研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

分割表示 1,236 件中 501 - 520 件目／全件表示 >>

[Mechanisms of asbestos-induced carcinogenesis]. 国際誌 Open Access

Toyokuni S, Jiang L, Hu Q, Nagai H, Okazaki Y, Akatsuka S, Yamashita Y

Nihon eiseigaku zasshi. Japanese journal of hygiene 66 巻 ( 3 ) 頁： 562 - 7 2011年5月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Nihon eiseigaku zasshi. Japanese journal of hygiene

Several types of fibrous stone called asbestos have been an unexpected cause of human cancer in the history. This form of mineral is considered precious in that they are heat-, friction-, and acid-resistant, are obtained easily from mines, and can be modified to any form with many industrial merits. However, it became evident that the inspiration of asbestos causes a rare cancer called malignant mesothelioma. Because of the long incubation period, the peak year for malignant mesothelioma is expected to be 2025 in Japan. Thus, it is necessary to elucidate the mechanisms of asbestos-induced mesothelial carcinogenesis. In this review, we summarize the cutting edge results of our 5-year project funded by a MEXT grant, in which local iron deposition and the characteristics of mesothelial cells are the key issues.

DOI： 10.1265/jjh.66.562

Roles of ASH1-miR-375 pathway in development of lung cancers with neuroendocrine features

Hirotaka, O; Nishikawa, E; Arima, C; Okazaki, Y; Tomida, S; Tatematsu, Y; Taguchi, A; Shimada, Y; Yanagisawa, K; Toyokuni, S; Sekido, Y; Takahashi, T

CANCER RESEARCH 71 巻 2011年4月

XCR1 expression and biased VH gene usage are distinct features of diffuse large B-cell lymphoma initially manifesting in the bone marrow. 査読有り国際誌

Yamashita Y, Kajiura D, Tang L, Hasegawa Y, Kinoshita T, Nakamura S, Akatsuka S, Toyokuni S, Mori N

American journal of clinical pathology 135 巻 ( 4 ) 頁： 556 - 64 2011年4月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：American Journal of Clinical Pathology

A total of 29 cases of diffuse large B-cell lymphoma initially manifesting in the bone marrow (BM-DLBCL) were analyzed for VH gene sequence, and expression microarray of chemokines and chemokine receptors and immunohistochemical analysis were done. Seminested polymerase chain reaction (PCR) and sequencing analyses of 18 cases revealed that the VH gene usage in 6 cases was restricted to VH3-7, in 3 cases to V H4-34, and in 2 cases to VH4-39, which were all previously reported to be autoreactive. In total, 14 of 18 VH genes were those associated with autoimmune diseases, including VH3-21, V H3-23, and VH3-48. Furthermore, cDNA microarray analysis specific for chemokine and chemokine receptors revealed that chemokine receptor XCR1 expression was significantly elevated in the BM-DLBCL cases (P < 05), which was confirmed by quantitative reverse transcriptase-PCR and immunohistochemical analysis. Expression of the chemokine receptor XCR1 and frequent usage of autoreactive VH genes seem to be distinct characteristics of BM-DLBCL. © American Society for Clinical Pathology.

DOI： 10.1309/AJCPCTDC5PY3LXBP

LATS2 is a tumor suppressor gene of malignant mesothelioma

Murakami H.

Cancer Research 71 巻 ( 3 ) 頁： 873 - 883 2011年2月

LATS2 is a tumor suppressor gene of malignant mesothelioma.

Murakami H, Mizuno T, Taniguchi T, Fujii M, Ishiguro F, Fukui T, Akatsuka S, Horio Y, Hida T, Kondo Y, Toyokuni S, Osada H, Sekido Y

Cancer research 71 巻 ( 3 ) 頁： 873 - 83 2011年2月

Stage-specific roles of fibulin-5 during oxidative stress-induced renal carcinogenesis in rats. 査読有り国際誌

Ohara H, Akatsuka S, Nagai H, Liu YT, Jiang L, Okazaki Y, Yamashita Y, Nakamura T, Toyokuni S

Free radical research 45 巻 ( 2 ) 頁： 211 - 20 2011年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Free Radical Research

By using a rat model of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA), this study performed genome-wide analysis to identify target genes during carcinogenesis. It screened for genes with decreased expression in RCCs, with simultaneous loss of heterozygosity, eventually to focus on the fibulin-5 (fbln5) gene. Oxidative damage via Fe-NTA markedly increased Fbln5 in the proximal tubules. RCCs presented lower levels of Fbln5. However, a fraction of RCCs presenting pulmonary metastasis revealed significantly higher levels of Fbln5 than those without metastasis, accompanied by immunopositivity of RCC cells and myofibroblast proliferation. Experiments revealed that RCC cell lines showed lower expression of fbln5 than its non-transformed counterpart NRK52E, but that fbln5 transfection to RCC cell lines changed neither proliferation nor migration/invasion. The data suggest that Fbln5 plays a role not only in the tissue repair and remodelling after renal tubular oxidative damage but also in RCC metastasis, presumably as a cytokine. © 2011 Informa UK, Ltd.

DOI： 10.3109/10715762.2010.523702

LATS2 Is a Tumor Suppressor Gene of Malignant Mesothelioma 査読有り

Hideki Murakami, Tetsuya Mizuno, Tetsuo Taniguchi, Makiko Fujii, Futoshi Ishiguro, Takayuki Fukui, Shinya Akatsuka, Yoshitsugu Horio, Toyoaki Hida, Yutaka Kondo, Shinya Toyokuni, Hirotaka Osada, Yoshitaka Sekido

CANCER RESEARCH 71 巻 ( 3 ) 頁： 873 - 883 2011年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER ASSOC CANCER RESEARCH

Malignant mesothelioma (MM) is an aggressive neoplasm associated with asbestos exposure. We carried out genome-wide array-based comparative genomic hybridization analysis with 14 MM cell lines. Three cell lines showed overlapping homozygous deletion at chromosome 13q12, which harbored the LATS2 (large tumor suppressor homolog 2) gene. With 6 other MM cell lines and 25 MM tumors, we found 10 inactivating homozygous deletions or mutations of LATS2 among 45 MMs. LATS2 encodes a serine/threonine kinase, a component of the Hippo tumor-suppressive signaling pathway, and we transduced LATS2 in MM cells with its mutation. Transduction of LATS2 inactivated oncoprotein YAP, a transcriptional coactivator, via phosphorylation, and inhibited MM cell growth. We also analyzed LATS2 immunohistochemically and found that 13 of 45 MM tumors had low expression of LATS2. Because NF2 is genetically mutated in 40% to 50% of MM, our data indicate that Hippo pathway dysregulation is frequent in MM cells with inactivation of LATS2 or an upstream regulator of this pathway, Merlin, which is encoded by NF2. Thus, our results suggest that the inactivation of LATS2 is one of the key mechanisms for constitutive activation of YAP, which induces deregulation of MM cell proliferation. Cancer Res; 71(3); 873-83. (C)2011 AACR.

DOI： 10.1158/0008-5472.CAN-10-2164

Web of Science

researchmap

CD8+CD122+ regulatory T cells (Tregs) and CD4+ Tregs cooperatively prevent and cure CD4+ cell-induced colitis. 査読有り国際誌 Open Access

Endharti AT, Okuno Y, Shi Z, Misawa N, Toyokuni S, Ito M, Isobe K, Suzuki H

Journal of immunology (Baltimore, Md. : 1950) 186 巻 ( 1 ) 頁： 41 - 52 2011年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Journal of Immunology

We identified CD8+CD122+ regulatory T cells (Tregs) and demonstrated their importance in the maintenance of immune homeostasis and in the recovery from experimental autoimmune encephalomyelitis. In this paper, we show that CD8+CD122+ Tregs effectively prevent and cure colitis in a mouse model. In our experiments, colitis was induced in lymphocyte-deficient RAG-2-/- mice by transferring CD4 +CD45RBhigh cells that were excluded with CD4+ Tregs. Cotransfer of CD8+CD122+ cells clearly suppressed the development of colitis, and this suppressive effect was similar to that of CD4+CD45RBlow cells that were mostly CD4+ Tregs. CD8+CD122+ cells obtained from IL-10-/- mice were unable to suppress colitis, indicating that IL-10 is an important effect-transmitting factor in the suppression of colitis. CD8 +CD122+ cells showed a suppressive effect when they were transferred 4 wk after CD4+CD45RBhigh cells, indicating the therapeutic potential of CD8+CD122+ cells. A mixture of CD8+CD122+ cells and CD4+CD45RB low cells was far more effective than single Tregs, indicating the synergistic effect of these Tregs. These overall findings demonstrate the potential role of CD8+ Tregs, and possibly together with CD4 + Tregs, in the medical care of inflammatory bowel disease patients. Copyright © 2010 by The American Association of Immunologists, Inc.

DOI： 10.4049/jimmunol.1000800

3-Morpholinosydnonimine participates in the attenuation of neointima formation via inhibition of annexin A2-mediated vascular smooth muscle cell migration 国際誌

Won, KJ; Lee, P; Jung, SH; Jiang, X; Lee, CK; Lin, HY; Kang, H; Lee, HM; Kim, J; Toyokuni, S; Kim, B

PROTEOMICS 11 巻 ( 2 ) 頁： 193 - 201 2011年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Proteomics

3-Morpholinosydnonimine (SIN-1) affects vascular smooth muscle cell migration and proliferation, processes essential for atherosclerosis. However, the mechanism by which SIN-1 exerts these effects has not been elucidated. We used 2-DE followed by MALDI-TOF/TOF MS to identify responses in protein expression to SIN-1 in rat aortic smooth muscle. Platelet-derived growth factor-BB increased cell migration and proliferation in rat aortic smooth muscle cells, and subsequent SIN-1 treatment inhibited it. Administration of SIN-1 in vivo attenuated neointima formation in balloon-injured rat carotid arteries. Proteomic analysis showed that glutathione peroxidase and 40S ribosomal protein S12 were differentially expressed in aortic strips exposed to SIN-1. Expression of annexin A2 was decreased by SIN-1. Platelet-derived growth factor-BB-induced cell migration was increased and inhibited in rat aortic smooth muscle cells with overexpression and knockdown of annexin A2 gene, respectively. The expression of annexin A2 was increased in vascular neointima compared with the intact control, which was inhibited by SIN-1 treatment. These results demonstrate that SIN-1 may attenuate vascular neointima formation by inhibiting annexin A2-mediated migration. Therefore, annexin A2 may be a potential target for therapeutic strategies for atherosclerosis. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

DOI： 10.1002/pmic.200900834

XCR1 expression and biased VH gene usage are distinct features of diffuse large B-cell lymphoma initially manifesting in the bone marrow. 査読有り

Yamashita Y, Kajiura D, Tang L, Hasegawa Y, Kinoshita T, Nakamura S, Akatsuka S, Toyokuni S and Mori N.

Am J Clin Pathol 135 巻頁： 556-564 2011年

Iron as a target of chemoprevention for longevity in humans. 査読有り

Toyokuni S.

Free Radic Res 45 巻頁： 906-917 2011年

The human cytomegalovirus gene products essential for late viral gene expression assemble into prereplication complexes before viral DNA replication. 査読有り

Isomura H, Stinski MF, Murata T, Yamashita Y, Kanda T, Toyokuni S and Tsurumi T.

J Virol 85 巻頁： 6629-6644 2011年

Dietary fish oil promotes colonic apoptosis and mitochondrial proton leak in oxidatively stressed mice. 査読有り

Fan YY, Ran Q, Toyokuni S, Okazaki Y, Callaway ES, Lupton JR, and Chapkin RS.

Cancer Prev Res 4 巻頁： 1267-1274 2011年

Age- and sun exposure-dependent differences in 8-hydroxy-2'-deoxyguanosine and Nε-(carboxymethyl)lysine in human epidermis. 査読有り

Toyokuni S, Hirao A, Wada T, Nagai R, Date A, Yoshii T, Akatsuka S, Yamashita Y, and Kawada A.

J Clin Biochem Nutr 49 巻頁： 1-4 2011年

Mysterious link between iron overload and CDKN2A/2B. 査読有り

Toyokuni S.

J 48 巻頁： 46-49 2011年

LATS2 is a tumor suppressor gene of malignancy mesothelioma. 査読有り

Murakami H, Mizuno T, Taniguchi T, Fujii M, Ishiguro F, Fukui T, Akatsuka S, Horio Y, HIda T, Kondo Y, Toyokuni S, Osada H and Sekido Y.

Cancer Res 71 巻頁： 873-883 2011年

Asbetos provides a niche for oxidative modification. 査読有り

Nagai H, Ishihara T, Lee WH, Ohara H, Okazaki Y, Okawa K and Toyokuni S.

Cancer Sci 102 巻頁： 2118-2125 2011年

miR-375 is activated by ASH1 and inhibits YAP1 in a lineage dependent manner in lung cancer. 査読有り

Nishikawa E, Osada H, Okazaki Y, Arima C, Tomida S, Tatematsu Y, Taguchi A, Shimada Y, Yanagisawa K, Yatabe Y, Toyokuni S, Sekido Y and Takahashi T

Cancer Res 71 巻頁： 6165-6173 2011年

Oxidative DNA Damage and Carcinogenesis

Jiang, L; Toyokuni, S

FREE RADICAL BIOLOGY IN DIGESTIVE DISEASES 29 巻頁： 55 - 63 2011年

Iron as a target of chemoprevention for longevity in humans. 査読有り

Toyokuni S

Free Radic Res 45 巻頁： 906-917 2011年

　前のページ - 次のページ　

<豊國 伸哉>

論文 - 豊國 伸哉

<豊國　伸哉>

論文 - 豊國　伸哉