2005年4月

記述言語：英語出版者・発行元：NATURE PUBLISHING GROUP

Replication-competent oncolytic viruses are being developed for human cancer therapy. We previously reported that an attenuated adenovirus (OBP-301, 'Telomelysin'), in which the hTERT promoter element drives expression of E1A and E1B genes linked with an IRES, could replicate in cancer cells, and causes selective lysis of cancer cells. We further constructed OBP-405 ('Telomelysin-RGD') that contains an RGD motif in the HI loop of the fiber knob. We examined whether OBP-405 could be effective in overcoming the limitations of OBP-301, specifically their inefficient infection into cells lacking the primary receptor, the coxsackievirus and adenovirus receptor ( CAR). By flow cytometric analysis, H1299 ( lung) and SW620 ( colorectal) tumor cells showed high levels of CAR expression, whereas LN444 ( glioblastoma), LNZ308 ( glioblastoma), and H1299-R5 ( lung) tumor cells were negative for CAR expression. A quantitative realtime PCR analysis demonstrated that fiber-modified OBP-405 infected more efficiently than OBP-301, although the intracellular replication rate of both viruses was consistent. The comparative antitumor effect of fiber-modified OBP-405 and unmodified OBP-301 for human cancer cells was evaluated in vitro by XTT assay as well as in vivo by using athymic mice carrying xenografts. OBP-405 had a profound oncolytic effect on human cancer cell lines compared to OBP-301, in particular on cells with low CAR expression. Intratumoral injection of 107 plaque-forming units of OBP-405 into CAR-negative H1299-R5 lung tumor xenografts in nu/nu mice resulted in a significant inhibition of tumor growth and long-term survival in all treated mice. Moreover, selective replication of OBP-405 in the distant, uninjected H1299-R5 tumors was demonstrated. Our results suggest that fiber-modified replication-competent adenovirus OBP-405 exhibits a broad target range by increasing infection efficiency, an outcome that has important implications for the treatment of human cancers.

DOI： 10.1038/sj.onc.1208460

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肺悪性腫瘍のラジオ波治療

金澤右, 三村秀文, 郷原英夫, 向井敦, 平木隆夫, 長谷総一郎, 藤原寛康, 田尻展久, 佐野由文, 清水信義, 藤原俊義, 田中紀章

成人病と生活習慣病 2005年

重症糖尿病合併胸部食道癌に対する糖質調整流動食Inslowの糖質・脂質代謝改善効果の検討

藤原俊哉, 猶本良夫, 元木崇之, 繁光薫, 白川靖博, 山辻知樹, 片岡正文, 羽井佐実, 羽井佐茂, 藤原俊義, 有馬裕史, 佐々木一, 松浦基, 田中紀章

外科治療 2005年

Human monocyte-derived dendritic cells pulsed with wild-type p53 protein efficiently induce cytotoxic T-lymphocytes against p53-overexpressing human cancer cells.

Tokunaga N, Murakami T, Endo Y, Nishizaki M, Kagawa S, Tanaka N, Fujiwara T

Cancer Res 2005年

癌に対する遺伝子治療：肺癌

藤原俊義, 香川俊輔, 田中紀章

遺伝子診療学（日本臨床増刊号） 63,507-511 2005年

悪性腫瘍に対するウイルス製剤：Telomelysinの開発と臨床応用の可能性

藤原俊義, 田中紀章

Medical Technology 33,961-966 2005年

P53遺伝子発現アデノウイルスベクターを用いた肺癌遺伝子治療

藤原俊義, 田中紀章

Surgery Frontier 12,53-56 2005年

遊離空腸パッチグラフトによる頚部食道再建術

桜間一史, 猶本良夫, 野間和広, 浅海信也, 白川靖博, 山辻知樹, 藤原俊義, 松原長秀, 羽井佐実

岡山医学会雑誌 116 ( 3 ) 2005年

Alport症候群に合併した食道びまん性平滑筋腫症の一例

西江学, 猶本良夫, 野間和広, 白川靖博, 浅海信也, 山辻知樹, 藤原俊義, 松原長秀, 羽井佐実, 岩垣博巳, 松岡順治, 田中紀章

岡山医学会雑誌 117 ( 2 ) 2005年

食道癌術後にみられたToxic Shock Syndromeの検討

山辻知樹, 楢本良夫, 渡辺信之, 野間和広, 桜間一史, 小林正彦, 白川靖博, 小林直哉, 藤原俊義, 松原長秀, 羽井佐実, 岩垣博巳, 松岡順治, 田中紀章

日本臨床外科学会雑誌 66 2005年

当科における食道部分切除術の検討

白川靖博, 猶本良夫, 野間和広, 西江学, 浅海信也, 山辻知樹, 藤原俊義, 松原長秀, 羽井佐実, 岩垣博巳, 松岡順治, 田中紀章

岡山医学会雑誌 117 ( 2 ) 2005年

DP皮弁を用いた食道再建法

猶本良夫, 渡辺信之, 野間和広, 桜間一史, 小林正彦, 白川靖博, 山辻知樹, 小林直哉, 藤原俊義, 松原長秀, 岩垣博巳, 田中紀章

日本臨床外科学会雑誌 66 2005年

集学的治療が奏功した胸部大動脈浸潤食道癌の一例

西江学, 猶本良夫, 野間和弘, 浅海信也, 白川靖博, 山辻知樹, 藤原俊義, 松原長秀, 岩垣博己, 田中紀章

岡山医学会雑誌 117 ( 2 ) 2005年

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