Updated on 2026/04/17

写真a

 
MATSUDA Yasunobu
 
Organization
Academic Assembly Institute of Medicine and Dentistry Health Sciences Associate Professor
Faculty of Medicine School of Health Sciences Associate Professor
Graduate School of Health Sciences Health Sciences Associate Professor
Title
Associate Professor
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Degree

  • 医学博士 ( 1998.4   新潟大学 )

Research Interests

  • 腫瘍再増殖

  • 代償性増殖

  • oncology

  • gastroenterologym

  • エクソソーム

Research Areas

  • Life Science / Gastroenterology

Research History (researchmap)

  • Niigata University   Graduate School of Health Sciences Health Sciences   Associate Professor

    2007.10

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  • Niigata University   Faculty of Medicine School of Health Sciences   Associate Professor

    2007.10

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  • Niigata University   University Medical and Dental Hospital   Assistant Professor

    2007.4 - 2007.9

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  • Niigata University   University Medical and Dental Hospital   Assistant

    2003.10 - 2007.3

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  • Niigata University   Faculty of Medicine   Assistant

    2001.9 - 2003.9

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  • Osaka University   Faculty of Medicine   Researcher

    1993.5 - 1994.3

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Research History

  • Niigata University   Faculty of Medicine School of Health Sciences   Associate Professor

    2007.10

  • Niigata University   Graduate School of Health Sciences Health Sciences   Associate Professor

    2007.10

  • Niigata University   Graduate School of Health Sciences Health Sciences   Associate Professor

    2007.10

  • Niigata University   University Medical and Dental Hospital   Assistant Professor

    2007.4 - 2007.9

  • Niigata University   University Medical and Dental Hospital   Research Assistant

    2003.10 - 2007.3

  • Niigata University   Faculty of Medicine   Research Assistant

    2001.9 - 2003.9

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Education

  • Niigata University   Faculty of Medicine   School of Medicine

    1982.4 - 1998.3

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Professional Memberships

 

Papers

  • Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells. International journal

    Mami Osawa, Yasunobu Matsuda, Jun Sakata, Toshifumi Wakai

    Anticancer research   42 ( 2 )   745 - 757   2022.2

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    BACKGROUND/AIM: Tumour repopulation is a major obstacle for successful cancer treatment. This study investigated whether anticancer agents contribute to tumour repopulation in TP53-mutated bile duct cancer cells. MATERIALS AND METHODS: TP53-mutated HuCCT1 and HuH28 cells were exposed to anticancer agents, and recipient cells were exposed to their conditioned media or exosomes. The effect of inhibitors and siRNA-mediated gene silencing of p38 mitogen-activated protein kinase (MAPK) and of TP53 was analyzed by cell proliferation assays and western blotting. RESULTS: Conditioned media from genotoxic agent-treated cells promoted proliferation of recipient cells (p<0.05), and this effect was abrogated by exosome inhibitors. Exosomes from gemcitabine- or cisplatin-treated cells increased cell proliferation by 1.6- to 2.2-fold (p<0.05) through p38 MAPK signalling. These effects of exosomes were inhibited by inhibition/silencing of p38 MAPK but not by TP53 silencing. CONCLUSION: Exosomal p38 MAPK plays a pivotal role in tumour repopulation in a TP53-independent manner.

    DOI： 10.21873/anticanres.15533

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  • [Retracted] Alteration of p53-binding protein 1 expression as a risk factor for local recurrence in patients undergoing resection for extrahepatic cholangiocarcinoma. International journal

    Toshifumi Wakai, Yoshio Shirai, Jun Sakata, Pavel V Korita, Yasunobu Matsuda, Masaaki Takamura, Riuko Ohashi, Masayuki Nagahashi, Yoichi Ajioka, Katsuyoshi Hatakeyama

    International journal of oncology   59 ( 4 )   2021.10

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    Following the publication of this paper, the Journal was alerted by an investigation committee of Niigata University to the fact that the paper had been identified as a duplicate publication, which had already been published. Therefore, in accordance with the rules of Niigata University Fraud Investigation committee, a request was made that the paper be retracted. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 38: 1227-1236, 2011; DOI: 10.3892/ijo.2011.959].

    DOI： 10.3892/ijo.2021.5258

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  • Dysregulation of sphingolipid metabolic enzymes leads to high levels of sphingosine-1-phosphate and ceramide in human hepatocellular carcinoma. Reviewed International journal

    Kohei Miura, Masayuki Nagahashi, Pankaj Prasoon, Yuki Hirose, Takashi Kobayashi, Jun Sakata, Manabu Abe, Kenji Sakimura, Yasunobu Matsuda, Ali L Butash, Eriko Katsuta, Kazuaki Takabe, Toshifumi Wakai

    Hepatology research : the official journal of the Japan Society of Hepatology   51 ( 5 )   614 - 626   2021.5

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    AIM: Sphingosine-1-phosphate (S1P) and ceramide are bioactive sphingolipids known to be important in regulating numerous processes involved in cancer progression. The aim of this study was to determine the absolute levels of sphingolipids in hepatocellular carcinoma (HCC) utilizing data obtained from surgical specimens. In addition, we explored the clinical significance of S1P in patients with HCC and the biological role of S1P in HCC cells. METHODS: Tumors and normal liver tissues were collected from 20 patients with HCC, and sphingolipids were measured by mass spectrometry. The Cancer Genome Atlas (TCGA) cohort was utilized to evaluate gene expression of enzymes related to sphingolipid metabolism. Immunohistochemistry of phospho-sphingosine kinase 1 (SphK1), an S1P-producing enzyme, was performed for 61 surgical specimens. CRISPR/Cas9-mediated SphK1 knockout cells were used to examine HCC cell biology. RESULTS: S1P levels were substantially higher in HCC tissue compared with normal liver tissue. Levels of other sphingolipids upstream of S1P in the metabolic cascade, such as sphingomyelin, monohexosylceramide and ceramide, were also considerably higher in HCC tissue. Enzymes involved in generating S1P and its precursor, ceramide, were found in higher levels in HCC compared with normal liver tissue. Immunohistochemical analysis found that phospho-SphK1 expression was associated with tumor size. Finally, in vitro assays indicated that S1P is involved in the aggressiveness of HCC cells. CONCLUSIONS: Sphingolipid levels, including S1P and ceramide, were elevated in HCC compared with surrounding normal liver tissue. Our findings suggest S1P plays an important role in HCC tumor progression, and further examination is warranted.

    DOI： 10.1111/hepr.13625

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  • Urokinase-type Plasminogen Activator Is a Therapeutic Target for Overcoming Sorafenib Resistance in Hepatoma Cells. Reviewed International journal

    Mami Osawa, Yasunobu Matsuda, Yoshiaki Kinoshita, Toshifumi Wakai

    Anticancer research   41 ( 2 )   645 - 660   2021.2

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    BACKGROUND/AIM: Sorafenib is a multikinase inhibitor approved as a first-line therapy for hepatocellular carcinoma. This study examined the sorafenib resistance mechanism. MATERIALS AND METHODS: Hepatoma HepG2 cells were exposed to sorafenib, and the biological activity of the conditioned media was analyzed using cell proliferation/apoptosis assays, multiplex immunoassays, ELISA, and western blot analyses. The effect of urokinase-type plasminogen activator (uPA) inhibitors or siRNA-mediated gene silencing was examined in culture experiments and a mouse xenograft tumor model. RESULTS: Sorafenib increased uPA secretion, which was abrogated by an Akt inhibitor. The growth-inhibitory effect of sorafenib was significantly enhanced by the uPA inhibitors UK122 and amiloride. Sorafenib-induced apoptosis was increased 2.4-fold in uPA siRNA-transduced cells (p<0.05). Combined therapy with sorafenib and amiloride significantly decreased tumor volumes [mean volume: 759 mm3 (sorafenib) vs. 283 mm3 (sorafenib plus amiloride), p<0.05]. CONCLUSION: uPA may play a critical role in sorafenib resistance.

    DOI： 10.21873/anticanres.14816

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  • Changes in disease characteristics of primary biliary cholangitis: An observational retrospective study from 1982 to 2016. Reviewed International journal

    Masaaki Takamura, Yasunobu Matsuda, Naruhiro Kimura, Masafumi Takatsuna, Toru Setsu, Atsunori Tsuchiya, Akihiko Osaki, Nobuo Waguri, Masahiko Yanagi, Toru Takahashi, Soichi Sugitani, Yuka Kobayashi, Akira Yoshikawa, Toru Ishikawa, Toshiaki Yoshida, Toshiaki Watanabe, Hitoshi Bannai, Tomoyuki Kubota, Kazuhiro Funakoshi, Hiroto Wakabayashi, So Kurita, Norio Ogata, Masashi Watanabe, Yuhsaku Mita, Shigeki Mori, Motoya Sugiyama, Toru Miyajima, Sumio Takahashi, Shuichi Sato, Kisei Ishizuka, Hironobu Ohta, Yutaka Aoyagi, Shuji Terai

    Hepatology research : the official journal of the Japan Society of Hepatology   51 ( 2 )   166 - 175   2021.2

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    AIM: Disease characteristics of primary biliary cholangitis have changed recently. However, detailed studies on the subject have been limited. Therefore, we aimed to clarify disease characteristics of patients with recent primary biliary cholangitis using the cohort from Niigata University and 21 affiliated hospitals. METHODS: Overall, 508 patients were enrolled in this study from 1982 to 2016, divided into three cohorts according to their year of diagnosis: ≤1999, 2000-2009 and ≥2010. We compared differences in clinical characteristics, response to ursodeoxycholic acid and prognosis. RESULTS: The male-to-female ratio increased incrementally from 1:16.4 (≤1999) to 1:3.8 (≥2010) (P < 0.001). In women, the median age at diagnosis increased incrementally from 54.0 years (≤1999) to 60.5 years (≥2010) (P < 0.001) and serum albumin decreased gradually (P = 0.001), which might have affected the increase in the Fibrosis-4 Index and albumin-bilirubin score. The ursodeoxycholic acid response rate according to the Barcelona criteria increased incrementally from 26.7% (≤1999) to 78.4% (≥2010) (P < 0.010), and those according to other criteria (Paris-I, Rotterdam and Toronto) were approximately ≥80% in all cohorts. Ten-year survival rate in the ≤1999 and 2000-2009 cohorts were 98.6% and 95.6%, respectively. These earlier cohorts were also characterized by a higher rate of asymptomatic state and mild histology (83.5% [≤1999] and 84.7% [2000-2009], and 93.6% [≤1999] and 91.1% [2000-2009]). CONCLUSIONS: Patients with primary biliary cholangitis were characterized by older age at diagnosis and an increase in male to female ratio as well as higher response rates of ursodeoxycholic acid and longer survival, resulting from the early recognition of primary biliary cholangitis.

    DOI： 10.1111/hepr.13586

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  • Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer. Reviewed International journal

    Kizuki Yuza, Masayuki Nagahashi, Hiroshi Ichikawa, Takaaki Hanyu, Masato Nakajima, Yoshifumi Shimada, Takashi Ishikawa, Jun Sakata, Shiho Takeuchi, Shujiro Okuda, Yasunobu Matsuda, Manabu Abe, Kenji Sakimura, Kazuaki Takabe, Toshifumi Wakai

    Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract   25 ( 9 )   2231 - 2241   2021.1

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    BACKGROUND: Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. METHODS: An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. RESULTS: ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. CONCLUSIONS: Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors.

    DOI： 10.1007/s11605-020-04889-9

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  • Epidermal growth factor receptor/heme oxygenase-1 axis is involved in chemoresistance to cisplatin and pirarubicin in HepG2 cell lines and hepatoblastoma specimens. Reviewed International journal

    Takashi Kobayashi, Masayuki Kubota, Yoshiaki Kinoshita, Yuki Arai, Toshiyuki Oyama, Naoki Yokota, Koichi Saito, Yasunobu Matsuda, Mami Osawa

    Pediatric surgery international   35 ( 12 )   1369 - 1378   2019.12

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    PURPOSE: To investigate the possibility that the antioxidant stress protein Heme oxygenase-1 (HO-1) is involved in the acquisition of chemoresistance in cisplatin and pirarubicin (CITA) therapy. METHODS: Human hepatoblastoma-derived cell line (HepG2) was used to generate a knockdown cell line of HO-1 by small interfering RNA (siRNA). Expression of HO-1, epidermal growth factor receptor (EGFR), Akt, and extracellular signal-regulated kinase1/2 (ERK1/2) was examined by Western blot. The cytotoxic effect of cisplatin, pirarubicin, and EGFR inhibitor was examined by trypan blue staining. In human hepatoblastoma specimens (n = 5), changes of HO-1 expression were examined immunohistochemically before and after CITA therapy. RESULTS: HO-1 expression in HepG2 cells was increased by the treatment of cisplatin (CDDP) and pirarubicin (THP) dose-dependently. In HO-1 knockdown HepG2 cells, the HO-1 was not expressed and the percentage of trypan blue-positive cells (dead cells) was significantly increased after treatment of CDDP and THP. The EGFR inhibitor decreased the levels of HO-1, phospho-Akt and phospho-ERK1/2 in HepG2 cells. Combination treatment of EGFR inhibitor with CDDP and THP increased the cytotoxic effect in HepG2 cells. In human hepatoblastoma specimens, 4 of the 5 patients (80%) showed HO-1 expression changed much stronger in the viable tumor cells after CITA therapy. CONCLUSION: The cytotoxic effects of CDDP and THP were both enhanced under HO-1 knockdown conditions as well as under conditions that inhibit the activation pathway of HO-1 by EGFR inhibitors. EGFR/HO-1 axis may be involved in acquiring chemoresistance in HepG2 cell lines as well as in human hepatoblastoma.

    DOI： 10.1007/s00383-019-04563-5

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  • Overexpression of a disintegrin and metalloproteinase 21 is associated with motility, metastasis, and poor prognosis in hepatocellular carcinoma. Reviewed International journal

    Hiroki Honda, Masaaki Takamura, Satoshi Yamagiwa, Takuya Genda, Ryoko Horigome, Naruhiro Kimura, Toru Setsu, Kentaro Tominaga, Hiroteru Kamimura, Yasunobu Matsuda, Toshifumi Wakai, Yutaka Aoyagi, Shuji Terai

    Scientific reports   7 ( 1 )   15485 - 15485   2017.11

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    DOI： 10.1038/s41598-017-15800-z

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  • Clinical significance of NQO1 expression in KRAS wild-type colorectal cancer Reviewed

    Hitoshi Kameyama, Yuki Hirose, Yasunobu Matsuda, Masayuki Nagahashi, Hiroshi Ichikawa, You Sato, Saki Yamada, Shinnosuke Hotta, Yosuke Tajima, Takuma Okamura, Mae Nakano, Masato Nakano, Yoshifumi Shimada, Jun Sakata, Takashi Kobayashi, Toshifumi Wakai

    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY   10 ( 5 )   5841 - 5849   2017

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  • Biological significance of a disintegrin and metalloproteinase 21 expression in hepatocellular carcinoma Reviewed

    Masaaki Takamura, Hiroki Honda, Satoshi Yamagiwa, Naruhiro Kimura, Toru Setsu, Kentaro Tominaga, Hiroteru Kamimura, Takuya Genda, Yasunobu Matsuda, Toshifumi Wakai, Shuji Terai

    HEPATOLOGY   64   639A - 639A   2016.10

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  • DNA damage response and sphingolipid signaling in liver diseases. Reviewed

    Masayuki Nagahashi, Yasunobu Matsuda, Kazuki Moro, Junko Tsuchida, Daiki Soma, Yuki Hirose, Takashi Kobayashi, Shin-Ichi Kosugi, Kazuaki Takabe, Masaaki Komatsu, Toshifumi Wakai

    Surgery today   46 ( 9 )   995 - 1005   2016.9

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    DOI： 10.1007/s00595-015-1270-8

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  • Comparison of Number Versus Ratio of Positive Lymph Nodes in the Assessment of Lymph Node Status in Extrahepatic Cholangiocarcinoma. Reviewed International journal

    Jun Sakata, Toshifumi Wakai, Yasunobu Matsuda, Taku Ohashi, Yuki Hirose, Hiroshi Ichikawa, Takashi Kobayashi, Masahiro Minagawa, Shin-Ichi Kosugi, Yu Koyama, Kouhei Akazawa, Yoichi Ajioka

    Annals of surgical oncology   23 ( 1 )   225 - 34   2016.1

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    DOI： 10.1245/s10434-015-4609-x

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  • Clinical significance of MED12 expression in colorectal cancer Reviewed

    Yoshifumi Shimada, Yosuke Tajima, Hitoshi Kameyama, Ryoma Yagi, Takuma Okamura, Yuki Hirose, Jun Sakata, Takashi Kobayashi, Yasunobu Matsuda, Yoichi Ajioka, Shin-ichi Kosugi, Toshifumi Wakai

    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY   9 ( 7 )   6937 - 6944   2016

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  • Prognostic significance of NQO1 expression in esophageal squamous cell carcinoma after preoperative chemotherapy with cisplatin and 5-fluorouracil followed by curative esophagectomy Reviewed

    Hiroshi Ichikawa, Shin-ichi Kosugi, Yuki Hirose, Yasunobu Matsuda, Takashi Ishikawa, Takaaki Hanyu, Kenji Usui, Yusuke Muneoka, Masayuki Nagahashi, Jun Sakata, Takashi Kobayashi, Hitoshi Kameyama, Toshifumi Wakai

    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY   9 ( 7 )   7393 - 7401   2016

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  • Oncogenic role of p21 in hepatocarcinogenesis suggests a new treatment strategy. Reviewed International journal

    Shogo Ohkoshi, Masahiko Yano, Yasunobu Matsuda

    World journal of gastroenterology   21 ( 42 )   12150 - 6   2015.11

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    DOI： 10.3748/wjg.v21.i42.12150

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  • Increase of fucosylated alpha-fetoprotein fraction at the onset of autoimmune hepatitis and acute liver failure. Reviewed International journal

    Satoshi Yamagiwa, Yasushi Tamura, Masaaki Takamura, Takuya Genda, Takafumi Ichida, Toru Ishikawa, Tomoteru Kamimura, Toru Takahashi, Takeshi Suda, Yasunobu Matsuda, Minoru Nomoto, Yutaka Aoyagi

    Hepatology research : the official journal of the Japan Society of Hepatology   44 ( 14 )   E368-75 - E375   2014.12

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    DOI： 10.1111/hepr.12318

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  • Imbalance between CD56+bright and CD56+dim natural killer cell subsets in the liver of patients with recurrent hepatitis C after liver transplantation. Reviewed

    Satoshi Yamagiwa, Yoshinobu Sato, Takafumi Ichida, Toru Setsu, Kentaro Tominaga, Hiroteru Kamimura, Atsunori Tsuchiya, Masaaki Takamura, Yasunobu Matsuda, Yutaka Aoyagi

    Biomedical research (Tokyo, Japan)   35 ( 3 )   177 - 84   2014.6

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  • Valproic acid overcomes transforming growth factor-β-mediated sorafenib resistance in hepatocellular carcinoma. Reviewed International journal

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Yuki Hirose, Jun Sakata, Takashi Kobayashi, Shun Fujimaki, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi

    International journal of clinical and experimental pathology   7 ( 4 )   1299 - 313   2014

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  • Sphingosine-1-phosphate transporters as targets for cancer therapy. Reviewed International journal

    Masayuki Nagahashi, Kazuaki Takabe, Krista P Terracina, Daiki Soma, Yuki Hirose, Takashi Kobayashi, Yasunobu Matsuda, Toshifumi Wakai

    BioMed research international   2014   651727 - 651727   2014

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    DOI： 10.1155/2014/651727

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  • Alcoholic liver disease complicated by deep bleeding into the muscles or retroperitoneum: report of three cases and a review of the literature. Reviewed

    Masaaki Takamura, Jun Watanabe, Akira Sakamaki, Yutaka Honda, Kenya Kamimura, Atsunori Tsuchiya, Satoshi Yamagiwa, Takeshi Suda, Yasunobu Matsuda, Yutaka Aoyagi

    Internal medicine (Tokyo, Japan)   53 ( 16 )   1763 - 8   2014

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    DOI： 10.2169/internalmedicine.53.2123

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  • Hepatitis B virus X stimulates redox signaling through activation of ataxia telangiectasia mutated kinase. Reviewed International journal

    Yasunobu Matsuda, Ayumi Sanpei, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Yuki Hirose, Jun Sakata, Takashi Kobayashi, Shun Fujimaki, Masaaki Takamura, Satoshi Yamagiwa, Masahiko Yano, Shogo Ohkoshi, Yutaka Aoyagi

    International journal of clinical and experimental pathology   7 ( 5 )   2032 - 43   2014

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  • Effects of rapamycin on granulation formation in response to centrally doubled coiled stents as a tracheal substitute. Reviewed International journal

    Masayuki Kubota, Yasunobu Matsuda, Shun Fujimaki, Mami Osawa, Toshifumi Wakai, Kengo Nakaya

    Journal of pediatric surgery   48 ( 12 )   2416 - 24   2013.12

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    DOI： 10.1016/j.jpedsurg.2013.08.013

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  • Clinical significance of cell cycle inhibitors in hepatocellular carcinoma. Reviewed

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi, Mami Osawa, Shun Fujimaki, Ayumi Sanpei, Takuya Genda, Takafumi Ichida

    Medical molecular morphology   46 ( 4 )   185 - 92   2013.12

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    DOI： 10.1007/s00795-013-0047-7

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  • p27 Is a critical prognostic biomarker in non-alcoholic steatohepatitis-related hepatocellular carcinoma. Reviewed International journal

    Yasunobu Matsuda, Toshifumi Wakai, Yuki Hirose, Mami Osawa, Shun Fujimaki, Masayuki Kubota

    International journal of molecular sciences   14 ( 12 )   23499 - 515   2013.11

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    DOI： 10.3390/ijms141223499

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  • Hepatitis B virus X induces cell proliferation in the hepatocarcinogenesis via up-regulation of cytoplasmic p21 expression Reviewed

    Masahiko Yano, Shogo Ohkoshi, Yo-Hei Aoki, Hiromichi Takahashi, Sou Kurita, Kazuhide Yamazaki, Kenta Suzuki, Satoshi Yamagiwa, Ayumi Sanpei, Shun Fujimaki, Toshifumi Wakai, Shin-Ei Kudo, Yasunobu Matsuda, Yutaka Aoyagi

    Liver International   33 ( 8 )   1218 - 1229   2013.9

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    DOI： 10.1111/liv.12176

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  • Mycotoxins are conventional and novel risk biomarkers for hepatocellular carcinoma. Reviewed International journal

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Ayumi Sanpei, Shun Fujimaki

    World journal of gastroenterology   19 ( 17 )   2587 - 90   2013.5

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    DOI： 10.3748/wjg.v19.i17.2587

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  • Involvement of liver-intestine cadherin in cancer progression. Reviewed

    Takamura M, Yamagiwa S, Matsuda Y, Ichida T, Aoyagi Y

    Medical Molecular Morphology   46 ( 1 )   1 - 7   2013.3

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    DOI： 10.1007/s00795-012-0003-y

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  • Risk of subsequent biliary malignancy in patients undergoing cyst excision for congenital choledochal cysts Reviewed

    Taku Ohashi, Toshifumi Wakai, Masayuki Kubota, Yasunobu Matsuda, Yuhki Arai, Toshiyuki Ohyama, Kengo Nakaya, Naoki Okuyama, Jun Sakata, Yoshio Shirai, Yoichi Ajioka

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   28 ( 2 )   243 - 247   2013.2

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    DOI： 10.1111/j.1440-1746.2012.07260.x

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  • Involvement of liver-intestine cadherin in cancer progression Reviewed

    Masaaki Takamura, Satoshi Yamagiwa, Yasunobu Matsuda, Takafumi Ichida, Yutaka Aoyagi

    Medical Molecular Morphology   46 ( 1 )   1 - 7   2013

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    DOI： 10.1007/s00795-012-0003-y

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  • p21-activated kinase-2 is a critical mediator of transforming growth factor-β-induced hepatoma cell migration Reviewed

    Munehiro Sato, Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Shun Fujimaki, Ayumi Sanpei, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi

    Journal of Gastroenterology and Hepatology (Australia)   28 ( 6 )   1047 - 1055   2013

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Blackwell Publishing  

    DOI： 10.1111/jgh.12150

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  • DNA damage sensor γ-H2AX is increased in preneoplastic lesions of hepatocellular carcinoma Reviewed

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi, Ayumi Sanpei, Shun Fujimaki

    The Scientific World Journal   2013   597095 - 597095   2013

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    DOI： 10.1155/2013/597095

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  • Risk of subsequent biliary malignancy in patients undergoing cyst excision for congenital choledochal cysts Reviewed

    Taku Ohashi, Toshifumi Wakai, Masayuki Kubota, Yasunobu Matsuda, Yuhki Arai, Toshiyuki Ohyama, Kengo Nakaya, Naoki Okuyama, Jun Sakata, Yoshio Shirai, Yoichi Ajioka

    Journal of Gastroenterology and Hepatology (Australia)   28 ( 2 )   243 - 247   2013

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    DOI： 10.1111/j.1440-1746.2012.07260.x

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  • Blockade of ataxia telangiectasia mutated sensitizes hepatoma cell lines to sorafenib by interfering with Akt signaling Reviewed

    Shun Fujimaki, Yasunobu Matsuda, Toshifumi Wakai, Ayumi Sanpei, Masayuki Kubota, Masaaki Takamura, Satoshi Yamagiwa, Masahiko Yano, Shogo Ohkoshi, Yutaka Aoyagi

    Cancer Letters   319 ( 1 )   98 - 108   2012.6

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  • Plasma cells and the chronic nonsuppurative destructive cholangitis of primary biliary cirrhosis Reviewed

    Toru Takahashi, Tomofumi Miura, Junichiro Nakamura, Satoshi Yamada, Tsutomu Miura, Masahiko Yanagi, Yasunobu Matsuda, Hiroyuki Usuda, Iwao Emura, Koichi Tsuneyama, Xiao-Song He, M. Eric Gershwin

    Hepatology   55 ( 3 )   846 - 855   2012.3

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  • Reduced NKG2D ligand expression in hepatocellular carcinoma correlates with early recurrence. Invited

    Kamimura Hiroteru, Yamagiwa Satoshi, Tsuchiya Atsunori, Takamura Masaaki, Matsuda Yasunobu, Ohkoshi Shogo, Inoue Makoto, Wakai Toshifumi, Shirai Yoshio, Nomoto Minoru, Aoyagi Yutaka

    J Hepatol   56 ( 2 )   381 - 388   2012.2

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    BACKGROUND &amp; AIMS: The activating receptor natural killer group 2, member D (NKG2D) and its ligands play a crucial role in immune response to tumors. NKG2D ligand expression in tumors has been shown to be associated with tumor eradication and superior patient survival, but the involvement of NKG2D ligands in the immune response against hepatocellular carcinoma (HCC) still remains to be elucidated. METHODS: We investigated the expression of NKG2D ligands in HCC tissues collected from 54 patients and HCC cell lines. We also examined the proteasome expression and the effect of inhibition of proteasome activity on NKG2D ligand expression in HCC tissues and cell lines. RESULTS: In dysplastic nodules (DN), well-differentiated (well-HCC), and moderately-differentiated HCCs (mod-HCC), UL16-binding protein (ULBP) 1 was expressed predominantly in tumor cells, but not in poorly-differentiated HCCs (poor-HCC). Remarkably, recurrence-free survival of patients with ULBP1-negative HCC was significantly shorter than that of patients with ULBP1-positive HCC (p=0.006). Cox regression analysis revealed that loss of ULBP1 expression was an independent predictor of early recurrence (p=0.008). We c

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  • Reduced NKG2D ligand expression in hepatocellular carcinoma correlates with early recurrence Reviewed

    Hiroteru Kamimura, Satoshi Yamagiwa, Atsunori Tsuchiya, Masaaki Takamura, Yasunobu Matsuda, Shogo Ohkoshi, Makoto Inoue, Toshifumi Wakai, Yoshio Shirai, Minoru Nomoto, Yutaka Aoyagi

    JOURNAL OF HEPATOLOGY   56 ( 2 )   381 - 388   2012.2

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  • Sorafenib: Complexities of Raf-dependent and Raf-independent signaling are now unveiled Reviewed

    Yasunobu Matsuda, Manabu Fukumoto

    Medical Molecular Morphology   44 ( 4 )   183 - 189   2011.12

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  • REDUCED NKG2D LIGAND EXPRESSION IN HEPATOCELLULAR CARCINOMA CORRELATES WITH EARLY RECURRENCE Reviewed

    Satoshi Yamagiwa, Hiroteru Kamimura, Atsunori Tsuchiya, Masaaki Takamura, Yasunobu Matsuda, Yoshio Shirai, Yutaka Aoyagi

    HEPATOLOGY   54   1100A - 1101A   2011.10

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  • Ribonucleotide Reductase M1 Expression in Intrahepatic Cholangiocarcinoma Reviewed

    Toshifumi Wakai, Yoshio Shirai, Jun Sakata, Masaaki Takamura, Yasunobu Matsuda, Pavel V. Korita, Katsuki Muneoka, Masataka Sasaki, Yoichi Ajioka, Katsuyoshi Hatakeyama

    HEPATO-GASTROENTEROLOGY   58 ( 110 )   1659 - 1663   2011.9

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  • Hepatocellular carcinoma and liver transplantation: Clinical perspective on molecular targeted strategies Reviewed

    Yasunobu Matsuda, Takafumi Ichida, Manabu Fukumoto

    Medical Molecular Morphology   44 ( 3 )   117 - 124   2011.9

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  • Failure to Achieve 2-log(10) Viral Decrease in First Four Weeks of Peg-IFN alpha-2b Plus Ribavirin Therapy for Chronic Hepatitis C with Genotype 1b and High Viral Titer is Useful in Predicting Non-response: Evaluation of Response-guided Therapy Reviewed

    Shogo Ohkoshi, Satoshi Yamagiwa, Masahiko Yano, Hiromichi Takahashi, Yoh-hei Aoki, Nobuo Waguri, Kentaro Igarashi, Soh-ichi Sugitani, Tohru Takahashi, Tohru Ishikawa, Tomoteru Kamimura, Hiroto Wakabayashi, Toshiaki Watanabe, Yasunobu Matsuda, Yutaka Aoyagi

    HEPATO-GASTROENTEROLOGY   58 ( 107 )   965 - 970   2011.5

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  • Alteration of p53-binding protein 1 expression as a risk factor for local recurrence in patients undergoing resection for extrahepatic cholangiocarcinoma. Reviewed

    Wakai Toshifumi, Shirai Yoshio, Sakata Jun, Korita Pavel V, Matsuda Yasunobu, Takamura Masaaki, Ohashi Riuko, Nagahashi Masayuki, Ajioka Yoichi, Hatakeyama Katsuyoshi

    Int J Oncol   38 ( 5 )   1227 - 1236   2011.5

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    P53-binding protein 1 (53BP1) is an early DNA damage response-protein that is rapidly recruited to sites of DNA double-strand breaks. The presence of 53BP1 nuclear foci can be considered as a cytologic marker for endogenous double-strand breaks reflecting genomic instability. This study aimed to clarify the early DNA damage response mediated by 53BP1 in tumor specimens of ductal resection margins and to elucidate its predictive value for clinically evident local recurrence at ductal stumps in 110 patients undergoing resection for extrahepatic cholangiocarcinoma. The ductal resection margin status was classified as negative (85 patients), positive with carcinoma in situ (14 patients), or positive with invasive carcinoma (11 patients). The nuclear staining pattern of 53BP1 was evaluated by immunofluorescence. TUNEL analysis was used to calculate apoptotic index. Ductal margin status was the only independent risk factor for local recurrence (P=0.001). The cumulative probability of local recurrence at 5 years was 10%, 40% and 100% in patients with negative ductal margins, positive with carcinoma in situ and positive with invasive carcinoma, respectively (P&lt;0.001). Of the 14 tumor

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  • A case with chronic hepatitis C who developed liver cirrhosis due to liver dysfunction caused by pegylated interferon plus ribavirin treatment despite negativity of serum HCV RNA, during therapy

    Shogo Ohkoshi, Shin-Ichi Morita, Yukari Tanaka, Masahiko Yano, Manabu Takeuchi, Hiromichi Takahashi, Haruo Ikeda, Satoshi Yamagiwa, Yasunobu Matsuda, Minoru Nomoto, Yutaka Aoyagi

    Journal of Japanese Society of Gastroenterology   108 ( 2 )   267 - 274   2011.2

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  • Characterization of elevated alanine aminotransferase levels during pegylated-interferon alpha-2b plus ribavirin treatment for chronic hepatitis C Reviewed

    Yo-hei Aoki, Shogo Ohkoshi, Satoshi Yamagiwa, Masahiko Yano, Hiromichi Takahashi, Nobuo Waguri, Kentaro Igarashi, Soh-ichi Sugitani, Toru Takahashi, Toru Ishikawa, Tomoteru Kamimura, Hiroto Wakabayashi, Toshiaki Watanabe, Yasunobu Matsuda, Minoru Nomoto, Yutaka Aoyagi

    HEPATOLOGY RESEARCH   41 ( 2 )   118 - 125   2011.2

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  • Multicentric occurrence of hepatocellular carcinoma with nonalcoholic steatohepatitis Reviewed

    Hirokazu Kawai, Minoru Nomoto, Takeshi Suda, Kenya Kamimura, Atsunori Tsuchiya, Yasushi Tamura, Masahiko Yano, Masaaki Takamura, Masato Igarashi, Toshifumi Wakai, Satoshi Yamagiwa, Yasunobu Matsuda, Shogo Ohkoshi, Isao Kurosaki, Yoshio Shirai, Masahiko Okada, Yutaka Aoyagi

    World Journal of Hepatology   3 ( 1 )   15 - 23   2011

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  • Prognostic significance of NQO1 expression in intrahepatic cholangiocarcinoma Reviewed

    Toshifumi Wakai, Yoshio Shirai, Jun Sakata, Yasunobu Matsuda, Pavel V. Korita, Masaaki Takamura, Yoichi Ajioka, Katsuyoshi Hatakeyama

    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY   4 ( 4 )   363 - 370   2011

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  • Multidrug resistance-associated protein 2 determines the efficacy of cisplatin in patients with hepatocellular carcinoma Reviewed

    Pavel V. Korita, Toshifumi Wakai, Yoshio Shirai, Yasunobu Matsuda, Jun Sakata, Masaaki Takamura, Masahiko Yano, Ayumi Sanpei, Yutaka Aoyagi, Katsuyoshi Hatakeyama, Yoichi Ajioka

    Oncology Reports   23 ( 4 )   965 - 972   2010.4

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  • Rectal administration of tranilast ameliorated acute colitis in mice through increased expression of heme oxygenase-1: Original Article Reviewed

    Xiaomei Sun, Kenji Suzuki, Masaki Nagata, Yusuke Kawauchi, Masahiko Yano, Shogo Ohkoshi, Yasunobu Matsuda, Hiroshi Kawachi, Kenichi Watanabe, Hitoshi Asakura, Yutaka Aoyagi

    Pathology International   60 ( 2 )   93 - 101   2010.2

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    DOI： 10.1111/j.1440-1827.2009.02490.x

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  • Loss of liver-intestine cadherin in human intrahepatic cholangiocarcinoma promotes angiogenesis by up-regulating metal-responsive transcription factor-1 and placental growth factor Reviewed

    Masaaki Takamura, Satoshi Yamagiwa, Toshifumi Wakai, Yasushi Tamura, Hiroteru Kamimura, Takashi Kato, Atsunori Tsuchiya, Yasunobu Matsuda, Yoshio Shirai, Takafumi Ichida, Yoichi Ajioka, Yutaka Aoyagi

    International Journal of Oncology   36 ( 1 )   245 - 254   2010.1

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  • Very-low-dose pegylated interferon α2a plus ribavirin therapy for advanced liver cirrhosis type C: A possible therapeutic alternative without splenic intervention Reviewed

    Shogo Ohkoshi, Satoshi Yamagiwa, Masahiko Yano, Hiromichi Takahashi, Yo-Hei Aoki, Yasunobu Matsuda, Yutaka Aoyagi

    Case Reports in Gastroenterology   4 ( 2 )   261 - 266   2010

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  • Clinicopathological analysis of CD133+and NCAM+ human hepatic stem/progenitor cells in damaged livers and hepatocellular carcinomas Reviewed

    Atsunori Tsuchiya, Hiroteru Kamimura, Masaaki Takamura, Satoshi Yamagiwa, Yasunobu Matsuda, Yoshinobu Sato, Minoru Nomoto, Takafumi Ichida, Yutaka Aoyagi

    HEPATOLOGY RESEARCH   39 ( 11 )   1080 - 1090   2009.11

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  • Impact of hepatitis B virus X protein on the DNA damage response during hepatocarcinogenesis Reviewed

    Yasunobu Matsuda, Takafumi Ichida

    Medical Molecular Morphology   42 ( 3 )   138 - 142   2009.9

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  • Loss of carcinoembryonic antigen-related cell adhesion molecule 1 expression predicts metachronous pulmonary metastasis and poor survival in patients with hepatoblastoma. Reviewed

    Tsukada Mami, Wakai Toshifumi, Matsuda Yasunobu, Korita Pavel V, Shirai Yoshio, Ajioka Yoichi, Hatakeyama Katsuyoshi, Kubota Masayuki

    J Pediatr Surg   44 ( 8 )   1522 - 1528   2009.8

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    PURPOSE: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a member of the carcinoembryonic antigen family of immunoglobulin-like adhesion molecules. The aim of this study was to test the hypothesis that loss of CEACAM1 expression in hepatoblastoma cells may promote hematogeneous metastasis and function as an adverse prognostic factor. METHODS: Immunohistochemical expression of CEACAM1 in surgically resected specimens from 19 patients with hepatoblastoma was examined retrospectively. The CEACAM1 expression in the epithelial area of the tumor was classified into 2 categories as follows: diffuse expression, characterized by positive staining throughout the tumor specimen, or loss of expression, in which there were distinct areas of negative staining within the tumor specimen. RESULTS: Of the 19 patients, 12 were classified as having tumors with diffuse expression, and 7 had loss-of-expression tumors. Survival after treatment was significantly worse in patients with tumors with loss of CEACAM1 expression (cumulative 5-year survival rate, 29%) than in patients with diffuse CEACAM1 expression (cumulative 5-year survival rate, 92%; P = .0062). Loss of CEACAM1 expr

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  • Blockade of Endogenous CD26 Activity Augments the Therapeutic Potential of Marrow Stem Cells for Mouse Liver Cirrhosis Reviewed

    Matsuda Yasunobu, Sanpei Ayumi, Wakai Toshifumi, Shirai Yoshio, Yano Masahiko, Sun Xiaomei, Tsuchiya Atsunori, Takamura Masaaki, Yamagiwa Satoshi, Suzuki Kenji, Ohkoshi Shogo, Suzuki Yutaka, Aoyagi Yutaka

    GASTROENTEROLOGY   136 ( 5 )   A817   2009.5

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  • Progression of hypermethylation of the p16(INK4A) gene from normal liver to nontumorous liver and hepatocellular carcinoma: an evaluation using quantitative PCR analysis. Reviewed

    Kurita So, Ohkoshi Shogo, Yano Masahiko, Yamazaki Kazuhide, Suzuki Kenta, Aoki Yo-hei, Matsuda Yasunobu, Wakai Toshifumi, Shirai Yoshio, Ichida Takafumi, Aoyagi Yutaka

    Dig Dis Sci   54 ( 1 )   80 - 88   2009.1

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    The aim of this study was to determine to what extent hypermethylation of the p16(INK4A) (p16) gene promoter is increased in nontumorous liver tissues compared with in normal liver, using two quantitative methylation-specific polymerase chain reaction (MS-PCR) methods and a bisulfite sequencing method. Methylation of the p16 gene was detected more frequently in nontumorous liver than in normal liver using the TaqMan PCR method. Methylation indices also were significantly higher in nontumorous than in normal liver. However, the bisulfite sequencing method did not detect significantly more methylation of the p16 gene in nontumorous than normal liver, nor was there a significant difference in the level of p16 mRNA. There may be a greater proportion of cells which contain methylated p16 in nontumorous than in normal liver. However, the difference was so small that the functional relevance to hepatocarcinogenesis remains elusive.

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  • A case of extra-hepatic lymph node metastasis of hepatocellular carcinoma with no evident sign of intra-hepatic recurrence

    Shinichi Morita, Yasunobu Matsuda, Tomoko Oshima, Tomoyuki Kubota, Yusuke Kawauchi, Makoto Kobayashi, Minoru Nomoto, Yutaka Aoyagi

    Journal of Japanese Society of Gastroenterology   106 ( 3 )   397 - 404   2009

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  • Successful Treatment in a Case of Massive Hepatocellular Carcinoma with Paraneoplastic Syndrome. Reviewed

    Tsuchiya Atsunori, Kubota Tomoyuki, Takizawa Kazuyoshi, Yamada Kazuki, Wakai Toshifumi, Matsuda Yasunobu, Honma Terasu, Watanabe Masashi, Shirai Yoshio, Maruyama Hiroki, Nomoto Minoru, Aoyagi Yutaka

    Case Rep Gastroenterol   3 ( 1 )   105 - 110   2009

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    Paraneoplastic syndromes of hepatocellular carcinoma (HCC) are not uncommon. However, the prognosis is poor and follow-up and improvement of paraneoplastic syndromes with treatment have been reported rarely. We report a successful case in an aged man of a massive HCC with paraneoplastic syndrome, treated by combined intraarterial chemotherapy and hepatic resection. Paraneoplastic syndrome (erythrocytosis and hyperlipidemia) was monitored throughout the treatment and erythropoietin (EPO) mRNA also was analyzed in the resected liver. The hemoglobin level and serum levels of EPO and total cholesterol (T-cho) decreased dramatically with treatment, along with a decrease in serum levels of alpha-fetoprotein and protein induced by vitamin vitamin K absence II (PIVKA-II). Semiquantitative reverse transcription polymerase chain reaction (RT-PCR) revealed that the residual cancer expressed EPO RNA but the nontumor tissue did not. This was a rare case of paraneoplastic syndrome of HCC that was treated successfully. This case indicates that paraneoplastic syndrome reflected tumor progression and that serum levels of both EPO and T-cho might be used as tumor markers.

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  • Overexpression of osteopontin independently correlates with vascular invasion and poor prognosis in patients with hepatocellular carcinoma. Reviewed

    Korita Pavel V, Wakai Toshifumi, Shirai Yoshio, Matsuda Yasunobu, Sakata Jun, Cui Xing, Ajioka Yoichi, Hatakeyama Katsuyoshi

    Hum Pathol   39 ( 12 )   1777 - 1783   2008.12

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    This study retrospectively evaluated the immunohistochemical expression of 3 cell adhesion molecules (CAMs), E-cadherin, beta-catenin, and osteopontin, according to tumor grade in 125 surgically resected specimens of hepatocellular carcinoma (HCC). The aims of this study were to identify factors associated with vascular invasion and to elucidate the prognostic value of CAMs. The median follow-up time was 110 months. The levels of E-cadherin, beta-catenin, and osteopontin immunoreactivity were significantly associated with Edmondson-Steiner grade but not with tumor size. There was increased loss of E-cadherin, nonnuclear overexpression of beta-catenin, and overexpression of osteopontin in tumors of higher histologic grade. Vascular invasion was found in 44 (35%) of 125 resected specimens. Logistic regression analysis identified 3 tumor-related factors that were independently associated with vascular invasion-tumor size more than 3 cm, Edmondson-Steiner grades III to IV, and overexpression of osteopontin. Among the tested CAMs, osteopontin (P = .0110) and E-cadherin (P = .0287) were significant prognostic factors by univariate analysis. The Cox proportional hazard regression analy

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  • Expression of liver-intestine cadherin in intrahepatic cholangiocarcinoma: Its prognostic significance and relationship to vascular invasion Reviewed

    Takamura M, Tamura Y, Wakai T, Yamagiwa S, Kato T, Tsuchiya A, Matsuda Y, Shirai Y, Ichida T, Ajioka Y, Aoyagi Y

    Hepatology (supplement)   48 ( S1 )   945A - 945A   2008.10

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  • THE BALANCE BETWEEN CD56(+BRIGHT) AND CD56(+DlM) NATURAL KILLER CELL SUBSETS IN THE LIVER OF PATIENTS WITH RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION Reviewed

    Yamagiwa Satoshi, Kamimura Hiroteru, Tsuchiya Atsunori, Takamura Masaaki, Matsuda Yasunobu, Sato Yoshinobu, Ichida Takafumi, Aoyagi Yutaka

    HEPATOLOGY   48 ( 4 )   769A - 770A   2008.10

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  • Successful treatment with lamivudine may correlate with reduction of serum ferritin levels in the patients with chronic hepatitis and liver cirrhosis type B Reviewed

    Shogo Ohkoshi, Akira Yoshimura, Satoshi Yamamoto, Masahiko Yano, So Kurita, Kazuhide Yamazaki, Yo-hei Aoki, Satoshi Yamagiwa, Hiroto Wakabayashi, Motoya Sugiyama, Tohru Takahashi, Tohru Ishikawa, Yasunobu Matsuda, Takafumi Ichida, Tomoteru Kamimura, Yutaka Aoyagi

    HEPATOLOGY INTERNATIONAL   2 ( 3 )   382 - 387   2008.9

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  • Sustained response to interferon-alpha plus ribavirin therapy for chronic hepatitis C is closely associated with increased dynamism of intrahepatic natural killer and natural killer T cells Reviewed

    Satoshi Yamagiwa, Yasunobu Matsuda, Takafumi Ichida, Yutaka Honda, Masaaki Takamura, Satoshi Sugahara, Toru Ishikawa, Shogo Ohkoshi, Yoshinobu Sato, Yutaka Aoyagi

    HEPATOLOGY RESEARCH   38 ( 7 )   664 - 672   2008.7

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  • Molecular mechanism underlying the functional loss of cyclindependent kinase inhibitors p16 and p27 in hepatocellular carcinoma Reviewed

    Yasunobu Matsuda

    WORLD JOURNAL OF GASTROENTEROLOGY   14 ( 11 )   1734 - 1740   2008.3

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  • Temporal treatment with interferon-beta prevents hepatocellular carcinoma in hepatitis B virus X gene transgenic mice Reviewed

    Kazuhide Yamazaki, Kenta Suzuki, Shogo Ohkoshi, Masahiko Yano, So Kurita, Yo-Hei Aoki, Ken Toba, Masa-aki Takamura, Satoshi Yamagiwa, Yasunobu Matsuda, Yutaka Aoyagi

    JOURNAL OF HEPATOLOGY   48 ( 2 )   255 - 265   2008.2

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  • Sca-1+ endothelial cells (SPECs) reside in the portal area of the liver and contribute to rapid recovery from acute liver disease Reviewed

    A. Tsuchiya, T. Heike, S. Baba, H. Fujino, K. Umeda, Y. Matsuda, M. Nomoto, T. Ichida, Y. Aoyagi, T. Nakahata

    Biochemical and Biophysical Research Communications   365 ( 3 )   595 - 601   2008.1

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  • Altered expression of TLR homolog RP105 on monocytes hypersensitive to LPS in patients with primary biliary cirrhosis Reviewed

    Yutaka Honda, Satoshi Yamagiwa, Yasunobu Matsuda, Masaaki Takamura, Takafumi Ichida, Yutaka Aoyagi

    JOURNAL OF HEPATOLOGY   47 ( 3 )   404 - 411   2007.9

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  • Tumor suppressor carcinoembryonic antigen-related cell adhesion molecule 1 potentates the anchorage-independent growth of human hepatoma HepG2 cells Reviewed

    Mariko Hokari, Yasunobu Matsuda, Toshifumi Wakai, Yoshio Shirai, Munehiro Sato, Atsunori Tsuchiya, Masaaki Takamura, Satoshi Yamagiwa, Kenji Suzuki, Shogo Ohkoshi, Takafumi Ichida, Hiroshi Kawachi, Yutaka Aoyagi

    LIFE SCIENCES   81 ( 4 )   336 - 345   2007.7

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  • Early upsurge in anti-HBs titer possibly caused by the immunomodulative, not by the mutagenetic effect of interferon and ribavirin Reviewed

    Kazuhide Yamazaki, Shogo Ohkoshi, Masaki Maruyama, Yo-hei Aoki, Masahiko Yano, So Kurita, Kenta Suzuki, Yasunobu Matsuda, Kazuhito Sugimura, Yutaka Aoyagi

    HEPATOLOGY RESEARCH   37 ( 6 )   477 - 481   2007.6

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  • An inhibitor of c-Jun NH2-terminal kinase, SP600125, protects mice from D-galactosamine/lipopolysaccharide-induced hepatic failure by modulating BH3-only proteins Reviewed

    Masaaki Takamura, Yasunobu Matsuda, Satoshi Yamagiwa, Yasushi Tamura, Yutaka Honda, Kenji Suzuki, Takafumi Ichida, Yutaka Aoyagi

    LIFE SCIENCES   80 ( 14 )   1335 - 1344   2007.3

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  • Long-term culture of postnatal mouse hepatic stem/progenitor cells and their relative developmental hierarchy Reviewed

    Atsunori Tsuchiya, Toshio Heike, Shiro Baba, Hisanori Fujino, Katsutsugu Umeda, Yasunobu Matsuda, Minoru Nomoto, Takafumi Ichida, Yutaka Aoyagi, Tatsutoshi Nakahata

    STEM CELLS   25 ( 4 )   895 - 902   2007

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  • p16 and p27 are functionally correlated during the progress of hepatocarcinogenesis Reviewed

    Yasunobu Matsuda, Takafumi Ichida

    MEDICAL MOLECULAR MORPHOLOGY   39 ( 4 )   169 - 175   2006.12

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  • Increase of CD4(+) CD25(+) regulatory T-cells in the liver of patients with hepatocellular carcinoma Reviewed

    Xiu Hua Yang, Satoshi Yamagiwa, Takafumi Ichida, Yasunobu Matsuda, Satoshi Sugahara, Hisami Watanabe, Yoshinobu Sato, Toru Abo, David A. Horwitz, Yutaka Aoyagi

    JOURNAL OF HEPATOLOGY   45 ( 2 )   254 - 262   2006.8

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    DOI： 10.1016/j.jhep.2006.01.036

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  • MEK/ERK signaling is a critical mediator for integrin-induced cell scattering in highly metastatic hepatocellular carcinoma cells Reviewed

    N Honma, T Genda, Y Matsuda, S Yamagiwa, M Takamura, T Ichida, Y Aoyagi

    LABORATORY INVESTIGATION   86 ( 7 )   687 - 696   2006.7

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    DOI： 10.1038/labinvest.3700427

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  • A primary follicular lymphoma of the duodenum treated successfully with radiation therapy Reviewed

    Masaaki Takamura, Rintaro Narisawa, Yudzuru Maruyama, Junji Yokoyama, Yasuo Fukuhara, Hirokazu Kawai, Satoshi Yamagiwa, Yuichi Sato, Yasunobu Matsuda, Kazuhito Sugimura, Takafumi Ichida, Yutaka Aoyagi

    Internal Medicine   45 ( 5 )   309 - 311   2006.4

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    DOI： 10.2169/internalmedicine.45.1464

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  • Long-term outcomes of hepatectomy vs percutaneous ablation for treatment of hepatocellular carcinoma &lt;= 4 cm Reviewed

    Toshifumi Wakai, Yoshio Shirai, Takeshi Suda, Naoyuki Yokoyama, Jun Sakata, Pauldion V. Cruz, Hirokazu Kawai, Yasunobu Matsuda, Masashi Watanabe, Yutaka Aoyagi, Katsuyoshi Hatakeyama

    WORLD JOURNAL OF GASTROENTEROLOGY   12 ( 4 )   546 - 552   2006.1

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  • Overexpressed Id-1 is associated with a high risk of hepatocellular carcinoma development in patients with cirrhosis without transcriptional repression of p16 Reviewed

    Y Matsuda, S Yamagiwa, M Takamura, Y Honda, Y Ishimoto, T Ichida, Y Aoyagi

    CANCER   104 ( 5 )   1037 - 1044   2005.9

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    DOI： 10.1002/cncr.21259

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  • Long-term extensive expansion of mouse hepatic stem/progenitor cells in a novel serum-free culture system Reviewed

    Atsunori Tsuchiya, Toshio Heike, Hisanori Fujino, Mitsutaka Shiota, Katsutsugu Umeda, Momoko Yoshimoto, Yasunobu Matsuda, Takafumi Ichida, Yutaka Aoyagi, Tatsutoshi Nakahata

    Gastroenterology   128 ( 7 )   2089 - 2104   2005.6

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    DOI： 10.1053/j.gastro.2005.03.030

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  • Complete disappearance of pulmonary metastases in a case of hepatocellular carcinoma treated with docetaxel-based systemic chemotherapy Reviewed

    T Ishikawa, T Ichida, J Yokoyama, Y Matsuda, T Watanabe, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   19 ( 12 )   1423 - 1426   2004.12

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    DOI： 10.1111/j.1400-1746.2004.03737.x

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  • A case of hepatocellular carcinoma on the liver surface successfully treated by laparoscopic radiofrequency ablation using a sector ultrasonic probe

    Masahiko Yano, Yasunobu Matsuda, Takayoshi Miura, Tomoko Ohshima, Yasuo Fukuhara, Nobuyuki Honma, Makoto Kobayashi, Masato Ikarashi, Takuya Genda, Nobuo Waguri, Hirokazu Kawai, Satoshi Yamagiwa, Yutaka Aoyagi

    Endoscopic Forum for Digestive Disease   20 ( 2 )   151 - 157   2004.11

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  • Overexpression of extracellular signal-regulated protein kinase and its correlation with proliferation in human hepatocellular carcinoma Reviewed

    Y Tsuboi, T Ichida, S Sugitani, T Genda, J Inayoshi, M Takamura, Y Matsuda, M Nomoto, Y Aoyagi

    LIVER INTERNATIONAL   24 ( 5 )   432 - 436   2004.10

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    DOI： 10.1111/j.1478-3231.2004.0940.x

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  • Reduced expression of liver-intestine cadherin is associated with progression and lymph node metastasis of human colorectal carcinoma Reviewed

    M Takamura, T Ichida, Y Matsuda, M Kobayashi, S Yamagiwa, T Genda, K Shioji, S Hashimoto, M Nomoto, K Hatakeyama, Y Ajioka, M Sakamoto, S Hirohashi, Y Aoyagi

    CANCER LETTERS   212 ( 2 )   253 - 259   2004.8

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    DOI： 10.1016/j.canlet.2004.03.016

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  • Recurrence of hepatocellular carcinoma 102 months after successful eradication and removal of membranous obstruction of the inferior vena cava Reviewed

    M Takamura, T Ichida, J Yokoyama, Y Matsuda, M Nomoto, Y Aoyagi

    JOURNAL OF GASTROENTEROLOGY   39 ( 7 )   681 - 684   2004.7

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    DOI： 10.1007/s535-004-1365-2

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  • Loss of p16 contributes to p27 sequestration by cyclin D-1-cyclindependent kinase 4 complexes and poor prognosis in hepatocellular carcinoma Reviewed

    Y Matsuda, T Ichida, T Genda, S Yamagiwa, Y Aoyagi, H Asakura

    CLINICAL CANCER RESEARCH   9 ( 9 )   3389 - 3396   2003.8

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  • Association between K469E allele of intercellular adhesion molecule 1 gene and inflammatory bowel disease in a Japanese population Reviewed

    J Matsuzawa, K Sugimura, Y Matsuda, M Takazoe, K Ishizuka, T Mochizuki, SS Seki, O Yoneyama, H Bannnai, K Suzuki, T Honma, H Asakura

    GUT   52 ( 1 )   75 - 78   2003.1

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    DOI： 10.1136/gut.52.1.75

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  • Thrombopoietin receptor (c-Mpl) is constitutively expressed on platelets of patients with liver cirrhosis, and correlates with its disease progression Reviewed

    T Ishikawa, T Ichida, S Sugahara, S Yamagiwa, Y Matsuda, K Uehara, T Kato, H Miyazaki, H Asakura

    HEPATOLOGY RESEARCH   23 ( 2 )   115 - 121   2002.6

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    DOI： 10.1016/S1386-6346(01)00170-X

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  • Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis Reviewed

    T Ishikawa, T Ichida, Y Matsuda, S Sugitani, M Sugiyama, T Kato, H Miyazaki, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   15 ( 6 )   647 - 653   2000.6

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    DOI： 10.1046/j.1440-1746.2000.02087.x

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  • Nuclear translocation of beta-catenin in colorectal cancer Reviewed

    M Kobayashi, T Honma, Y Matsuda, Y Suzuki, R Narisawa, Y Ajioka, H Asakura

    BRITISH JOURNAL OF CANCER   82 ( 10 )   1689 - 1693   2000.5

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    DOI： 10.1054/bjoc.1999.1112

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  • Interaction between hyaluronan and CD44 in the development of dimethylnitrosamine-induced liver cirrhosis Reviewed

    T Satoh, T Ichida, Y Matsuda, M Sugiyama, K Yonekura, T Ishikawa, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   15 ( 4 )   402 - 411   2000.4

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    DOI： 10.1046/j.1440-1746.2000.02164.x

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  • A case suggestive of primary biliary cirrhosis-autoimmune hepatitis overlap syndrome

    Y. Mita, T. Takahashi, Y. Matsuda, S. Matsui, M. Takimoto, T. Ishikawa, H. Kawai, Y. Tsuboi, N. Waguri, N. Yamada, T. Kuroiwa, K. Uehara, M. Igarashi, J. Inayoshi, K. Watanabe, T. Ichida, Y. Aoyagi, H. Asakura

    Endoscopic Forum for Digestive Disease   16 ( 2 )   158 - 173   2000

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  • p16(INK4) is inactivated by extensive CpG methylation in human hepatocellular carcinoma Reviewed

    Y Matsuda, T Ichida, J Matsuzawa, K Sugimura, H Asakura

    GASTROENTEROLOGY   116 ( 2 )   394 - 400   1999.2

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    DOI： 10.1016/S0016-5085(99)70137-X

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  • Areas of sinusoidal surface hepatocyte nuclear predominance in type C chronic hepatitis Reviewed

    Y Tanaka, T Ichida, M Nomoto, Y Matsuda, H Asakura

    LIVER   18 ( 6 )   383 - 390   1998.12

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  • Reduced expression of thrombopoietin is involved in thrombocytopenia in human and rat liver cirrhosis Reviewed

    T Ishikawa, T Ichida, Y Matsuda, S Sugitani, M Sugiyama, T Kato, H Miyazaki, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   13 ( 9 )   907 - 913   1998.9

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  • Hepatocyte growth factor suppresses the onset of liver cirrhosis and abrogates lethal hepatic dysfunction in rats. Reviewed

    Matsuda Y, Matsumoto K, Ichida T, Nakamura T

    J Biochem   118 ( 3 )   643 - 649   1998.4

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  • Autoantibodies against a 210 kDa glycoprotein of the nuclear pore complex as a prognostic marker in patients with primary biliary cirrhosis Reviewed

    S Itoh, T Ichida, T Yoshida, A Hayakawa, M Uchida, T Tashiro-Itoh, Y Matsuda, K Ishihara, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   13 ( 3 )   257 - 265   1998.3

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  • Expression of activin A is increased in cirrhotic and fibrotic rat livers Reviewed

    M Sugiyama, T Ichida, T Sato, T Ishikawa, Y Matsuda, H Asakura

    GASTROENTEROLOGY   114 ( 3 )   550 - 558   1998.3

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    DOI： 10.1016/S0016-5085(98)70539-6

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  • Selective depletion of neutrophils by a monoclonal antibody, RP-3, suppresses dextran sulphate sodium-induced colitis in rats Reviewed

    M Natsui, K Kawasaki, H Takizawa, SI Hayashi, Y Matsuda, K Sugimura, K Seki, R Narisawa, F Sendo, H Asakura

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   12 ( 12 )   801 - 808   1997.12

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  • Metallothionein expression and concentrations of copper and zinc are associated with tumor differentiation in hepatocellular carcinoma Reviewed

    T Tashiro-Itoh, T Ichida, Y Matsuda, T Satoh, M Sugiyama, Y Tanaka, T Ishikawa, S Itoh, M Nomoto, H Asakura

    LIVER   17 ( 6 )   300 - 306   1997.12

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  • Preventive and therapeutic effects in rats of hepatocyte growth factor infusion on liver fibrosis/cirrhosis Reviewed

    Yasunobu Matsuda, Kunio Matsumoto, Akira Yamada, Takafumi Ichida, Hitoshi Asakura, Yasunobu Komoriya, Eiji Nishiyama, Toshikazu Nakamura

    Hepatology   26 ( 1 )   81 - 89   1997

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    DOI： 10.1002/hep.510260111

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  • Localization of hyaluronan in human liver sinusoids: A histochemical study using hyaluronan-binding protein Reviewed

    T Ichida, S Sugitani, T Satoh, Y Matsuda, M Sugiyama, K Yonekura, T Ishikawa, H Asakura

    LIVER   16 ( 6 )   365 - 371   1996.12

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  • Hepatocyte growth factor suppresses the onset of liver cirrhosis and abrogates lethal hepatic dysfunction in rats Reviewed

    Yasunobu Matsuda, Kunio Matsumoto, Toshikazu Nakamura, Takafumi Ichida

    Journal of Biochemistry   118 ( 3 )   643 - 649   1995

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    DOI： 10.1093/oxfordjournals.jbchem.a124958

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  • [Molecular biology of hepatocyte growth factor (HGF)].

    Matsuda Y, Nakamura T

    Nihon Rinsho   51 ( 2 )   435 - 445   1993.2

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    Hepatocyte growth factor (HGF) is the most potent mitogen of mature hepatocytes in primary culture, and is a molecule composed of 69 kD alpha-chain and 34 kD beta-chain. HGF predominantly acts on various epithelial cells as a mitogen, motogen and a morphogen. HGF mRNA and HGF protein increases rapidly in the liver and plasma of rats with liver injury such as hepatitis, ischemia, physical crush and partial hepatectomy. Production of HGF in the liver occurs in Kupffer cells, sinusoidal endothelial cells, and Ito cells, but not in hepatocytes. HGF mRNA is also rapidly increased in the intact organs such as lung, kidney and spleen. Thus, HGF may act as a hepatotrophic factor for liver regeneration through two mechanisms: a paracrine mechanism and an endocrine mechanism. Moreover, intravenously injected HGF enhances liver regeneration and protects hepatitis in vivo. Consequently, HGF may prove to be useful for the clinical treatment of patients with liver disease. Recently, we found a factor which specially appears in the blood of rats with organ injury and increases the synthesis of HGF, and it was named &quot;injurin&quot;. IL-1 alpha and IL-1 beta are also positive regulators for the exp

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  • [Molecular biology of hepatocyte growth factor (HGF)].

    Matsuda Y, Nakamura T

    Nihon Rinsho   51 ( 2 )   435 - 445   1993.2

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    Hepatocyte growth factor (HGF) is the most potent mitogen of mature hepatocytes in primary culture, and is a molecule composed of 69 kD alpha-chain and 34 kD beta-chain. HGF predominantly acts on various epithelial cells as a mitogen, motogen and a morphogen. HGF mRNA and HGF protein increases rapidly in the liver and plasma of rats with liver injury such as hepatitis, ischemia, physical crush and partial hepatectomy. Production of HGF in the liver occurs in Kupffer cells, sinusoidal endothelial cells, and Ito cells, but not in hepatocytes. HGF mRNA is also rapidly increased in the intact organs such as lung, kidney and spleen. Thus, HGF may act as a hepatotrophic factor for liver regeneration through two mechanisms: a paracrine mechanism and an endocrine mechanism. Moreover, intravenously injected HGF enhances liver regeneration and protects hepatitis in vivo. Consequently, HGF may prove to be useful for the clinical treatment of patients with liver disease. Recently, we found a factor which specially appears in the blood of rats with organ injury and increases the synthesis of HGF, and it was named &quot;injurin&quot;. IL-1 alpha and IL-1 beta are also positive regulators for the exp

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  • TENASCIN EXPRESSION IN HUMAN CHRONIC LIVER-DISEASE AND IN HEPATOCELLULAR-CARCINOMA Reviewed

    S YAMADA, T ICHIDA, Y MATSUDA, Y MIYAZAKI, T HATANO, K HATA, H ASAKURA, N HIROTA, A GEERTS, E WISSE

    LIVER   12 ( 1 )   10 - 16   1992.2

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▶ display all

Books

  • p27

    MATSUDA Yasunobu（ Role： Sole author）

    “Encyclopedia of Cancer” Springer Publishing  2014.1 

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  • Sorafenib

    MATSUDA Yasunobu（ Role： Sole author）

    “Encyclopedia of Cancer” Springer Publishing  2014.1 

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  • Sorafenib-Inhibited Signaling: Emerging Evidence of RAF Independent Pathways as Potential Therapeutic Targets in Hepatocellular Carcinoma.

    MATSUDA Yasunobu（ Role： Sole author）

    InTech publisher  2013.10  （ ISBN:9789535112020 ）

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    Responsible for pages：239-253   Language：English Book type：Scholarly book

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  • Molecular Mechanism of DNA Damage Response Pathway During Hepatic Carcinogenesis.

    MATSUDA Yasunobu（ Role： Sole author）

    InTech publisher  2012.2  （ ISBN:9789535100232 ）

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    Responsible for pages：313-324   Language：English Book type：Scholarly book

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  • Hepatocellular carcinoma – etiology, risk factors and prevention

    MATSUDA Yasunobu（ Role： Sole author）

    “Encyclopedia of Cancer” Springer Publishing  2012.1 

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MISC

  • アジア人の非B非C肝細胞癌においてATM高発現は予後不良因子である:TCGA Cohort

    廣瀬雄己, 小林隆, 三浦宏平, 松田康伸, 若井俊文

    肝臓   62 ( Supplement 2 )   2021

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  • NAFLD/NAFLD関連肝細胞癌におけるDNA損傷修復因子pATMおよびpCHK2発現の意義

    廣瀬 雄己, 小林 隆, 松田 康伸, 若井 俊文

    肝臓   60 ( Suppl.2 )   A682 - A682   2019.10

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  • 肝癌薬剤耐性におけるエクソソームの有用性および課題

    松田 康伸, 寺井 崇二

    BIO Clinica   34 ( 7 )   737 - 740   2019.7

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  • 当院における高齢発症原発性胆汁性胆管炎患者の予後予測マーカーについて

    高村 昌昭, 木村 成宏, 薛 徹, 上村 博輝, 坂牧 僚, 横尾 健, 土屋 淳紀, 上村 顕也, 松田 康伸, 寺井 崇二

    肝臓   60 ( Suppl.1 )   A407 - A407   2019.4

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  • 当院における高齢発症原発性胆汁性胆管炎患者の予後予測マーカーについて

    高村 昌昭, 木村 成宏, 薛 徹, 上村 博輝, 坂牧 僚, 横尾 健, 土屋 淳紀, 上村 顕也, 松田 康伸, 寺井 崇二

    肝臓   60 ( Suppl.1 )   A407 - A407   2019.4

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  • 家兎気管大欠損モデルにおける代用気管と欠損部再生様式

    窪田 正幸, 小林 隆, 松田 康伸

    日本小児外科学会雑誌   54 ( 2 )   356 - 356   2018.4

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  • NAFLDにおけるイベント発生の前方視的検討

    川合 弘一, 松田 康伸, 阿部 聡司, 坂牧 僚, 上村 顕也, 土屋 淳紀, 高村 昌昭, 石川 達, 山際 訓, 杉谷 想一, 渡辺 雅史, 寺井 崇二

    日本消化器病学会雑誌   114 ( 臨増大会 )   A769 - A769   2017.9

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  • uPA/FGF-2経路は肝がん細胞におけるソラフェニブ耐性因子である

    大澤 まみ, 松田 康伸, 窪田 正幸, 若井 俊文

    日本癌学会総会記事   76回   P - 3295   2017.9

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  • 肝癌薬剤耐性におけるエクソソームの有用性および課題

    松田 康伸, 寺井 崇二

    Medical Science Digest   43 ( 7 )   334 - 337   2017.6

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    J-GLOBAL

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  • 肝細胞癌におけるa disintegrin and metalloprotease(ADAM)21発現の意義:in vivoでの検討と切除症例での臨床病理学的意義の検討

    高村昌昭, 本田博樹, 山際訓, 玄田拓哉, 松田康伸, 若井俊文, 寺井崇二

    肝臓   58 ( Supplement 1 )   A289 - A289   2017.4

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  • ベザフィブラート投与原発性胆汁性胆管炎症例におけるUDCA投与量の検討

    山際訓, 松田康伸, 寺井崇二

    肝臓   57 ( Supplement 3 )   A664   2016.10

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  • 自己免疫性肝疾患における基礎と臨床 新たな臨床試験の可能性まで ベザフィブラート投与原発性胆汁性胆管炎症例におけるUDCA投与量の検討

    山際 訓, 松田 康伸, 寺井 崇二

    肝臓   57 ( Suppl.3 )   A664 - A664   2016.10

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  • 原発性胆汁性肝硬変に対するUDCA至適投与量の再検討

    山際訓, 松田康伸, 寺井崇二

    肝臓   57 ( Supplement 2 )   A505   2016.9

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  • 自己免疫性肝疾患 これからの課題 原発性胆汁性肝硬変に対するUDCA至適投与量の再検討

    山際 訓, 松田 康伸, 寺井 崇二

    肝臓   57 ( Suppl.2 )   A505 - A505   2016.9

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  • 肝細胞癌におけるa disintegrin and metalloprotease 21発現の生物学的意義に関する検討

    本田 博樹, 高村 昌昭, 山際 訓, 玄田 拓哉, 木村 成宏, 薛 徹, 冨永 顕太郎, 上村 博輝, 松田 康伸, 若井 俊文, 寺井 崇二

    肝臓   57 ( Suppl.1 )   A247 - A247   2016.4

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  • ラジオ波焼灼術を施行した肝細胞癌患者に対するNomogramを用いた生命予後予測モデルの開発と術前ICG‐PDR測定の臨床的意義

    安住基, 須田剛士, 横尾健, 上村博輝, 土屋淳紀, 上村顕也, 高村昌昭, 川合弘一, 松田康伸, 山際訓, 寺井崇二

    肝臓   57 ( Supplement 1 )   A158 - A158   2016.4

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  • 各種肝疾患における肝細胞ロゼット形成の臨床的意義

    野本実, 上村博輝, 土屋淳紀, 寺井崇二, 松田康伸

    新潟医学会雑誌   129 ( 10 )   632‐633 - 633   2015.10

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  • 44 各種肝疾患における肝細胞ロゼット形成の臨床的意義（Ⅰ．一般演題, 第39回リバーカンファレンス）

    野本 実, 上村 博輝, 土屋 淳紀, 寺井 崇二, 松田 康伸

    新潟医学会雑誌   129 ( 10 )   632 - 632   2015.10

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  • DJ-1 labeling index is a novel diagnostic biomarker for predicting progression of nonalcoholic steatohepatitis

    Masaaki Takamura, Satoshi Yamagiwa, Yasunobu Matsuda, Minoru Nomoto, Toshifumi Wakai, Shuji Terai

    HEPATOLOGY   62   1263A - 1263A   2015.10

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  • 肝がん細胞株におけるオーロラキナーゼ阻害剤・ソラフェニブ併用療法の解析

    大澤 まみ, 松田 康伸, 若井 俊文, 廣瀬 雄己, 永橋 昌幸, 坂田 純, 小林 隆, 藤巻 隼, 窪田 正幸

    新潟大学保健学雑誌   12 ( 1 )   57 - 63   2015.9

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  • 「細胞間相互作用からみた胆管系腫瘍進展の分子機構」

    松田康伸

    日本膵・胆管合流異常研究会プロシーディングス   38th   16 - 17   2015.9

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  • 非アルコール性脂肪肝炎におけるDJ‐1核内発現および血清DJ‐1濃度測定の有用性

    高村昌昭, 山際訓, 松田康伸, 野本実, 青柳豊, 若井俊文, 寺井崇二

    肝臓   56 ( Supplement 1 )   A353 - A353   2015.4

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  • 肝胆膵 非アルコール性脂肪肝疾患関連肝細胞癌における肝切除の術後成績およびp27発現の臨床的意義

    廣瀬 雄己, 松田 康伸, 油座 築, 相馬 大輝, 岡部 康之, 森本 悠太, 三浦 宏平, 佐藤 良平, 滝沢 一泰, 永橋 昌幸, 坂田 純, 小林 隆, 亀山 仁史, 皆川 昌広, 小杉 伸一, 小山 諭, 若井 俊文

    日本外科学会定期学術集会抄録集   115回   YIA - 1   2015.4

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  • 46 当院における他科依頼肝疾患の現状（Ⅰ.一般演題, 第38回リバーカンファレンス）

    安住 基, 須田 剛士, 横尾 健, 山本 幹, 土屋 淳紀, 五十嵐 正人, 田村 康, 高村 昌昭, 川合 弘一, 山際 訓, 野本 実, 青柳 豊, 松田 康伸

    新潟医学会雑誌   128 ( 9 )   484 - 484   2014.9

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  • 非アルコール性脂肪肝炎におけるDJ-1発現の有用性の検討

    高村 昌昭, 許 波, 山際 訓, 松田 康伸, 野本 実, 若井 俊文, 山本 格, 青柳 豊

    肝臓   55 ( Suppl.2 )   A628 - A628   2014.9

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  • 当院における他科依頼肝疾患の現状

    安住 基, 須田 剛士, 横尾 健, 山本 幹, 土屋 淳紀, 五十嵐 正人, 田村 康, 高村 昌昭, 川合 弘一, 山際 訓, 野本 実, 青柳 豊, 松田 康伸

    新潟医学会雑誌   128 ( 9 )   484 - 484   2014.9

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  • Akt-FGF経路は肝がん細胞におけるソラフェニブ耐性機構に関与する(Hepatoma Cells Acquire Sorafenib Resistance through Akt-Fibroblast Growth Factor Signaling)

    大澤 まみ, 松田 康伸, 若井 俊文, 窪田 正幸

    日本癌学会総会記事   73回   P - 1391   2014.9

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  • TGF-BETAはソラフェニブ薬剤耐性の促進因子である(TGF-beta Is a Critical Mediator Of Sorafenib Resistance In Hepatocellular Carcinoma)

    松田 康伸, 大澤 まみ, 若井 俊文, 窪田 正幸

    日本癌学会総会記事   73回   P - 1405   2014.9

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  • 食道癌術前補助化学療法抵抗性におけるNQO1発現の関与

    市川 寛, 小杉 伸一, 松田 康伸, 皆川 昌広, 小林 隆, 亀山 仁史, 坂田 純, 羽入 隆晃, 石川 卓, 若井 俊文

    日本食道学会学術集会プログラム・抄録集   68回   107 - 107   2014.7

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  • 細胞周期調節因子p27はNASH関連肝細胞癌再発の予測因子である

    廣瀬 雄己, 松田 康伸, 滝沢 一泰, 島田 能史, 石川 卓, 亀山 仁史, 坂田 純, 小林 隆, 皆川 昌広, 小杉 伸一, 若井 俊文

    日本肝胆膵外科学会・学術集会プログラム・抄録集   26回   488 - 488   2014.6

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  • Molecular mechanism of compensatory proliferation

    Osawa Mami, Matsuda Yasunobu, Wakai Toshifumi, Hirose Yuki, Sakata Jun, Kobayashi Takashi, Fujimaki Shun, Kubota Masayuki

    新潟大学保健学雑誌 = Journal of health sciences of Niigata University   11 ( 1 )   1 - 6   2014.3

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    近年，アポトーシス細胞が周囲の細胞に生存・増殖を促す「代償性増殖作用」をもつことが明らかとなったが，そのメカニズムについては未だ不明な点が多い。最近の研究報告により，アポトーシスを進行させる因子であるカスパーゼが，ストレスキナーゼJNKやプロスタグランジンE2を介して，細胞増殖を誘導させる作用を併せ持つことが明らかになった。また酸化ストレスに関与するインターロイキン-11も，代償性増殖に関与する可能性が報告されており，本機構が多彩な因子によって調節されている可能性が推測されている。今後，さらなる研究の発展により，代償性増殖を利用した医療の発展に期待がもたれる。Recent studies have suggested that dying apoptotic cells are involved in various types of extracellular stimuli, termed compensatory proliferation. For example, caspase-9 (Dronc), a type of enzyme which induced cell apoptosis, stimulates JNK or prostaglandin E2, leading to the pronounced cell proliferation. Moreover, interleukin-11, which is produced by reactive oxygen stress, has been also found to be involved in the compensatory proliferation. For more understanding the mechanism of cell death and proliferation, further investigation of the compensatory proliferation is awaited.

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  • p70S6 kinase is activated in non-alcoholic steatohepatitis-related hepatocellular carcinoma

    Matsuda Yasunobu, Wakai Toshifumi, Hirose Yuki, Sakata Jun, Kobayashi Takashi, Osawa Mami, Fujimaki Shun, Kubota Masayuki

    新潟大学保健学雑誌 = Journal of health sciences of Niigata University   11 ( 1 )   51 - 56   2014.3

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    【目的】非アルコール性脂肪肝炎（NASH）は，近年急速に増加している原因不明の肝疾患である。本研究では，肝がん治療に有効とされる分子標的薬ラパマイシンの標的シグナルp70S6キナーゼが，NASH肝がんの病態に関与している可能性について検討した。 【方法】根治的外科手術療法を施行したNASH肝がん22例の病変組織に対して，リン酸化型（活性型）p70S6キナーゼの免疫組織化学染色を行い，臨床因子・予後の比較検討を行った。 【結果】NASH肝がん22例中12例（54.5%）がリン酸化型p70S6キナーゼを高発現しており，組織未分化度と相関した（p = 0.047）。リン酸化型P70S6キナーゼ高発現群は，外科切除後３年以内再発率が有意に増加していた（p = 0.045）。 【総括】p70S6キナーゼを高発現しているNASH肝がんは，再発頻度が高い傾向がある。同シグナルを阻害する分子標的薬ラパマイシンは，本疾患の再発防止に有効である可能性が示唆された。Objective: Non-alcoholic steatohepatitis（NASH）is a recently identified liver disease which causes hepatocellular carcinoma（HCC）. In this study, we addressed whether p70S6 kinase（p70S6K）, a main target of the anti-cancer agent rapamycin, is involved in the clinicopathological factors in NASH-related HCC. Methods: HCC tissue samples were obtained from 22 NASH patients with radical surgical treatment. Phosphorylation level of p70S6K was analyzed by immunohistochemical analysis, and the correlation with the clinicopathological factors were examined. Results: Phosphorylated p70S6K was detected in 54.5%（12/22）of NASH-related HCCs. The levels of phosphop70S6K were correlated with histological grade of HCC（p = 0.047）, but not with clinical factors. Phosphorylation of p70S6K was correlated with increased cancer recurrence after 3 years of the treatment（p= 0.045）. Conclusion: Phosphorylation level of p70S6K was correlated with cancer recurrence of NASH-related HCC. Rapamycin might be a useful agent for treating NASH-associated HCC.

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  • Blockade of CD26 Augments the Therapeutic Potential of Marrow Stem Cells in the Liver

    Matsuda Yasunobu, Wakai Toshifumi, Hirose Yuki, Sakata Jun, Kobayashi Takashi, Osawa Mami, Fujimaki Shun, Kubota Masayuki

    11 ( 1 )   39 - 49   2014.3

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  • 42 当科におけるsorafenib治療の検討（Ⅰ．一般演題, 第37回リバーカンファレンス）

    長島 藍子, 須田 剛士, 倉岡 直亮, 罇 陽介, 山本 幹, 横山 純二, 五十嵐 正人, 川合 弘一, 山際 訓, 青柳 豊, 松田 康伸, 大越 省吾, 小林 真

    新潟医学会雑誌   127 ( 10 )   580 - 580   2013.10

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  • 全生存期間からみたTACEとchemolipiodolizationの比較検討

    兼藤 努, 吉川 成一, 上村 顕也, 田村 康, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 須田 剛士, 野本 実, 青柳 豊, 松田 康伸, 和栗 暢生

    新潟医学会雑誌   127 ( 10 )   578 - 579   2013.10

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  • 音響放射圧を用いた肝内せん断弾性波速度測定による肝細胞癌発癌リスク評価

    高村 昌昭, 須田 剛士, 兼藤 努, 吉川 成一, 上村 顕也, 田村 康, 五十嵐 正人, 川合 弘一, 山際 訓, 野本 実, 青柳 豊, 松田 康伸

    新潟医学会雑誌   127 ( 10 )   580 - 580   2013.10

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  • 当科におけるsorafenib治療の検討

    長島 藍子, 須田 剛士, 倉岡 直亮, もたい 陽介, 山本 幹, 横山 純二, 五十嵐 正人, 川合 弘一, 山際 訓, 青柳 豊, 松田 康伸, 大越 省吾, 小林 真

    新潟医学会雑誌   127 ( 10 )   580 - 580   2013.10

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  • 39 全生存期間からみたTACEとchemolipiodolizationの比較検討（Ⅰ．一般演題, 第37回リバーカンファレンス）

    兼藤 努, 吉川 成一, 上村 顕也, 田村 康, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 須田 剛士, 野本 実, 青柳 豊, 松田 康伸, 和栗 暢生

    新潟医学会雑誌   127 ( 10 )   578 - 579   2013.10

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  • 40 APM2は肝細胞癌に対するシスプラチンの効果予測マーカー候補である（Ⅰ．一般演題, 第37回リバーカンファレンス）

    上村 顕也, 吉川 成一, 兼藤 努, 田村 康, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 須田 剛士, 松田 康伸, 野本 実, 青柳 豊

    新潟医学会雑誌   127 ( 10 )   579 - 579   2013.10

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  • 44 音響放射圧を用いた肝内せん断弾性波速度測定による肝細胞癌発癌リスク評価（Ⅰ．一般演題, 第37回リバーカンファレンス）

    高村 昌昭, 須田 剛士, 兼藤 努, 吉川 成一, 上村 顕也, 田村 康, 五十嵐 正人, 川合 弘一, 山際 訓, 野本 実, 青柳 豊, 松田 康伸

    新潟医学会雑誌   127 ( 10 )   580 - 580   2013.10

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  • APM2は肝細胞癌に対するシスプラチンの効果予測マーカー候補である

    上村 顕也, 吉川 成一, 兼藤 努, 田村 康, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 須田 剛士, 松田 康伸, 野本 実, 青柳 豊

    新潟医学会雑誌   127 ( 10 )   579 - 579   2013.10

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  • A disintegrin and metalloprotease 21発現は肝細胞癌の細胞運動に関与し術後再発に影響を与える

    高村 昌昭, 玄田 拓哉, 山際 訓, 松田 康伸, 若井 俊文, 青柳 豊

    肝臓   54 ( Suppl.2 )   A593 - A593   2013.9

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  • 化学療法により根治的切除可能となった肝・リンパ節転移を伴う胃内分泌細胞癌の1例

    渡辺 庄治, 富所 隆, 高綱 将史, 外池 祐子, 堂森 浩二, 佐藤 明人, 福原 康夫, 佐藤 知巳, 北見 智恵, 川原 聖佳子, 牧野 成人, 西村 淳, 河内 保之, 新国 恵也, 松田 康伸, 五十嵐 俊彦, 吉川 明

    ENDOSCOPIC FORUM for digestive disease   29 ( 1 )   21 - 27   2013.5

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  • 非アルコール性脂肪性肝疾患モデルマウス肝組織のプロテオーム解析による新規バイオマーカーの探索

    高村 昌昭, 許 波, 山際 訓, 松田 康伸, 野本 実, 山本 格, 青柳 豊

    日本臨床分子医学会学術総会プログラム・抄録集   50回   64 - 64   2013.4

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  • 深部出血を合併した肝硬変症例における生存例と死亡例の比較検討

    高村 昌昭, 渡邊 順, 坂牧 僚, 本田 穣, 兼藤 努, 吉川 成一, 上村 顕也, 田村 康, 五十嵐 正人, 川合 弘一, 山際 訓, 須田 剛士, 松田 康伸, 野本 実, 青柳 豊

    肝臓   54 ( Suppl.1 )   A328 - A328   2013.4

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  • Presence of antibodies against self-HLA class II molecules in autoimmune hepatitis

    Satoshi Yamagiwa, Masaaki Takamura, Yasunobu Matsuda, Takuya Genda, Toru Takahashi, Takafumi Ichida, Yutaka Aoyagi

    HEPATOLOGY   56   989A - 989A   2012.10

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  • An insulin resistance-inducing factor, RBP4, is a negative predictor of outcome of Peg-IFN plus ribavirin therapy for patients with chronic heatitis C

    Masahiko Yano, Shogo Ohkoshi, Hiromichi Takahashi, Satoshi Yamagiwa, Yasunobu Matsuda, Masanori Ikeda, Nobuyuki Kato, Yutaka Aoyagi

    HEPATOLOGY   56   269A - 269A   2012.10

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  • Comparative proteomic analysis of the liver in a murine model of non-alcoholic steatohepatitis

    Masaaki Takamura, Bo Xu, Satoshi Yamagiwa, Yasunobu Matsuda, Shuichiro Shimada, Ying Zhang, Yutaka Yoshida, Eishin Yaoita, Minoru Nomoto, Tadashi Yamamoto, Yutaka Aoyagi

    HEPATOLOGY   56   855A - 855A   2012.10

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  • C型肝炎基礎 C型慢性肝炎とインスリン抵抗性因子RBP4 RBP4はインターフェロン治療抵抗性をもたらす

    高橋 弘道, 大越 章吾, 矢野 雅彦, 山際 訓, 松田 康伸, 池田 正徳, 加藤 宣之, 青柳 豊

    肝臓   53 ( Suppl.1 )   A342 - A342   2012.4

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  • p21細胞内局在制御によるIFN-βのシスプラチン制癌効果増強機構

    矢野 雅彦, 大越 章吾, 高橋 弘道, 藤巻 隼, 松田 康伸, 青柳 豊, 工藤 進英

    肝臓   53 ( Suppl.1 )   A427 - A427   2012.4

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  • 実験的NASHモデルマウス肝組織のプロテオーム解析

    高村 昌昭, 許 波, 嶋田 修一郎, 張 瑩, 吉田 豊, 矢尾板 永信, 山際 訓, 松田 康伸, 野本 実, 山本 格, 青柳 豊

    日本消化器病学会雑誌   109 ( 臨増総会 )   A325 - A325   2012.3

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  • Sorafenib: complexities of Raf-dependent and Raf-independent signaling are now unveiled

    Yasunobu Matsuda, Manabu Fukumoto

    MEDICAL MOLECULAR MORPHOLOGY   44 ( 4 )   183 - 189   2011.12

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  • Long-term Outcome of Surgical Resection for Hepatocellular Carcinoma in Nonalcoholic Fatty Liver Disease

    Wakai Toshifumi, Sakata Jun, Shirai Yoshio, Hatakeyama Katsuyoshi, Ajioka Yoichi, Kawai Hirokazu, Nomoto Minoru, Suda Takeshi, Tamura Yasushi, Takamura Masaaki, Yamagiwa Satoshi, Matsuda Yasunobu, Aoyagi Yutaka

    新潟医学会雑誌   125 ( 10 )   557 - 565   2011.10

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    【目的】非アルコール怪脂肪性肝疾患 (nonalcoholic fatty liver disease, 以下NAFLD) における肝細胞癌に対する外科治療成績を明らかにする. 【対象・方法】肝細胞癌に対して肝切除を施行した225例を対象とし, HBs抗原単独陽性群 (以下, B群) 61例, HCV抗体単独陽性群 (以下, C群) 147例, NAFLD群17例の3群に分類した. 3群間における臨床病理学的背景因子, 術後遠隔成績を比較検討した. 【結果】NAFLD群はB群, C群と比較して有意に高齢であり (P &lt;0.001), body mass index は高く (P &lt;0.001), 腫瘍径が大きかった (P =0.002). NAFLD群17例中8例は組織学的に非アルコール性脂肪肝炎 (nonalcoholic steatohepatitis, 以下NASH) と診断された. 術後合併症発生率, 在院死亡率は, B群 (各々28%, 8%), C群 (各々31%, 1.4%) と比較してNAFLD群 (各々59%, 12%) で有意に高かった (各々P =0.043, P =0.030). NAFLD群での在院死亡は2例であり, NASHに関連した肝硬変に合併した肝細胞癌に対して肝右葉切除が施行されていた. 術後累積5年無再発生存率は, B群39%, C群29%, NAFLD群66%であった. 術後累積無再発生存率はNAFLD群が単変量解析 (P =0.048), 多変量解析 (P =0.020) の両者で有意に良好な成績であった. 【結論】NAFLD関連肝細胞癌に対する外科治療は予後を改善する. NASH関連肝硬変患者に対して肝葉切除を行う際には細心の注意が必要である.

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  • 肝細胞癌におけるNK細胞活性化レセプターリガンド発現低下とその臨床的意義

    山際 訓, 上村 博輝, 土屋 淳紀, 高村 昌昭, 松田 康伸, 白井 良夫, 野本 実, 青柳 豊

    肝臓   52 ( Suppl.2 )   A624 - A624   2011.9

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  • Hepatocellular carcinoma and liver transplantation: clinical perspective on molecular targeted strategies

    Yasunobu Matsuda, Takafumi Ichida, Manabu Fukumoto

    MEDICAL MOLECULAR MORPHOLOGY   44 ( 3 )   117 - 124   2011.9

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  • 5 部分的膵動脈塞栓術後の血小板数予測の試み(I.一般演題,第63回新潟画像医学研究会)

    大崎 暁彦, 須田 剛士, 石川 達, 和栗 暢生, 川合 弘一, 土屋 淳紀, 上村 顕也, 矢野 雅彦, 田村 康, 高村 昌昭, 五十嵐 正人, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    新潟医学会雑誌   125 ( 6 )   339 - 340   2011.6

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  • 部分的脾動脈塞栓術後の血小板数予測の試み

    大崎 暁彦, 須田 剛士, 石川 達, 和栗 暢生, 川合 弘一, 土屋 淳紀, 上村 顕也, 矢野 雅彦, 田村 康, 高村 昌昭, 五十嵐 正人, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    新潟医学会雑誌   125 ( 6 )   339 - 340   2011.6

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  • ウイルス肝炎・肝癌制圧の分子基盤 B型肝炎ウイルスX遺伝子によるDNA酸化傷害機構の解析および制御方法の検討

    松田 康伸, 大越 章吾, 青柳 豊

    肝臓   52 ( Suppl.1 )   A26 - A26   2011.4

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  • 肝細胞癌におけるLiver-intestine(LI)-cadherinの発現とその臨床病理学的意義

    高村 昌昭, 山際 訓, 若井 俊文, 上村 博輝, 土屋 淳紀, 松田 康伸, 白井 良夫, 青柳 豊

    肝臓   52 ( Suppl.1 )   A324 - A324   2011.4

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  • DNA傷害修復因子ATMによる肝癌細胞の細胞死抑制機構の解析

    藤巻 隼, 松田 康伸, 矢野 雅彦, 大越 章吾, 若井 俊文, 白井 良夫, 三瓶 歩, 平野 茂樹

    肝臓   52 ( Suppl.1 )   A194 - A194   2011.4

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  • INTERFERON-beta PREVENTS HBX-TRIGGERED HEPATOCARCINOGENESIS BY DOWN-REGULATING CYTOPLASMIC P21 OVEREXPRESSION

    M. Yano, S. Ohkoshi, Y. Aoki, K. Yamazaki, S. Kurita, K. Suzuki, S. Fujimaki, A. Sanpei, Y. Matsuda, Y. Aoyagi

    JOURNAL OF HEPATOLOGY   54   S448 - S448   2011.3

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  • TRANSFORMING GROWTH FACTOR-beta/P38 MAP KINASE SIGNALING CONTRIBUTES TO SORAFENIB RESISTANCE IN HEPATOMA

    Y. Matsuda, T. Wakai, Y. Shirai, M. Yano, S. Ohkoshi, Y. Aoyagi, S. Fujimaki, A. Sanpei, S. Hirano

    JOURNAL OF HEPATOLOGY   54   S272 - S273   2011.3

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  • ATAXIA TELANGIECTASIA MUTATED PLAYS A PIVOTAL ROLE ON THE CELL SURVIVAL IN HEPATOMA VIA SUPPRESSING ENDOPLASMIC RETICULUM STRESS

    S. Fujimaki, Y. Matsuda, A. Sanpei, M. Yano, S. Ohkoshi, T. Wakai, Y. Shirai, S. Hirano

    JOURNAL OF HEPATOLOGY   54   S271 - S271   2011.3

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  • ペグインターフェロンとリバビリンの併用療法中HCV RNAの陰性化にもかかわらず肝機能障害が継続し組織学的に肝硬変への進展が確認されたC型慢性肝炎の1例

    大越 章吾, 森田 慎一, 田中 由佳里, 矢野 雅彦, 竹内 学, 高橋 弘道, 池田 晴夫, 山際 訓, 松田 康伸, 野本 実, 青柳 豊

    日本消化器病学会雑誌   108 ( 2 )   267 - 274   2011.2

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    DOI： 10.11405/nisshoshi.108.267

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  • HEPATITIS B VIRUS X PROTEIN ACTIVATES MAMMALIAN TARGET OF RAPAMYCIN MTOR VIA REACTIVE OXYGEN SPECIES GENERATION

    Ayumi Sanpei, Yasunobu Matsuda, Toshifumi Wakai, Jun Sakata, Yoshio Shirai, Masahiko Yano, Shogo Ohkoshi, Syun Fujimaki, Katsuyoshi Hatakeyama

    HEPATOLOGY   52 ( 4 )   591A - 592A   2010.10

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  • 肝細胞癌に対する術前CDDP肝動注施行例における組織学的腫瘍壊死率とmultidrug resistant-associated protein 2過剰発現との関連

    若井 俊文, 白井 良夫, 坂田 純, 松田 康伸, 高村 昌昭, 青柳 豊, 味岡 洋一, 畠山 勝義

    日本消化器病学会雑誌   107 ( 臨増大会 )   A891 - A891   2010.9

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  • 1型高ウイルス量C型慢性肝炎に対するPEG-IFNα2b+Rib併用療法の治療効果予測因子及びにフルバスタチン、テプレノンの上乗せ療法の検討

    大越 章吾, 山際 訓, 矢野 雅彦, 高橋 弘道, 和栗 暢生, 五十嵐 健太郎, 杉谷 想一, 高橋 達, 石川 達, 上村 朝輝, 渡辺 庄治, 武井 伸一, 津端 俊介, 若林 博人, 渡辺 俊明, 前田 裕伸, 松田 康伸, 青柳 豊

    肝臓   51 ( Suppl.2 )   A593 - A593   2010.9

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  • HBx遺伝子誘導性肝発癌に対するインターフェロンβの分子学的制御機構(Molecular mechanism of interferon-beta on prevention of HBx-induced hepatocarcinogenesis)

    矢野 雅彦, 大越 章吾, 青木 洋平, 山崎 和秀, 栗田 聡, 鈴木 健太, 三瓶 歩, 松田 康伸, 青柳 豊

    日本癌学会総会記事   69回   91 - 91   2010.8

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  • 肝細胞癌における分子標的としてのNK細胞活性化レセプターリガンドとその発現調節による抗腫瘍効果

    上村 博輝, 山際 訓, 土屋 淳紀, 高村 昌昭, 松田 康伸, 井上 真, 若井 俊文, 白井 良夫, 野本 実, 青柳 豊

    肝臓   51 ( Suppl.1 )   A167 - A167   2010.4

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  • 非蛋白性呼吸商の治療侵襲に対する耐容性指標としての有用性

    山田 一樹, 須田 剛士, 大崎 暁彦, 上村 博輝, 土屋 淳紀, 矢野 雅彦, 田村 康, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    肝臓   51 ( Suppl.1 )   A306 - A306   2010.4

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  • HBx誘導性肝発癌に対するIFN-βの制御機構の分子学的解析

    矢野 雅彦, 大越 章吾, 青木 洋平, 山崎 和秀, 栗田 聡, 鈴木 健太, 三瓶 歩, 松田 康伸, 青柳 豊

    肝臓   51 ( Suppl.1 )   A212 - A212   2010.4

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  • 肝内胆管癌におけるLI-cadherinの発現消失はMTF-1およびPlGFの発現を上昇することにより血管新生を誘導する

    高村 昌昭, 山際 訓, 若井 俊文, 田村 康, 井上 真, 上村 博輝, 加藤 卓, 土屋 淳紀, 松田 康伸, 白井 良夫, 市田 隆文, 味岡 洋一, 青柳 豊

    日本消化器病学会雑誌   107 ( 臨増総会 )   A266 - A266   2010.3

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  • 慢性DSS腸炎に対するPlasmid-IL-10注腸治療効果の検討

    野々村 頼子, 孫 暁梅, 鈴木 健司, 大坪 亜矢, 遠藤 悠, 河内 裕介, 横山 純二, 串田 良裕, 大根田 輝, 細野 正道, 丸山 弘樹, 渡辺 賢一, 松田 康伸, 青柳 豊

    消化器と免疫   ( 46 )   140 - 144   2010.3

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  • マウス肝発癌モデルを用いたインターフェロン-βによる肝発癌予防効果

    矢野 雅彦, 大越 章吾, 青木 洋平, 山崎 和秀, 鈴木 健太, 栗田 聡, 松田 康伸, 青柳 豊

    日本内科学会雑誌   99 ( Suppl. )   209 - 209   2010.2

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  • OXIDATIVE STRESS INDUCES ANTI-HCV STATUS VIA THE ACTIVATION OF MEK-ERK1/2 SIGNALING PATHWAY

    Masahiko Yano, Masanori Ikeda, Ken-ichi Abe, Yoshinari Kawai, Misao Kuroki, Kyoko Mori, Hiromichi Dansako, Yasuo Ariumi, Yasunobu Matsuda, Shougo Ohkoshi, Yutaka Aoyagi, Nobuyuki Kato

    HEPATOLOGY   50 ( 4 )   965A - 965A   2009.10

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  • 音響放射圧刺激に基づく肝硬度測定の臨床的意義

    窪田 智之, 須田 剛士, 土屋 淳紀, 田村 康, 矢野 雅彦, 高村 昌昭, 五十嵐 正人, 川合 弘一, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    肝臓   50 ( Suppl.2 )   A553 - A553   2009.9

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  • 胆管癌における53BP1を介したDNA損傷修復機構の解明及びその臨床的意義

    若井 俊文, 白井 良夫, 松田 康伸, 坂田 純, 味岡 洋一, 畠山 勝義

    日本消化器病学会雑誌   106 ( 臨増大会 )   A907 - A907   2009.9

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  • C型慢性肝炎関連非アルコール性脂肪性肝炎(NASH)の検討

    野本 実, 吉川 成一, 五十嵐 正人, 青柳 豊, 松田 康伸

    肝臓   50 ( Suppl.2 )   A551 - A551   2009.9

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  • ラジオ波焼灼術における硬膜外麻酔の鎮痛効果の検討

    五十嵐 聡, 川合 弘一, 窪田 智之, 土屋 淳紀, 矢野 雅彦, 田村 康, 高村 昌昭, 五十嵐 正人, 山際 訓, 須田 剛士, 松田 康伸, 大越 章吾, 岡本 学, 野本 実, 青柳 豊

    肝臓   50 ( Suppl.2 )   A576 - A576   2009.9

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  • Impact of hepatitis B virus X protein on the DNA damage response during hepatocarcinogenesis

    Yasunobu Matsuda, Takafumi Ichida

    MEDICAL MOLECULAR MORPHOLOGY   42 ( 3 )   138 - 142   2009.9

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    DOI： 10.1007/s00795-009-0457-8

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  • 劇症肝炎に対する生体部分肝移植におけるMELDスコアの意義

    山本 智, 佐藤 好信, 大矢 洋, 小林 隆, 小海 秀央, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊, 畠山 勝義

    肝臓   50 ( Suppl.1 )   A200 - A200   2009.4

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  • 慢性DSS腸炎におけるリザベン注腸治療効果の検討

    孫 暁梅, 鈴木 健司, 河内 裕介, 横山 純二, 斉藤 翼, 熊谷 さやか, 串田 良裕, 大根田 輝, 細野 正道, 渡辺 賢一, 松田 康伸, 永田 昌毅, 青柳 豊

    消化器と免疫   ( 45 )   139 - 143   2009.3

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  • DSS腸炎におけるplasmid-IL-10注腸治療効果の検討

    河合 裕子, 孫 暁梅, 鈴木 健司, 河内 裕介, 横山 純二, 北澤 侑恵, 斉藤 翼, 大根田 輝, 熊谷 さやか, 串田 良裕, 細野 正道, 丸山 弘樹, 渡辺 賢一, 松田 康伸, 青柳 豊

    消化器と免疫   ( 45 )   144 - 148   2009.3

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  • A case of extra-hepatic lymph node metastasis of hepatocellular carcinoma with no evident sign of intra-hepatic recurrence

    Shinichi Morita, Yasunobu Matsuda, Tomoko Oshima, Tomoyuki Kubota, Yusuke Kawauchi, Makoto Kobayashi, Minoru Nomoto, Yutaka Aoyagi

    Journal of Japanese Society of Gastroenterology   106 ( 3 )   397 - 404   2009

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    DOI： 10.11405/nisshoshi.106.397

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  • 術前CDDP肝動注療法にて、肝機能を保ちかつ著効し狭心症加療後切除し長期生存した多血症、高脂血症の腫瘍随伴症候群を伴う高齢者巨大肝細胞癌の一例

    土屋 淳紀, 窪田 智之, 滝澤 一休, 山田 一樹, 松田 康伸, 本間 照, 渡辺 雅史, 丸山 弘樹, 野本 実, 青柳 豊

    肝臓   49 ( Suppl.3 )   A717 - A717   2008.10

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  • 原発巣の切除約5年後に肺転移を認めたbiliary mucinous cystadenocarcinomaの1例

    山際 訓, 松田 康伸, 野本 実, 須田 剛士, 白井 良夫, 青柳 豊

    肝臓   49 ( Suppl.3 )   A776 - A776   2008.10

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  • 31 アルコール性肝硬変に合併し, マロリー体の集簇を認めた結節性病変の1例(I.一般演題,第29回リバーカンファレンス)

    大崎 暁彦, 津端 俊介, 佐藤 俊大, 福原 康夫, 矢野 雅彦, 石本 結子, 横山 純二, 川合 弘一, 山際 訓, 松田 康伸, 杉村 一仁, 野本 実, 青柳 豊

    新潟医学会雑誌   122 ( 10 )   599 - 600   2008.10

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  • アルコール性肝硬変に合併し、マロリー体の集簇を認めた結節性病変の1例

    大崎 暁彦, 津端 俊介, 佐藤 俊大, 福原 康夫, 矢野 雅彦, 石本 結子, 横山 純二, 川合 弘一, 山際 訓, 松田 康伸, 杉村 一仁, 野本 実, 青柳 豊

    新潟医学会雑誌   122 ( 10 )   599 - 600   2008.10

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  • 生体肝移植後に急速に進行したC型肝硬変症の1例

    山際 訓, 松田 康伸, 杉村 一仁, 野本 実, 青柳 豊, 佐藤 好信, 畠山 勝義, 市田 隆文

    新潟医学会雑誌   122 ( 10 )   599 - 599   2008.10

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  • 29 生体肝移植後に急速に進行したC型肝硬変症の1例(I.一般演題,第29回リバーカンファレンス)

    山際 訓, 松田 康伸, 杉村 一仁, 野本 実, 青柳 豊, 佐藤 好信, 畠山 勝義, 市田 隆文

    新潟医学会雑誌   122 ( 10 )   599 - 599   2008.10

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  • 8 セクタ型探触子使用により腹腔鏡下RFA術が可能であった被膜下肝細胞癌の1経験例(I.一般演題,第28回リバーカンファレンス)

    矢野 雅彦, 松田 康伸, 三浦 隆義, 大嶋 智子, 福原 康夫, 本間 信之, 小林 真, 五十嵐 正人, 玄田 拓哉, 和栗 暢生, 川合 弘一, 山際 訓, 青柳 豊

    新潟医学会雑誌   122 ( 9 )   530 - 530   2008.9

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  • セクタ型探触子使用により腹腔鏡下RFA術が可能であった被膜下肝細胞癌の1経験例

    矢野 雅彦, 松田 康伸, 三浦 隆義, 大嶋 智子, 福原 康夫, 本間 信之, 小林 真, 五十嵐 正人, 玄田 拓哉, 和栗 暢生, 川合 弘一, 山際 訓, 青柳 豊

    新潟医学会雑誌   122 ( 9 )   530 - 530   2008.9

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  • 非アルコール性脂肪性肝炎を背景に多中心性発生したと思われる肝細胞癌の3例

    川合 弘一, 野本 実, 窪田 智之, 田村 康, 高村 昌昭, 五十嵐 正人, 山際 勲, 須田 剛士, 松田 康伸, 大越 章吾, 岡田 正彦, 青柳 豊

    日本消化器病学会雑誌   105 ( 臨増大会 )   A857 - A857   2008.9

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  • 3 新規超音波造影剤ソナゾイドの肝細胞癌診療における有用性(I.一般演題,第56回新潟画像医学研究会)

    津端 俊介, 川合 弘一, 窪田 智之, 栗田 聡, 田村 康, 高村 昌昭, 五十嵐 正人, 山際 訓, 松田 康信, 大越 章吾, 野本 実, 青柳 豊, 渡辺 雅史

    新潟医学会雑誌   122 ( 5 )   292 - 292   2008.5

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  • 当科における肝硬変の成因別分類

    野本 実, 五十嵐 正人, 松田 康伸, 青柳 豊

    肝臓   49 ( Suppl.1 )   A85 - A85   2008.4

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  • 当科で経験した薬物性肝障害の実態

    野本 実, 五十嵐 正人, 松田 康伸, 青柳 豊

    肝臓   49 ( Suppl.1 )   A116 - A116   2008.4

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  • 肝内胆管癌におけるLiver-intestine(LI)-cadherinの発現の検討

    高村 昌昭, 田村 康, 若井 俊文, 山際 訓, 加藤 卓, 土屋 淳紀, 松田 康伸, 白井 良夫, 市田 隆文, 味岡 洋一, 青柳 豊

    肝臓   49 ( Suppl.1 )   A167 - A167   2008.4

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  • p21はHBxトランスジェニックマウスモデルにおけるIFN-βの肝発癌予防効果に関与する

    青木 洋平, 大越 章吾, 栗田 聡, 山崎 和秀, 高村 昌昭, 山際 訓, 松田 康伸, 青柳 豊

    肝臓   49 ( Suppl.1 )   A359 - A359   2008.4

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  • 肝移植後C型慢性肝炎再発における肝内NK細胞の関与

    山際 訓, 松田 康伸, 土屋 淳紀, 高村 昌昭, 佐藤 好信, 大越 章吾, 市田 隆文, 青柳 豊

    肝臓   49 ( Suppl.1 )   A346 - A346   2008.4

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  • アンジオテンシンII受容体拮抗薬の抗ウイルス療法非適応C型慢性肝炎・肝硬変に対する臨床効果の検討

    松田 康伸, 佐藤 宗弘, 土屋 淳紀, 高村 昌昭, 山際 訓, 大越 章吾, 野本 実, 青柳 豊

    日本消化器病学会雑誌   105 ( 臨増総会 )   A306 - A306   2008.3

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  • 若年性皮膚筋炎に合併し、5年の経過で線維化の進行を肝組織像にて確認し得た非アルコール性脂肪性肝炎(NASH)の一例

    窪田 智之, 小林 真, 高村 昌昭, 五十嵐 正人, 川合 弘一, 松田 康伸, 野本 実, 青柳 豊

    日本消化器病学会雑誌   105 ( 臨増総会 )   A265 - A265   2008.3

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  • 抗ウイルス療法非適応C型慢性肝疾患に対するアンギオテンシンII受容体拮抗薬少量長期投与の臨床効果

    松田 康伸, 佐藤 宗広, 土屋 淳紀, 高村 昌昭, 山際 訓, 大越 章吾, 野本 実, 青柳 豊

    日本内科学会雑誌   97 ( Suppl. )   180 - 180   2008.2

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  • 原発性胆汁性肝硬変におけるToll-like receptor homolog RP105の発現低下

    山際 訓, 松田 康伸, 高村 昌昭, 土屋 淳紀, 野本 実, 青柳 豊

    日本内科学会雑誌   97 ( Suppl. )   179 - 179   2008.2

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  • 原発性胆汁性肝硬変合併筋炎の3例 臨床的特徴の検討

    津端 俊介, 青柳 智也, 田村 康, 川合 弘一, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    日本消化器病学会雑誌   104 ( 臨増大会 )   A686 - A686   2007.9

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  • 皮膚筋炎を合併した抗ミトコンドリア抗体陰性無症候性原発性胆汁性肝硬変の一例

    津端 俊介, 川合 弘一, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    ENDOSCOPIC FORUM for digestive disease   23 ( 1 )   72 - 72   2007.6

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  • 原発性胆汁性肝硬変におけるToll-like receptor homolog RP105の発現とLPS高反応性

    山際 訓, 本田 穣, 高村 昌昭, 松田 康伸, 市田 隆文, 青柳 豊

    肝臓   48 ( Suppl.1 )   A38 - A38   2007.4

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  • IFN-βによる肝発癌予防効果とその機序

    青木 洋平, 山崎 和秀, 鈴木 健太, 大越 章吾, 矢野 雅彦, 栗田 聡, 高村 昌昭, 山際 訓, 松田 康伸, 青柳 豊

    肝臓   48 ( Suppl.1 )   A280 - A280   2007.4

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  • ヘパリン置換療法下にESDを施行した早期胃癌の1例

    廣野 玄, 東海林 俊之, 竹内 学, 佐藤 祐一, 大嶋 智子, 河内 裕介, 塩路 和彦, 横山 純二, 佐々木 俊哉, 小林 正明, 松田 康伸, 杉村 一仁, 成澤 林太郎, 青柳 豊, 曽川 正和, 林 純一

    ENDOSCOPIC FORUM for digestive disease   22 ( 2 )   152 - 152   2006.11

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  • 細胞周期調節因子Id-1/p16/p27を指標にした肝硬変患者の発癌リスク予測診断システムの確立

    松田 康伸

    新潟県医師会報   ( 679 )   2 - 7   2006.10

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  • Early treatment by beta-IFN prevents the occurrence of HCC by inhibition of DNA synthesis and cell cycle progression: A study using a hepatocarcinogenic mouse model

    Kazuhide Yamazaki, Shogo Ohkoshi, Kenta Suzuki, Masahiko Yano, So Kurita, Yohhei Aoki, Masa-aki Takamura, Satoshi Yamagiwa, Yasunobu Matsuda, Yutaka Aoyagi

    HEPATOLOGY   44 ( 4 )   619A - 619A   2006.10

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  • 新潟大学関連施設におけるC型慢性肝炎に対するPEG-IFNα-2a療法の現状と血清CXCL10による治療効果予測

    山際 訓, 松田 康伸, 大越 章吾, 和栗 暢生, 杉山 幹也, 杉谷 想一, 宮島 透, 若林 博人, 高橋 達, 渡辺 俊明, 上村 朝輝, 青柳 豊

    肝臓   47 ( Suppl.2 )   A401 - A401   2006.9

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  • 肝内血流の不均衡によって興味深い画像及び組織所見を呈した原因不明の肝静脈血栓症の1例

    塙 孝泰, 青木 洋平, 橋本 哲, 竹内 学, 山際 訓, 松田 康伸, 大越 章吾, 野本 実, 青柳 豊

    ENDOSCOPIC FORUM for digestive disease   22 ( 1 )   72 - 72   2006.6

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  • 検査値の読み方 比較的若年の女性に起こった原因不明の肝静脈閉塞症の1例

    塙 孝泰, 大越 章吾, 青木 洋平, 竹内 学, 山際 訓, 松田 康伸, 野本 実, 青柳 豊

    臨床消化器内科   21 ( 8 )   1197 - 1202   2006.6

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  • 【レジデントのための内視鏡診療マニュアル】 「肝」 各肝疾患における腹腔鏡所見の特徴

    渡辺 俊明, 坂内 均, 瀧本 光弘, 高橋 達, 松田 康伸

    消化器内視鏡   18 ( 5 )   888 - 892   2006.5

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  • インターフェロンβによる肝発癌抑制効果へのアプローチ 正常肝細胞に対するインターフェロンβの効果について

    山崎 和秀, 大越 章吾, 鈴木 健太, 栗田 聡, 矢野 雅彦, 高村 昌昭, 山際 訓, 松田 康伸, 青柳 豊

    肝臓   47 ( Suppl.1 )   A263 - A263   2006.4

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  • マウス急性肝不全モデルにおけるc-Jun N-terminal kinase(JNK)阻害剤による肝細胞のアポトーシス抑制効果

    高村 昌昭, 松田 康伸, 山際 訓, 本田 穣, 市田 隆文, 青柳 豊

    肝臓   47 ( Suppl.1 )   A100 - A100   2006.4

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  • 生体肝移植症例における肝内樹状細胞の経時的検討

    山際 訓, 富山 智香子, 渡部 久実, 市田 隆文, 松田 康伸, 高村 昌昭, 本田 穣, 佐藤 好信, 青柳 豊

    消化器と免疫   ( 42 )   146 - 149   2006.4

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    生体肝移植症例の移植肝生着とDCとの関連性について検討することを目的とし,移植前後で経時的に肝臓内樹状細胞(DC)の変動を解析した.生体肝移植を施行したレシピエント12例,およびそのドナー12例を対象とした.移植後の拒絶反応の有無は,血液生化学的データと肝生検による病理組織学的検討により診断した.肝組織および末梢血よりFicoll比重遠心法でリンパ球を分離後,各種蛍光モノクローナル抗体で染色しフローサイトメトリーで解析した.正常肝内DCは成熟あるいは活性化型が多く,未熟型が多い末梢血中DCとは異なるフェノタイプを示した.拒絶反応の有無により移植肝内DCの違いを認め,移植肝生着に関与していることが示唆された

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  • 【Innate immunityと肝病態】 各種肝疾患と自然免疫 PBC病態における自然免疫の関与

    山際 訓, 松田 康伸, 石本 結子, 高村 昌昭, 本田 穣, 市田 隆文

    肝・胆・膵   52 ( 4 )   563 - 570   2006.4

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  • CEACAM1発現調節による肝癌細胞株の足場非依存性増殖能の獲得

    小林 万李子, 松田 康伸, 青柳 豊, 若井 俊文, 白井 良夫

    肝臓   47 ( Suppl.1 )   A80 - A80   2006.4

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  • C型慢性肝炎症例のNK細胞におけるNKG 2A高発現とその機序

    山際 訓, 松田 康伸, 本田 穣, 高村 昌昭, 市田 隆文, 青柳 豊

    肝臓   47 ( Suppl.1 )   A217 - A217   2006.4

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  • CXCL10によるC型慢性肝炎に対するPEG化インターフェロン治療効果予測

    山際 訓, 松田 康伸, 本田 穣, 高村 昌昭, 大越 章吾, 野本 実, 青柳 豊

    日本内科学会雑誌   95 ( Suppl. )   215 - 215   2006.2

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  • 肝臓 肝細胞癌の病態と診断

    山際 訓, 松田 康伸, 青柳 豊

    Annual Review消化器   2006   276 - 282   2006.1

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  • 【胆管系と自然免疫:生体防御と病態形成への関与】 胆管系の自然免疫 生体防御因子 Toll-like receptors PBC病態形成への関与

    山際 訓, 本田 穣, 高村 昌昭, 松田 康伸, 市田 隆文

    肝・胆・膵   51 ( 4 )   565 - 572   2005.10

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  • C型慢性肝炎に対するPEG-IFN治療効果と血清CXCL10及び肝臓内NK細胞を中心としたCXCR3陽性リンパ球との関連

    山際 訓, 松田 康伸, 本田 穣, 高村 昌昭, 市田 隆文, 青柳 豊

    肝臓   46 ( Suppl.2 )   A409 - A409   2005.9

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  • 肝再生医療の研究と臨床応用 G-CSF-CD26/DPPIV時間差調節を介した骨髄幹細胞による肝障害治療

    松田 康伸, 山際 訓, 青柳 豊

    日本消化器病学会雑誌   102 ( 臨増大会 )   A611 - A611   2005.9

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  • 肝硬変組織におけるId-1過剰発現と肝癌発症リスクの相互関係

    松田 康伸, 山際 訓, 高村 昌昭, 本田 譲, 市田 隆文, 青柳 豊

    日本癌学会総会記事   64回   176 - 176   2005.9

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  • マウス胎児肝幹前駆細胞の無血清長期継代培養およびその階層性の解析

    土屋 淳紀, 平家 俊男, 藤野 寿典, 塩田 光隆, 梅田 雄嗣, 吉本 桃子, 松田 康伸, 市田 隆文, 青柳 豊, 中畑 龍俊

    炎症・再生   25 ( 4 )   304 - 304   2005.7

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  • マウス急性肝傷害モデルにおける予防的HGF遺伝子治療の検討

    塙 孝泰, 鈴木 健司, 河内 裕介, 松田 康伸, 丸山 弘樹, 韓 基東, 河内 裕, 清水 不二雄, 宮崎 純一, 朝倉 均, 青柳 豊

    消化器と免疫   ( 41 )   172 - 175   2005.5

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    四塩化炭素によるマウス急性肝障害モデルに対し,ハイドロダイナミクス法を用いて肝臓にHGF(肝細胞増殖因子)遺伝子導入を行った群とControl gene導入群を作製し,治療効果を比較した.HGF遺伝子導入群は血清ALT値が有意に低く,組織学的には傷害がより軽度であり,免疫組織学的にはBrdU陽性細胞数の増加と炎症細胞の肝浸潤抑制がより顕著であった.また,Control gene導入群でTUNEL陽性細胞数が増加したのに対してHGF遺伝子導入群では有意に減少した

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  • 原発性胆汁性肝硬変におけるtoll様レセプターを介した単核球活性化の検討

    本田 穣, 山際 訓, 青柳 豊, 松田 康伸, 石本 結子, 高村 昌明, 野本 実, 市田 隆文

    肝臓   46 ( Suppl.1 )   A170 - A170   2005.5

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  • C型慢性肝炎における末梢血単核球レクチン結合能の特性

    山際 訓, 松田 康伸, 青柳 豊, 市田 隆文, 本田 穣, 高村 昌昭, 富山 智香子, 渡部 久実

    肝臓   46 ( Suppl.1 )   A227 - A227   2005.5

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  • 消化器領域におけるプロテオーム研究の現状と新しい展開 肝癌周囲組織のプロテオーム解析により推定されたoval cell由来肝細胞の発現蛋白異常

    松田 康伸, 市田 隆文, 青柳 豊

    日本消化器病学会雑誌   102 ( 臨増総会 )   A67 - A67   2005.3

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  • 大腸癌におけるliver-intestine cadherin(LI-cadherin)発現の臨床病理学的意義の検討

    高村 昌昭, 市田 隆文, 松田 康伸, 小林 正明, 山際 訓, 玄田 拓哉, 塩路 和彦, 橋本 哲, 野本 実, 畠山 勝義, 味岡 洋一, 坂元 亨宇, 広橋 説雄, 青柳 豊

    日本消化器病学会雑誌   102 ( 臨増総会 )   A284 - A284   2005.3

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  • 肝癌周囲組織に発現上昇するferritin light chain(FLC)の発癌危険因子としての臨床学的検討

    松田 康伸, 山際 訓, 高村 昌昭, 石本 結子, 本田 穣, 青柳 豊

    日本内科学会雑誌   94 ( Suppl. )   121 - 121   2005.2

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  • 多彩な内視鏡像を呈したサルコイドーシス胃病変の一例

    大嶋 智子, 三浦 隆義, 佐藤 祐一, 松田 康伸, 杉村 一仁, 本間 照, 小林 正明, 味岡 洋一, 稲庭 謙一, 成澤 林太郎, 青柳 豊

    ENDOSCOPIC FORUM for digestive disease   20 ( 2 )   172 - 172   2004.11

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  • セクタ型超音波探触子により腹腔鏡下ラジオ波焼灼術(LRFA)が可能であった表在性肝細胞癌の1例

    矢野 雅彦, 松田 康伸, 三浦 隆義, 大嶋 智子, 福原 康夫, 本間 信之, 小林 真, 五十嵐 正人, 玄田 拓哉, 和栗 暢生, 川合 弘一, 山際 訓, 青柳 豊

    ENDOSCOPIC FORUM for digestive disease   20 ( 2 )   151,162 - 157,162   2004.11

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    78歳男.肝被膜下表面のS3-4およびS3に存在する径12mm大と5mm大の肝細胞癌再発巣に対し,制癌剤動注療法後にLRFAを施行した.腹腔鏡下に病変を直視することはできなかったが,トロカールから挿入したセクタ型超音波探触子によって2つの病変が確認でき,正確な焼灼が行えた

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  • 薬物性肝障害の実態と今後の課題 薬剤性肝障害の診断と予後予測における組織学的検討の意義と自己免疫性肝炎急性型との比較

    野本 実, 松田 康伸, 青柳 豊

    肝臓   45 ( Suppl.3 )   A542 - A542   2004.11

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  • 検査値の読み方 抗ミトコンドリア抗体陰性原発性胆汁性肝硬変の1例

    大越 章吾, 小林 久里子, 見田 有作, 山際 訓, 松田 康伸, 野本 実, 青柳 豊

    臨床消化器内科   19 ( 13 )   1806 - 1810   2004.11

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  • Increase of regulatory CD4(+)CD25(+) T cells in the liver of patients with hepatocellular carcinoma.

    S Yamagiwa, XH Yang, S Sugahara, Y Honda, Y Matsuda, Y Aoyagi, DA Horwitz, T Ichida

    HEPATOLOGY   40 ( 4 )   311A - 311A   2004.10

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  • G-CSF/SDF-1系を介した骨髄細胞の肝細胞分化

    松田 康伸, 市田 隆文, 青柳 豊

    肝臓   45 ( Suppl.2 )   A358 - A358   2004.9

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  • 薬物性肝障害をめぐる諸問題 薬剤性肝障害の診断と予後推定に対する組織学的検討の意義

    野本 実, 松田 康伸, 青柳 豊

    日本消化器病学会雑誌   101 ( 臨増大会 )   A605 - A605   2004.9

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  • 再生医療は移植医療にとってかわるか? G-CSF/SDF-1系を介した骨髄細胞の肝細胞分化

    松田 康伸, 市田 隆文, 青柳 豊

    日本消化器病学会雑誌   101 ( 臨増大会 )   A421 - A421   2004.9

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  • 肝癌周囲正常組織における肝細胞のプロテオーム解析

    松田 康伸, 市田 隆文, 山際 訓, 高村 昌昭, 青柳 豊

    日本癌学会総会記事   63回   451 - 451   2004.9

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  • 薬剤性肝障害の診断と予後推定に対する組織学的検討の意義

    野本 実, 松田 康伸, 青柳 豊

    肝臓   45 ( Suppl.2 )   A416 - A416   2004.9

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  • マウス胎児肝幹前駆細胞の長期継代培養の試み

    土屋 淳紀, 平家 俊男, 藤野 寿典, 塩田 光隆, 梅田 雄嗣, 吉本 桃子, 松田 康伸, 市田 隆文, 青柳 豊, 中畑 龍俊

    炎症・再生   24 ( 4 )   500 - 500   2004.7

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  • 【内視鏡ことわざ・寸言集】 肝 豹紋はPBCを疑え

    渡辺 俊明, 坂内 均, 瀧本 光弘, 松田 康伸

    消化器内視鏡   16 ( 6 )   1019 - 1020   2004.6

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  • p27強発現肝癌組織におけるCDK2活性及び関連細胞周期調節因子の解析

    松田 康伸, 市田 隆文, 山際 訓, 玄田 拓也, 青柳 豊

    肝臓   45 ( Suppl.1 )   A158 - A158   2004.4

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  • 肝炎ウイルス増殖機構の解明と治療戦略 C型慢性肝炎に対するInterferonとRibavirin併用療法の治療反応性の違いにおける肝臓内リンパ球及び肝臓発現遺伝子の変動

    山際 訓, 市田 隆文, 青柳 豊, 松田 康伸

    肝臓   45 ( Suppl.1 )   A18 - A18   2004.4

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  • Attenuation of acute liver injury of mice by hepatocyte growth factor gene transfer to the liver via tail vein

    T Hanawa, K Suzuki, Y Kawauchi, Y Matsuda, H Yoneyama, H Maruyama, GD Han, H Kawachi, F Shimizu, JI Miyazaki, H Asakura, Y Aoyagi

    GASTROENTEROLOGY   126 ( 4 )   A492 - A492   2004.4

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  • 8 画像学的に診断し得なかった肝腫瘍の一例(I.一般演題,第26回リバーカンファレンス総会)

    藤村 健夫, 佐藤 明人, 松田 康伸, 小林 真, 和栗 暢生, 須田 剛士, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 山本 哲史, 加村 毅

    新潟医学会雑誌   117 ( 11 )   653 - 653   2003.11

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  • 37 当科における自己免疫性肝炎に合併した肝細胞癌の検討(I.一般演題,第27回リバーカンファレンス総会)

    大橋 和政, 土屋 淳紀, 松田 康伸, 市田 隆文, 野本 実, 青柳 豊

    新潟医学会雑誌   117 ( 11 )   674 - 674   2003.11

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  • 19 PIVKA-II高値を呈した肝限局性結節性過形成の一例(I.一般演題,第27回リバーカンファレンス総会)

    東海林 俊之, 丸山 弦, 松田 康伸, 市田 隆文, 野本 実, 青柳 豊, 畑 耕治郎

    新潟医学会雑誌   117 ( 11 )   668 - 668   2003.11

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  • 22 好酸球増多と類上皮肉芽腫を認めた原発性硬化性胆管炎の一例(I.一般演題,第26回リバーカンファレンス総会)

    浦川 佳美, 江部 和人, 松田 康伸, 高橋 達, 野本 実, 市田 隆文, 青柳 豊, 朝倉 均

    新潟医学会雑誌   117 ( 11 )   658 - 658   2003.11

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  • 当科における自己免疫性肝炎に合併した肝細胞癌の検討

    大橋 和政, 土屋 淳紀, 松田 康伸, 市田 隆文, 野本 実, 青柳 豊

    新潟医学会雑誌   117 ( 11 )   674 - 674   2003.11

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  • PIVKA-II高値を呈した肝限局性結節性過形成の一例

    東海林 俊之, 丸山 弦, 松田 康伸, 市田 隆文, 野本 実, 青柳 豊, 畑 耕治郎

    新潟医学会雑誌   117 ( 11 )   668 - 668   2003.11

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  • 好酸球増多と類上皮肉芽腫を認めた原発性硬化性胆管炎の一例

    浦川 佳美, 江部 和人, 松田 康伸, 高橋 達, 野本 実, 市田 隆文, 青柳 豊, 朝倉 均

    新潟医学会雑誌   117 ( 11 )   658 - 658   2003.11

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  • 画像学的に診断し得なかった肝腫瘍の一例

    藤村 健夫, 佐藤 明人, 松田 康伸, 小林 真, 和栗 暢生, 須田 剛士, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 山本 哲史, 加村 毅

    新潟医学会雑誌   117 ( 11 )   653 - 653   2003.11

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  • 【偶発症とその対策 こんな時どうする】 腹腔鏡 前処置・診断 気腹操作による腹腔内出血

    松田 康伸, 高橋 達, 渡辺 俊明

    消化器内視鏡   15 ( 10 )   1450 - 1451   2003.10

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  • 【偶発症とその対策 こんな時どうする】 腹腔鏡 前処置・診断 腹腔鏡下肝生検による出血

    松田 康伸, 高橋 達, 渡辺 俊明

    消化器内視鏡   15 ( 10 )   1452 - 1453   2003.10

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  • Integrin-stimulated cell scattering is regulated by extracellular signal-regulated kinase (ERK) pathways in highly metastatic hepatocellular carcinoma cells.

    N Honma, T Genda, Y Matsuda, T Ichida, Y Aoyagi

    HEPATOLOGY   38 ( 4 )   567A - 567A   2003.10

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  • Serial phenotypic profiling of intrahepatic lymphocytes in patients with chronic hepatitis C before and after combination interferon alpha-2b and ribavirin therapy.

    S Yamagiwa, T Ichida, S Okoshi, XH Yang, Y Ishimoto, T Genda, Y Matsuda, T Abo, Y Aoyagi, H Watanabe

    HEPATOLOGY   38 ( 4 )   460A - 460A   2003.10

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  • 生体肝移植症例における原発性胆汁性肝硬変の肝内リンパ球解析

    石本 結子, 山際 訓, 市田 隆文, 菅原 聡, 佐藤 好信, 松田 康伸, 青柳 豊

    肝臓   44 ( Suppl.1 )   A111 - A111   2003.4

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  • CDC25Aホスファターゼの発現は肝細胞癌の脱分化と悪性度に強い関連性を示す

    栗田 聡, 市田 隆文, 松田 康伸, 玄田 拓哉, 山際 訓, 青柳 豊

    肝臓   44 ( Suppl.1 )   A174 - A174   2003.4

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  • MAPK pathwayの活性化は高転移性肝がん細胞のscatteringを誘導する

    本間 信之, 玄田 拓哉, 松田 康伸, 市田 隆文, 青柳 豊

    肝臓   44 ( Suppl.1 )   A163 - A163   2003.4

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  • Docetaxel/CDDP/UFT-E全身化学療法が奏効した肝細胞癌肺転移の1例

    石川 達, 市田 隆文, 横山 純二, 松田 康伸, 渡辺 俊明, 青柳 豊

    日本消化器病学会雑誌   100 ( 臨増総会 )   A268 - A268   2003.3

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  • <学会記事>23 CT・MRI で描出できず, CTA で腫瘤性病変を明瞭に描出可能であった膵癌の一治験例(一般演題)(第 71 回新潟消化器病研究会)

    渡辺 史郎, 杉谷 想一, 竹内 学, 和栗 暢生, 川合 弘一, 須田 剛士, 松田 康伸, 藤原 敬人, 本山 展隆, 渡辺 雅史, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 黒崎 功, 畠山 勝義, 加村 毅

    新潟医学会雑誌   116 ( 8 )   410 - 410   2002.8

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  • CT・MRIで描出できず,CTAで腫瘤性病変を明瞭に描出可能であった膵癌の一治験例

    渡辺 史郎, 杉谷 想一, 竹内 学, 和栗 暢生, 川合 弘一, 須田 剛士, 松田 康伸, 藤原 敬人, 本山 展隆, 渡辺 雅史, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 黒崎 功, 畠山 勝義, 加村 毅

    新潟医学会雑誌   116 ( 8 )   410 - 410   2002.8

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    Other Link： http://search.jamas.or.jp/link/ui/2003147049

  • 肝臓癌におけるp27発現レベルと機能の相互関係の解析

    松田 康伸, 市田 隆文, 栗田 聡, 朝倉 均

    日本癌学会総会記事   60回   329 - 329   2001.9

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  • Nonalcoholic steatohepatitis(NASH)の3例

    和栗 暢生, 高橋 達, 川合 弘一, 塩路 和彦, 杉山 幹也, 小林 真, 渡辺 孝治, 五十嵐 正人, 稲吉 潤, 上原 一浩, 石川 達, 見田 有作, 松田 康伸, 市田 隆文, 野本 実, 朝倉 均

    ENDOSCOPIC FORUM for digestive disease   17 ( 1 )   88 - 88   2001.6

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  • 原発性胆汁性肝硬変と自己免疫性肝炎の境界症例と考えられた1例

    見田 有作, 高橋 達, 松田 康伸, 松井 茂, 瀧本 光弘, 石川 達, 川合 弘一, 坪井 康紀, 和栗 暢生, 山田 尚志, 黒岩 敬, 上原 一浩, 五十嵐 正人, 稲吉 潤, 渡辺 孝治, 市田 隆文, 青柳 豊, 朝倉 均

    ENDOSCOPIC FORUM for digestive disease   16 ( 2 )   158,173 - 164,173   2000.11

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    71歳女.胆道系優位の肝機能異常を認め,抗ミトコンドリア抗体は陰性であったが,抗核抗体および抗平滑筋抗体は陽性であり,自己免疫性肝炎の国際診断基準によるスコアは11点であった.腹腔鏡では溝状陥凹を有する起伏状変化の上に,大小不同の半球状結節が散在する肝表面像で,自己免疫性肝炎に近い像であった.組織では門脈域にpiecemeal necrosisを伴う細胞浸潤を認め,granulomaは認めないものの,ductpeniaと変性した隔壁胆管を認め,原発性胆汁性肝硬変も否定できない所見であった.これらの所見から,自己免疫性肝炎と原発性胆汁性肝硬変の境界に位置する症例と考え,ursodesoxycholic acid 300mg/日を投与し,経過をみているが,現在まで肝機能の悪化は認めていない

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  • 原発性胆汁性肝硬変(PBC)と自己免疫性肝炎(AIH)との境界症例と考えられた一例

    見田 有作, 高橋 達, 松田 康伸, 松井 茂, 瀧本 光弘, 石川 達, 川合 弘一, 菅原 聡, 坪井 康紀, 和栗 暢生

    ENDOSCOPIC FORUM for digestive disease   16 ( 2 )   187 - 187   2000.11

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  • 腹腔鏡下マイクロ波凝固療法(LMCT)を行った表在型肝癌3例

    松田 康伸, 高橋 達, 松井 茂, 朴 載広, 石川 達, 川合 弘一, 見田 有作, 和栗 暢生, 黒岩 敬, 上原 一浩, 市田 隆文, 青柳 豊, 朝倉 均

    ENDOSCOPIC FORUM for digestive disease   15 ( 2 )   199,238 - 204,238   1999.11

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    腹腔鏡下マイクロ波凝固治療(laparoscopic microwave coagulation therapy:LMCT)が有用であった表在型肝癌を3例(症例1:69歳女,症例2:70歳男,症例3:72歳女)を経験した.全例共にS3区域肝表面に存在する肝細胞癌であった.症例1の腫瘍は径6mmで肝表面に突出しており,腹腔鏡施行時に発見された.症例2の腫瘍は径2cmで,肝表面に腫瘍を視認できなかったが,腹腔鏡下超音波走査により描出可能であった.症例の3の腫瘍は径1cmで肝表面に突出しており,腹腔鏡で視認できたが,腹膜癒着のためLMCTのみでは十分なtreated marginを確保できず,LMCT施行時に経皮エタノール注入(PEIT)を追加した.いずれの症例も術後,画像検査で十分なtreated marginが得られた

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  • 腹腔鏡下マイクロ波凝固治療(LMCT)を行った表在型肝癌3例

    松田 康伸, 高橋 達, 松井 茂, 朴 載広, 石川 達, 川合 弘一, 見田 有作, 和栗 暢生, 黒岩 敬, 上原 一浩

    ENDOSCOPIC FORUM for digestive disease   15 ( 2 )   247 - 247   1999.11

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  • 血漿DNAを用いた膵・胆管癌スクリーニングの試み

    松田 康伸, 市田 隆文, 朝倉 均

    Gastroenterological Endoscopy   41 ( Suppl.2 )   1745 - 1745   1999.9

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  • 臨床応用可能な分子生物学 血漿DNAを用いた膵・胆管癌スクリーニングの試み

    松田 康伸, 市田 隆文, 朝倉 均

    胆道   13 ( 3 )   207 - 207   1999.9

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  • 肝癌におけるp16INK4遺伝子不活化機構の検討

    松田 康伸, 市田 隆文, 松澤 純, 杉村 一仁, 朝倉 均

    日本癌学会総会記事   58回   558 - 558   1999.8

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  • 【症候・病態の分子メカニズム】 消化器 主要疾患・症候群 膵・胆管癌

    松田 康伸, 朝倉 均

    Molecular Medicine   35 ( 臨増 )   167 - 168   1998.12

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  • 非B非C型肝疾患及び自己免疫性肝炎におけるTTV感染に関する検討

    高橋 達, 朴 載広, 松井 茂, 松田 康伸, 武田 康男, 大越 章吾, 市田 隆文, 朝倉 均

    肝臓   39 ( Suppl.3 )   82 - 82   1998.10

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  • 血漿DNAを用いた膵癌・胆管癌診断の試み

    松田 康伸, 小林 正明, 鈴木 裕, 新井 太, 坪井 康紀, 市田 隆文, 波多野 徹, 若井 俊文, 斎藤 英樹, 清水 武昭

    日本癌学会総会記事   57回   237 - 237   1998.8

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  • 18)多発性筋炎(PM)を合併した無症候性原発性胆汁性肝硬変(a-PBC)の2例(一般演題, 第65回新潟消化器病研究会 )

    丸山 貴広, 馬場 靖幸, 小柳 佳成, 松田 康伸, 鈴木 康史, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 高野 政彦, 広瀬 慎太郎, 小山 裕子, 粟森 和明, 姉崎 利治, 中野 亮一

    新潟医学会雑誌   112 ( 5 )   287 - 287   1998.5

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  • 多発性筋炎(PM)を合併した無症候性原発性胆汁性肝硬変(a-PBC)の2例

    丸山 貴広, 馬場 靖幸, 小柳 佳成, 松田 康伸, 鈴木 康史, 高橋 達, 野本 実, 青柳 豊, 朝倉 均, 高野 政彦

    新潟医学会雑誌   112 ( 5 )   287 - 287   1998.5

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  • 食塩水を併用した針電極組織内加温の検討

    斎藤 義明, 堀 潤一, 市田 隆文, 松田 康伸, 渡辺 雅史

    日本ハイパーサーミア学会誌   13 ( 4 )   245 - 245   1997.12

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  • 肝細胞癌におけるp16/INK4A/CDKN2遺伝子発現変動の検討

    松田 康伸

    肝臓   38 ( Suppl.2 )   157 - 157   1997.9

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  • Extention of Heating Range of Interstitial Needle RF Hyperthermia Using Saline

    SAITOH Yoshiaki, ICHIDA Takafumi, HORI Jun-ichi, MATSUDA Yasunobu, WATANABE Masafumi

    日本ハイパーサーミア学会誌 = Japanese journal of hyperthermic oncology   13 ( 2 )   68 - 74   1997.6

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    組織内癌温熱療法の一つである針電極によるRF加温の場合, 加温領域が狭いという問題があった.本研究では, 加温対象に食塩水を注入し, 導電率を高めることによって, 加温領域を拡大することを試みた.切離した豚の肝臓を対象として加温実験を行った結果, 食塩水の濃度が高いほど, また針電極の直径が太いほど加温領域が拡大した.Interstitial hyperthermia by using a needle electrode has problem that heating range is too narrow to apply for massive tissues. In this study, we tried to extend the heating range by using high-conductivity saline pouring into the heating object. In experiments of RF power heating using pig livers, the higher salt concentration or the thicker the diameter of the needle electrode, the wider the heating range.

    DOI： 10.3191/thermalmedicine.13.68

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  • Extention of heating range of interstitial needle RF hyperthermia using saline

    Yoshiaki Saitoh, Takafumi Ichida, Junichi Hori, Yasunobu Matsuda, Masafumi Watanabe

    Japanese Journal of Hyperthermia Oncology   13 ( 2 )   68 - 74   1997

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  • 腹腔鏡アトラス アルコール性肝障害

    高橋 達, 松田 康伸, 佐藤 万成

    消化器内視鏡   8 ( 10 )   1414 - 1417   1996.10

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  • ラット肝硬変モデルにおけるアクチビンA発現変動の検討

    杉山 幹也, 松田 康信, 市田 隆文, 朝倉 均

    日本分子生物学会年会プログラム・講演要旨集   19   698 - 698   1996.8

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  • 31) 肝細胞癌に対する経皮的マイクロ波凝固療法(I. 一般演題, 第20回リバーカンファレンス総会)

    渡辺 雅史, 市田 隆文, 松田 康伸, 佐藤 知巳, 原田 武, 小柳 佳成, 五十嵐 広隆, 藤井 久一, 内田 守昭, 柳 雅彦, 青柳 豊, 朝倉 均

    新潟医学会雑誌   110 ( 8 )   358 - 358   1996.8

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  • 肝癌の治療 肝細胞癌に対する化学療法

    市田 隆文, 松田 康伸, 渡辺 雅史

    臨床成人病   26 ( 4 )   475 - 479   1996.4

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  • 肝癌治療症例のプロトコール 新潟大学医学部第3内科

    市田 隆文, 松田 康伸, 渡辺 雅史

    臨床成人病   26 ( 4 )   506 - 507   1996.4

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  • 28)特異な発育形態を示した大腸ポリープの1例(一般演題, 第61回新潟消化器病研究会)

    菅原 聡, 松田 康伸, 波田野 徹, 窪田 久, 富所 隆, 戸枝 一明, 杉山 一教

    新潟医学会雑誌   109 ( 9 )   439 - 439   1995.10

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  • ヒトリコンビナントHGF投与によるラット肝硬変の抑制および肝不全死の防止作用

    松田 康伸

    肝臓   36 ( Suppl.1 )   206 - 206   1995.6

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  • ヒトリコンビナントHFG投与によるラット肝線維症/肝硬変ならびに肝不全死の防止作用

    松田 康伸

    日本癌学会総会記事   53回   474 - 474   1994.10

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  • リコンビナントヒトHGF外因性投与はラット肝線維症/肝硬変および肝不全死を抑制する

    松田 康伸

    生化学   66 ( 7 )   748 - 748   1994.7

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  • 肝細胞増殖因子(HGF)による肝再生調節

    松田 康伸, 中村 敏一

    BIO Clinica   9 ( 4 )   243 - 249   1994.4

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  • 肝臓の分子病態生理学 肝再生 肝細胞増殖因子(HGF)の分子生物学

    松田 康伸, 中村 敏一

    日本臨床   51 ( 2 )   435 - 445   1993.2

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  • 7) 腹腔内にimplantationしたと思われた肝細胞癌の1例(I.一般演題, 第24回新潟画像医学研究会）

    尾崎 俊彦, 松田 康伸, 本間 明, 相場 哲朗, 川口 正樹

    新潟医学会雑誌   106 ( 5 )   455 - 455   1992.5

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  • 肝細胞癌初期病変におけるAgNOR染色による腫瘍細胞増殖能の検討

    松田 康伸, 市田 隆文, 宮崎 裕

    肝臓   33 ( 1 )   76 - 76   1992.1

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    核1個当りのAgNOR個数は,正常肝1.34±0.11 (mean±SD),慢性肝炎1.83±0.22,肝硬変1.93±0.40,細小肝癌2.64±0.52,進行性肝細胞癌3.93±0.60であった.細小肝癌は,肝硬変に比し,統計学的に有意差(p&lt;0.01)をもって個数の増加が認められた.進行性肝細胞癌との間にも有意差(p&lt;0.01)を認めた

    DOI： 10.2957/kanzo.33.76

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  • 経過中に尿崩症を呈した再膨脹性肺水腫(RPE)の1例

    松田 康伸, 星野 重幸, 八幡 和明

    日本胸部臨床   50 ( 12 )   1010 - 1015   1991.12

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    24歳男,ショック状態を呈したRPE.この時,経過中に一過性に尿崩症を併発し,その他に脳下垂体ホルモンの低下をきたした

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  • 肝細胞癌における5年以上長期生存例の臨床的検討

    松田 康伸

    肝臓   32 ( Suppl.3 )   87 - 87   1991.10

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  • 16) 腹腔内にimplantationしたと思われた肝細胞癌の1例(II.一般演題, 第15回リバーカンファレンス総会)

    松田 康伸, 本間 明, 尾崎 俊彦, 相場 哲朗, 川口 正樹

    新潟医学会雑誌   105 ( 8 )   567 - 567   1991.8

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  • 7) 穿孔性腹膜炎を来たした腸管ベーチェット病の1例(I.一般演題, 第232回新潟外科集談会）

    相場 哲朗, 川口 正樹, 前田 和夫, 尾崎 俊彦, 本間 明, 松田 康伸

    新潟医学会雑誌   105 ( 8 )   570 - 570   1991.8

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  • 16) 大腸におけるstrip biopsy症例の検討(一般演題, 第53回新潟消化器病研究会）

    本間 明, 松田 康伸, 尾崎 俊彦, 相場 哲朗, 川口 正樹, 太田 玉紀

    新潟医学会雑誌   105 ( 7 )   498 - 498   1991.7

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  • 腹腔内に発生した血管周被細胞腫の1例

    松田 康伸

    日本消化器病学会雑誌   88 ( 臨増 )   1038 - 1038   1991.3

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  • 腸結核瘢痕に合併した大腸癌の1例

    松田 康伸

    日本消化器病学会雑誌   88 ( 臨増 )   591 - 591   1991.2

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  • UEA-I染色を用いた肝内小結節性病変の組織化学的検討

    波田野 徹, 市田 隆文, 畑 耕治郎, 山田 慎二, 松田 康伸, 宮崎 裕, 上村 朝輝, 朝倉 均

    肝臓   32 ( 10 )   967 - 967   1991

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  • 10）胃全摘後空腸重積症の1例（I.一般演題, 第23回新潟画像医学研究会）

    松田 康伸, 尾崎 俊彦, 本間 明, 相場 哲朗, 川口 正樹

    新潟医学会雑誌   104 ( 11 )   979 - 979   1990.11

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  • 胃全摘後空腸重積症の1例

    松田 康伸

    新潟医学会雑誌   104 ( 11 )   979 - 979   1990.11

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  • 3) ステロイド剤大量投与に起因するB型重症肝炎にインターフェロンが著効を奏した1例（一般演題, 第14回リバーカンファレンス総会）

    佐々木 亮, 小方 則夫, 田中 泰樹, 松田 康伸, 野本 実, 上村 朝輝, 朝倉 均, 須田 剛士, 宮武 正

    新潟医学会雑誌   104 ( 9 )   804 - 804   1990.9

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Awards

  • travel grant award

    2013.10   欧州消化器病学会  

    MATSUDA Yasunobu

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  • 奨励賞

    2011.10   日本臨床分子形態学会  

    松田 康伸

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  • 学術奨励賞

    2006.10   新潟県医師会  

    松田 康伸

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  • 市田賞

    2002.6   新潟大学医学部消化器内科学  

    松田 康伸

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  • JB論文賞

    1996.6   日本生化学会  

    松田 康伸

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Research Projects

  • 胆管がん腫瘍再増殖の予防法確立を目指したエクソソーム蛋白活性化機構の解析

    Grant number：22K07979

    2022.4 - 2025.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    松田 康伸, 小林 隆, 坂田 純

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    Grant amount：\3900000 （ Direct Cost: \3000000 、 Indirect Cost：\900000 ）

    本研究の目的は、胆管がんにおける化学療法後の腫瘍再増殖(TR)現象を、エクソソーム制御により予防する方法を確立することである。本研究では、この目的をさぐるために、i) 予備検討で明らかになった、胆管がんエクソソームの化学療法後のセリン・スレオニンキナーゼp38MAPK活性化機構を検討するとともに、ii) 化学療法休薬中のがんエクソソーム蛋白を網羅的解析して、p38MAPKの以外のTR促進因子の探索も行うことを計画した。
    本年度においては、上記の実験計画i)を主に行った。具体的には、胆道がん細胞（胆管がんHuCCT1、胆のうがんNOZ)に抗がん剤（ゲムシタビン、シスプラチン）を投与し、エクソソーム量・活性（増殖/転移促進）を解析するとともに、エクソソーム内部のp38MAPKのリン酸化レベルをウエスタン・ブロット法を用いて解析した。
    その結果、胆管がんのエクソソーム分泌量は抗がん剤刺激で1.7-3倍程度に増加していたが、エクソソーム内部のp38MAPK含有量は、有意な変化を認めなかった。一方、p38MAPKのリン酸化レベルは10数倍に増加しており、化学療法で刺激されたがん細胞のエクソソーム内部では、p38MAPK経路が著明に活性かしていることが明らかになった。次に、エクソソーム内部のp38MAPKシグナル経路をさらに詳細に調べたところ、がん抑制遺伝子p53変異を伴うHuCCT1細胞においては、p38MAPKの下流シグナル因子であるMAPKAP-2も同様に10-15倍レベルに活性化していることが明らかになった。以上の結果をもとに、次年時以降はp53-p38MAPK-TR現象の関連をさらに探索するとともに、上述の実験計画ii)も併せて行う予定である。
    なお、以上の実験は、既存の試薬・機器・消耗品を用いて行えたので、当該年度での支出を可能な限り抑えることができた。

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  • Development of Artificial Intelligence by Deep Learning Based on Genomic High-Dimensional Data Analysis System for Gastrointestinal Cancer

    Grant number：21H02998

    2021.4 - 2024.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\17420000 （ Direct Cost: \13400000 、 Indirect Cost：\4020000 ）

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  • Extend islet graft survival in pancreatic islet transplantation by applying the immunoregulatory mechanism of ceramide

    Grant number：20K21628

    2020.7 - 2023.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Challenging Research (Exploratory)

    Awarding organization：Japan Society for the Promotion of Science

    Kobayashi Takashi

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    Grant amount：\6500000 （ Direct Cost: \5000000 、 Indirect Cost：\1500000 ）

    Insulin independence after pancreatic islet transplant for diabetes mellitus is mainly limited by early immunological reaction, such as instant blood-mediated inflammatory reaction (IBMIR). It induces a high rate of post-procedure beta cell apoptosis and leads to islet graft loss. Ceramide is a lipid mediator and acts as a signal transmitter. Ceramide is also reported to activate regulatory T cell and modulate local immunity to prevent excessive immune reactions. The purpose of this study is to clarify whether ceramide may improve the function of pancreatic islet grafts. The results of this study suggest that administration of ceramide induced regulatory T cells and contributed to functional improvement of pancreatic islet grafts.

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  • Molecular analysis of the drug resistance mediated by exosomes in biliary tract cancer

    Grant number：19K08365

    2019.4 - 2022.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    MATSUDA YASUNOBU

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    Grant amount：\4030000 （ Direct Cost: \3100000 、 Indirect Cost：\930000 ）

    [Aim of research] Biliary tract cancer is a malignant disease for which life-prolonging treatment by chemotherapy is difficult. The purpose of this study is to explore the possibility of anticancer drug resistance in exosomes released by biliary tract cancer cells.
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    [Results & Conclusion] Results of experiments using chemical inhibitors and gene silencing techniques showed that exosomes released from biliary tract cancer play a vital role in tumor regrowth or drug resistance via the stress kinase p38MAPK.

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  • 消化器発癌における免疫老化による免疫監視不全の関与の解明と新規先制医療の開発

    Grant number：18K07965

    2018.4 - 2021.3

    System name：科学研究費助成事業 基盤研究(C)

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    山際 訓, 寺井 崇二, 高村 昌昭, 松田 康伸

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    Grant amount：\4290000 （ Direct Cost: \3300000 、 Indirect Cost：\990000 ）

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  • Creation of next-generation cell therapy for diabetes with focus on nesidioblastic change

    Grant number：17H04270

    2017.4 - 2020.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：Japan Society for the Promotion of Science

    Kobayashi Takashi

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    Grant amount：\17160000 （ Direct Cost: \13200000 、 Indirect Cost：\3960000 ）

    It was confirmed that stress protein expression was nesidioblastic changes observed in chronic pancreatitis tissue, and that similar proteins were also induced in drug induced pancreatitis models. Although stress proteins have been reported to promote graft engraftment, it is likely that stress-related proteins are also involved in graft engraftment with nesidioblastic changes. In addition, the usefulness of GLP-1 was suggested as a drug that may promote the regeneration of transplanted islets after engraftment of islets and improve blood glucose.

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  • Elucidation of clinical significance and chemotherapy resistance mechanism of NAD(P)H:quinone oxidoreductase 1 (NQO1) expression for colorectal liver metastasis

    Grant number：17K10663

    2017.4 - 2020.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Nakano Mae

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    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

    NQO1 is an antioxidant stress protein. The expression of NQO1 is enhanced under stressed environment in vivo. We studied how NQO1 expression affects response of preoperative chemotherapy and prognosis in colorectal liver metastasis. In this study, immunohistochemistry using monoclonal antibody was performed on the resected specimen of colorectal liver metastasis, and the expression of NQO1 was analyzed. The NQO1 positive group had worse overall survival than the NQO1 negative group, and the presence of NQO1 polymorphism was associated with a better response to preoperative chemotherapy. The expression pattern of NQO1 can predict the prognosis and the response of preoperative chemotherapy in patients with colorectal liver metastasis.

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  • Regenetative medicine using decidouous teeth preparing for future diseases

    Grant number：17K08966

    2017.4 - 2020.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Shogo Ohkoshi

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    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    Dental pulp-derived mesenchymal stem cells were differentiated into polygonal hepatocyte-like cells(HLCs) under the presence of Activin A, FGF and HGF in culture media. These cells could convert ammonium into urea and expressed HGFd HGF-4, that revealed mature hepatocyte function of the cells. We observed the suppression of severity of experimental chemical hepatitis by infusing cells via tail veins.We also developed specific PCR primers that could specifically differentiate human cells from rat cells. We clarified the dynamic changes of HLCs in nude-rat livers when infused directly into portal veins.

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  • The mechanism of exosome-mediated drug resistance in hepatoma cells

    Grant number：16K09347

    2016.4 - 2019.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Yasunobu MATSUDA

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    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    Recently, it has been regarded that cells secret exosome (nano-sized vesicles (20-100 nm)), which participate in various types of cell-cell communication. In this study, we examined the mechanism of exosome secretion in hepatoma cells, and found that exosome exert drug resistance to anticancer drugs. Our obtained results showed that anticancer drugs (cisplatin and 5-fluorouracil) stimulate the secretion of exosome in human hepatoma cells. When cells were incubated with anticancer drug-treated cells-derived exosome, they acquired strong resistance to anticancer drugs. We found that activated type of mTOR, a serine-threonine kinase which plays a pivotal role in the cell survival, was significantly increased in exosome. Collectively, exosome exerts drug resistance through mTOR signaling in hepatoma cells.

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  • Histochemical analysis and modification of the natural healing process of the large defect of rabbit trachea.

    Grant number：16K11343

    2016.4 - 2019.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Kubota Masayuki

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    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    The purpose of the present study is to establish a technique to induce more physiological healing process without a granulation formation in the large tracheal defect of rabbits. Firstly, a natural healing process was examined histochemically. Tracheal defect was covered with inflammatory tissue one week after operation, and granulation tissue created inside was covered with tracheal epithelium two weeks after operation. Exogenous application of TNFα monoclonal antibody induced general and local inflammatory responses probably due to suppression of natural immune system. Then, combined application of somatostatin analog (an inhibitor of growth hormone) and rapamycin (an inhibitor of intracellular mTOR signal pathway for fibrosis) were tried with a careful consideration of their dosages and timing of application. As a result, more physiological healing process without granulation formation could be induced.

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  • Elucidation of the signal expression mechanism in the mTOR cell and development of the rapamycin treatment in the hepatoblastoma

    Grant number：16K11341

    2016.4 - 2019.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Arai Yuhki

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    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    After examining 27 hepatoblastoma cases in our hospital for the past 30 years, I compared the clinical data such as the prognosis and the biological malignancy with the result of the immunostaining due to the mTOR (Ser2448) antibody of the preparation, and the tendency that a value of provided Labeling index related to was recognized by a malignancy and immunostaining. It did not lead to number of cases before finding enough significant difference, but, in the expression of hepatoblastoma, it is thought that PI3K/Akt/mTOR course participates, and the possibility that the drug which inhibited mTOR signaling course could become the therapeutic agent of the hepatoblastoma in the future was suggested.

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  • Establishment of new treatment strategy for NASH by elucidating the mechanisms of fibrosis progression due to nocturnal intermittent hypoxia.

    Grant number：16K09564

    2016.4 - 2019.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    HIRONO Haruka, WATANABE kazuhiko

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    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

    The fatty liver disease which is not related to drinking is so called NAFLD（non-alcoholic fatty liver disease). Most of it is the simple fatty liver, not resulting in a big trouble. However, a part of it could be NASH(non-alcoholic steatohepatitis), which has mimicking pathology of alcoholic liver injury and has a potential of progression to liver cirrhosis. Though the most important cause of NAFLD is obesity, chronic intermittent nocturnal hypoxia in OSAS(obstructive sleep apnea syndrome) patients is regarded as one of the causes for NAFLD independently without obese factor.The first choice of the treatment of OSAS is CPAP(continuous positive airway pressure), resulting in improvement of nocturnal hypoxia. We demonstrated the effectiveness of CPAP therapy for hypoxic liver injury by using 50 OSAS patients with NAFLD.

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  • Elucidation of molecular mechanism of lipid mediator involved in metastatic ability of biliary tract cancer / pancreatic cancer and clinical application

    Grant number：15H04927

    2015.4 - 2018.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：Japan Society for the Promotion of Science

    WAKAI TOSHIFUMI, Komatsu Masaaki, Sarah Spiegel, Hylemon Phillip B., Takabe Kazuaki

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    Grant amount：\16640000 （ Direct Cost: \12800000 、 Indirect Cost：\3840000 ）

    We have developed a method to measure sphingosine-1-phosphate levels in the interstitial fluid that bathes cancer cells in the tumor microenvironment, and reported that high levels of sphingosine-1-phosphate exist in the tumor interstitial fluid. Importantly, sphingosine-1-phosphate can be secreted from cancer cells and non-cancer components such as immune cells and vascular/lymphatic endothelial cells in the tumor microenvironment. We elucidate the roles of sphingosine-1-phosphate in the interaction between cancer and non-cancer cells in tumor microenvironment, and discuss future possibilities for targeted therapies against sphingosine-1-phosphate signaling for cancer patients.

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  • 肝内免疫監視不全の回復と抗体関連型拒絶反応を応用した肝癌に対する新規治療法の開発

    Grant number：15K08991

    2015.4 - 2018.3

    System name：科学研究費助成事業 基盤研究(C)

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    山際 訓, 高村 昌昭, 松田 康伸

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    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    ナチュラルキラー（NK）細胞と自然リンパ球（ILCs）およびNK細胞機能に影響する液性免疫に着目して，肝細胞癌（HCC）発癌・再発に関与する免疫病態，特に肝内免疫監視不全を分子・細胞レベルで解明することを目的とした研究を当初の研究計画に沿って実施した。
    １．研究対象の選定，同意を得た上での肝組織と末梢血の採取，臨床データのまとめ → HCC症例とHCC非合併慢性ウイルス性肝炎症例，および対照群として自己免疫性肝疾患症例より適切に肝組織と末梢血の採取を行い，研究に使用するとともにHCC再発の有無など臨床データのまとめと経過観察を継続中である。
    ２．肝組織と末梢血より分離したNK細胞やILCsにおける細胞傷害性リガンド，サイトカイン・ケモカインレセプターの発現解析 → フローサイトメトリーと免疫組織染色によりNK細胞機能に関与する分子を中心に検討するとともに，液性免疫に対する重要な調節作用を持つ濾胞性ヘルパーT（Tfh）細胞にも着目して解析を追加し，Tfh細胞分画の中でCCR7陰性PD-1陽性Tfh分画が自己免疫性肝炎の病態と関連することを見出し，現在，英文論文を投稿中である。
    ３．肝細胞癌株と血管内皮細胞株に対する細胞傷害活性，特に抗体添加による効果の解析 → 末梢血から磁気ビーズにて分離したNK細胞を用いて，各種肝癌細胞株に対する細胞傷害活性と抗MHC class I-related chain A（MICA）抗体の添加による作用を確認するとともに，血管内皮細胞株を用いて同様の実験を進めている。
    ４．抗MICA抗体のallele解析 → 血清中に抗MICA抗体が陽性となるHCC症例について，抗体が認識するallele解析済みの症例では自己のMICA以外のalleleに対する抗体が多く認められた。

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  • Elucidation of the mechanism of drug resistance in colorectal cancer by p62-Keap 1-Nrf2 pathway

    Grant number：26462006

    2014.4 - 2017.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    KAMEYAMA Hitoshi, KOMATSU Masaaki

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    Grant amount：\4940000 （ Direct Cost: \3800000 、 Indirect Cost：\1140000 ）

    p62-Keap1-Nrf2 pathway induce the antioxidants like NQO1. In cancer cells, NQO1 confers resistance against anticancer agents. The aim of this study was to evaluate the association between NQO1 expression and prognosis in patients with advanced colorectal cancer (CRC). Among the patients with KRAS wild CRC, NQO1-negative patients showed significantly better disease control rate than NQO1-positive patients. Moreover, NQO1-negative patients had longer progression-free survival and overall survival than NQO1-positive patients. NQO1 expression in the tumor may be a predictor of therapeutic efficacy and prognosis in patients with KRAS wild advanced CRC.

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  • Discovery of new insulin-resistance marker which determines the effect of IFN for chronic hepatitis C

    Grant number：25461012

    2013.4 - 2016.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    Ohkoshi Shogo, MATSUDA Yasunobu, YAMAGIWA Satoshi, YANO Masahiko

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    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

    We examined whether RBP4(Retinol binding protein 4) was a significant factor which determined the outcome of the CH C patients with genotype 1b who were treated with PEG-IFN plus ribavirin.
    Because RBP4 was a marker of insulin resistance, we speculated that this might be the key molecule which determined the association between IFN therapy and insulin resistance. We performed in vitro experiments to examine whether RBP4 suppressed IFN signalling, resulting in the resistance of HCV replication against IFN. As a result, in RBP4-knockdown hepatoma cell, ISG genes were activatied and HCV replication was enhanced when compared to RBP4 (+) cells. Thus we found that RBP4 interfered the action of IFN against HCV and result in IFN resistance.
    However, RBP4 was not proved to be a significant factor for the prediction of clinical data from more number of patients. In conclusion, we could not verify the significance of RBP4 levels for the prediction of IFN therapy.

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  • Importance of NK cell function in the mechanisms responsible for tumor evasion of immune surveillance against hepatocellular carcinoma after liver transplantation

    Grant number：24590963

    2012.4 - 2015.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    YAMAGIWA Satoshi, TAKAMURA Masaaki, MATSUDA Yasunobu

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    Grant amount：\5330000 （ Direct Cost: \4100000 、 Indirect Cost：\1230000 ）

    We analysed mainly the function of natural killer (NK) cells in the liver and blood of patients with hepatocellular carcinoma (HCC) before and after liver transplantation (LT), but any specific immune markers associated with the recurrence of HCC after LT could not be defined. However, we revealed that anti-NK cell activation ligand antibody and soluble immune checkpoint molecule were detected in the blood of patients with HCC. Our results may help unveiling the mechanisms responsible for tumor evasion of immune surveillance against HCC.

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  • Effects of rapamycin on granulation formation in response to centrally-doubled coiled stents as a tracheal substitute.

    Grant number：24659773

    2012.4 - 2015.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Research category：Grant-in-Aid for Challenging Exploratory Research

    Awarding organization：Japan Society for the Promotion of Science

    KUBOTA Masayuki, MATSUDA Yasunobu

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    Grant amount：\3900000 （ Direct Cost: \3000000 、 Indirect Cost：\900000 ）

    In order to prevent a formation of granulation tissue around the original artificial trachea, made of super-elastic wire, mTOR signal system in the granulation tissue was examined using rabbit tracheal defect model. In granulation tissue, mTOR activity was increased up to 20―40 folds in comparison with tracheal epithelium. Application of rapamycin, which blocked the mTOR signal system, partially blocked the mTOR activation. At the same time, the granulation tissue changed into the pathological condition, which induced respiratory infection. We have examined the proper method of application of rapamycin and it was found that the application of rapamycin starting from the 2 weeks after operation induced the favorable results. It is also suggested that the natural healing process of the tracheal wall defect is compromised and obtaining an improvement in this healing process should be one of the treatment strategies for tracheal pathologies.

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  • Early DNA damage response in residual carcinoma in situ at ductal stumps and local recurrence in patients undergoing resection for extrahepatic cholangiocarcinoma

    Grant number：24592021

    2012.4 - 2015.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    WAKAI Toshifumi, MATSUDA Yasunobu, AJIOKA Yoichi, KOYAMA Yu, NAGAHASHI Masayuki

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    Grant amount：\5330000 （ Direct Cost: \4100000 、 Indirect Cost：\1230000 ）

    Clinically evident local recurrence of residual carcinoma in situ at ductal stumps is closely associated with 53BP1 inactivation and decreased apoptosis. In contrast, apoptosis associated with early 53BP1-mediated DNA damage response is one of the molecular biological mechanisms that permit a small proportion of patients with residual carcinoma in situ at ductal stumps to survive in the long term with no evidence of local recurrence. Based on the Early DNA damage response, 50% of patients with formation of intraepithelial spread of invasive carcinoma, whereas 50% of patients with formation of field carcinogenesis. The formation of superficial intraepithelial spread results from both intraepithelial spread of invasive carcinoma and field carcinogenesis.

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  • Molecular Analysis of Cytokine-mediated Sorafenib Resistance

    Grant number：24590962

    2012.4 - 2015.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    MATSUDA YASUNOBU, WAKAI Toshifumi, TKAMURA Masaaki, YAMAGIWA Satoshi

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    Sorafenib is a multi-kinase inhibitor for hepatocellular carcinoma. To address whether cytokine-mediated signaling is involved in the drug resistance, hepatoma cells were treated with sorafenib in the presence of several cytokines/growth factors. Obtained results showed that the effect of sorafenib on cell growth was significantly inhibited by TGF-beta. When TGF-beta-treated cells were treated with sorafenib and valproic acid, apoptotic cell numbers were increased as compared with those treated with sorafenib alone. Collectively, combination treatment of valproic acid and sorafenib might improve the efficacy of sorafenib.

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  • DNA障害の修復機構をマーカーとした新しいインターフェロン治療の開発

    2010.4 - 2013.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    大越章吾

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    Grant type：Competitive

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  • 肝がんにおける分子標的薬耐性機構の解析

    2010.1 - 2010.12

    System name：その他の研究制度

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    Grant type：Competitive

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  • Development of new IFN-strategy that based on DNA repair mechanism

    Grant number：22590722

    2010 - 2012

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    OHKOSHI Shogo, MATSUDA Yasunobu, YAMAGIWA Satoshi, YANO Masahiko

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    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    The aim of this study is to clarify the molecular mechanisms of preventive effect of IFN-beta for the occurrence of hepatocellular carcinoma (HCC) and to establish the strategy of chemoprevention of HCC. We found that aberrant expression of p21, that was a known cyclin-dependent kinase (CDK) inhibitor, was a key mechanism for hepatocarcinogenesis and it’s prevention. IFN-beta shifted cytoplasmic p21, which was oncogenic, to nucleus, making them to exert original anti-proliferative function. We may explore this anti-cancer mechanism of IFN-beta in order to apply to clinical studies.

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  • 臓器移植における再生間葉系肝幹細胞門脈内投与による新たな免疫寛容誘導法の確立

    2009.4 - 2013.3

    System name：科学研究費助成事業

    Research category：基盤研究(B)

    Awarding organization：日本学術振興会

    佐藤好信

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    Grant type：Competitive

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  • 胆管癌における53BP1を介したDNA損傷修復機構の解明及びその臨床的意義

    2009.4 - 2011.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    若井俊文

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    Grant type：Competitive

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  • Development of New Strategy of Immunological Tolerance Inductionby Intraportal administration of donor specific Mesenchymal hepatic stem cell in OrganTransplantation

    Grant number：21390356

    2009 - 2012

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：Japan Society for the Promotion of Science

    SATO Yoshinobu, ABO Toru, MATSUDA Yasunobu, TOMIYAMA Chikako

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    Grant amount：\17420000 （ Direct Cost: \13400000 、 Indirect Cost：\4020000 ）

    The purpose of this study was to analyze the mechanisms of theinduction of operational tolerance in clinical liver transplantation by the intra-portaladministration of donor specific antigen and make the new method of induction of toleranceby hepatic stem cell. In the basic examination, the CD133+ NCAM+ human hepaticstem/progenitor cell was recognized around the region with existence of ductular reactionin the human liver with chronic or acute hepatitis. Especially, its existence was moreclearly in the human liver with higher hepatic injury. However, it was not recognizedin the normal human liver. In the immunological analysis of intra-portal administrationof super donor antigens, the population of FoxP3^+/CD4^+CD25^+ regulatory T cells increasedin the transplant patients with no immunosuppressants.
    Treg. cells increased in the patients above MELD score 20. It was proved that the graspof preoperative immunological situation of transplant patients take the betteradministration of immunosuppressants.

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  • Prospective analysis of DNA damage and repair markers in the patients with high risk of hepatocellular cancer

    Grant number：21590835

    2009 - 2011

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    MATSUDA Yasunobu

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    Background : It has been widely considered that the DNA damage response is strongly involved in the step of early carcinogenesis. In case of hepatocellular carcinoma(HCC), however, it has been remained unclear whether DNA damage response molecules are useful for the tumor markers of the patients with high risk of HCC.
    Methods : We evaluated the phosphorylation levels of DNA damage response markers in animal models with HCC by Western blotting or immunohistochemical staining. Based on the animal model experiments, we addressed whether any of the DNA-damage response molecules are involved in the cancer development of the patients with high risk of HCC.
    Results : Western blotting and immunohistochemical analysis showed that the levels of gamma-H2A were significantly increased in HCC-prone mice. Interestingly, increase in the levels of gamma-H2AX was observed from several months before the development of HCC. The increase in the levels of gamma-H2AX and Wip1 activity was also observed in human liver tissues adjacent to HCC.
    Conclusion : DNA damage response molecules gamma-H2AX and Wip1 might be useful markers for predicting the development of HCC.

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  • Development of a new endoscopic therapy using RNAi for intestinal fibrosis of Crohn's disease

    Grant number：21590807

    2009 - 2011

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    SUZUKI Kenji

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    Grant type：Competitive

    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    We have developed a new siRNA medicine, STNM-01 with Stelic Institute. In this project, we studied the therapeutic effects and the mechanism of endoscopic submucosal injection of the STNM-01 for the treatment of intestinal fibrosis using animal models. We have successfully developed a novel endoscopic injection therapy of STNM-01 for the treatment of intestinal fibrosis of Crohn's disease. Using this technique, we have started a phase I clinical trial for patients with Crohn's disease in Japan since January, 2012.

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  • Importance of NK cells and intrahepatic immune responses for the acceleration of hepatitis C after liver transplantation

    Grant number：21590834

    2009 - 2011

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    YAMAGIWA Satoshi, TAKAMURA Masaaki, MATSUDA Yasunobu, SATO Yoshinobu

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    Grant type：Competitive

    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

    The activating receptor natural killer group 2, member D(NKG2D) and its ligands play a crucial role in immune response to infections and tumors. Among the human NKG2D ligands, ULBP1 is prevalently expressed in hepatocellular carcinoma(HCC), but loss of its expression correlates with tumor progression and early recurrence. Although we could not find any significant changes in the gene expression profiles among the recurrent hepatitis C patients and chronic hepatitis C patients yet, our results suggest that the status of intrahepatic NK cell subsets and NK cell receptor ligand expressions might be associated with the rapid progression of recurrent hepatitis C infection.

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  • Manipulating the stromal-derived factor 1 function in mouse liver cirrhosis

    Grant number：19590753

    2007 - 2008

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    MATSUDA Yasunobu

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

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  • Analysis of the innate immune responses in the liver of patients with chronic hepatitis C following liver transplantation to develop a novel immunotherapy for the recurrent hepatitis C infection

    Grant number：18590723

    2006 - 2007

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    YAMAGIWA Satoshi, MATSUDA Yasunobu, TAKAMURA Masaaki, SATO Yoshinobu

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    Grant type：Competitive

    Grant amount：\3920000 （ Direct Cost: \3500000 、 Indirect Cost：\420000 ）

    (1) Natural killer (NK) cell subsets in the liver of patients with recurrent hepatitis C following liver transplantation
    Human NK cells can be divided into two subsets based on their cell-surface density of CD56 - CD56^(+bright) and CD56^(+dim) - each with distinct phenotypic properties. We investigated the NK cell subsets in the liver of patients with recurrent hepatitis C following living-donor liver transplantation (LDLT). The patients with chronic hepatitis C (CHC) and the donors for LDLT were also investigated as controls. We revealed that the CD56^(+bright) subset was significantly decreased in the liver of patients with recurrent hepatitis C than that in the patients with CHC and the normal donors. The expression of an activation marker CD69 on the CD56^(+dim) subset was significantly increased in the liver of LDLT. Our results suggest that further examination of the status of intrahepatic NK cell subsets might provide a new insight into the mechanism of rapid progression of recurrent hepatitis C infection.
    (2) Gene expression profiles in the liver of patients with recurrent hepatitis C following liver transplantation
    We investigated the gene expression profiles in the liver of patients with recurrent hepatitis C after LDLT using liver biopsy samples. However, we could not find any significant changes in the gene expression profiles among the recurrent hepatitis C patients and CHC patients yet.
    (3) NK and NKT cells in the liver of patients with chronic hepatitis C before and after interferon plus ribavirin therapy
    Previous studies have revealed that functional impairment of NK and NKT cells might be associated with the persistence of hepatitis C virus (HCV). However, the involvement of these cells, which predominate in the liver, in therapeutic HCV clearance is still unclear. We found a close relationship between the significant increase of intrahepatic NK/NKT cells and sustained HCV clearance in CHC patients treated with interferon-a plus ribavirin therapy.

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  • C型肝炎に対するインターフェロン・リバビリン併用療法の治療マーカーの探索同定

    2005.1 - 2005.3

    System name：共同研究

    Awarding organization：株式会社バイオマーカーサイエンス

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    Grant type：Competitive

    Grant amount：\100000

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  • 糖鎖を標的とした肝癌遺伝子治療戦略

    2004.4 - 2006.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    青柳豊

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    Grant type：Competitive

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  • Development of a new cell therapy by adoptive transfer of regulatory T cells to induce immunological tolerance for the transplanted liver

    Grant number：14570455

    2002 - 2003

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    ICHIDA Takafumi, YAMAGIWA Satoshi, WATANABE Hisami, MATSUDA Yasunobu

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    Grant type：Competitive

    Grant amount：\3400000 （ Direct Cost: \3400000 ）

    (1)Generation of human regulatory CD4^+CD25^+ T cells
    We confirmed that naive CD4^+ cells stimulated with alloantigens in the presence of TGF-β(transforming growth factor-β) differentiate into suppressor cells with a phenotype and functional properties similar if not identical with natural regulatory CD4^+CD25^+ T cells. We also studied the regulatory properties of other cytokines, separately or together with TGF-β, on CD4^+CD25^+ T cells generated by allo-stimulation. Although it has been reported that CD4^+ cells become regulatory T cells ('Tr1 cells') when repeatedly stimulated with IL-10,IL-10 inhibited CD25 expression on CD4^+* cells. Moreover, when naive CD4^+ cells were stimulated with alloantigens in the presence of both IL-10 and TGF-β,IL-10 inhibited the effect of TGF-β on the generation of CD4^+CD25^+ T cells.
    (2)Generation of murine regulatory CD4^+CD25^+ T cells
    We found that treatment of murine alio-activated CD4^+ T cells with TGF-β and IL-2 also enhanced expression of CD25 and enabled these cells to develop potent suppressive activity. We are planning to use those CD4^+CD25^+ T cells generated ex vivo in skin transplantation model to examine whether transfer of those cells can prevent graft rejection.
    (3)CD4^+CD25^+ T cells in the human liver
    We also investigated CD4^+CD25^+ T cells in human livers. Although the proportion of CD4^+CD25^+ T cells in the liver was lower than in the peripheral blood, we found a significant increase of CD4^+CD25^+ T cells in the marginal regions of hepatocellular carcinoma(HCC), but not in unaffected areas of the liver. CD4^+CD25^+ T cells isolated from peri-tumor regions of HCC displayed phenotype markers characteristic of regulatory T cells, and inhibited autologous CD8^+ cell proliferation. Our results suggest that CD4^+*CD25^+ T cells in the peri-tumor region of HCC inhibit the generation of tumor-specific CD8^+ cytotoxic T cell activity and, thereby, contribute to the progression of HCC.

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  • 肝がんにおける細胞周期調節機構の解析

    1999.1 - 1999.12

    System name：その他の研究制度

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    Grant type：Competitive

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  • Development of a new system identifying mutated DNA in the plasma

    Grant number：11670483

    1999 - 2000

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    TAKAHASHI Toru, ICHIDA Takafumi, MATSUDA Yasunobu

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    Grant type：Competitive

    Grant amount：\3500000 （ Direct Cost: \3500000 ）

    It is now being described that detection of mutated DNA using MutS protein is highly sensitive and accurate. because MutS can specifically bind mis-matched double strand of DNA, identifying mutated DNA(e.g., point mutation, deletion and insertion)is capable by referring to the amount of DNA-bound MutS.We addressed whether MutS could be useful in the detection of mutated DNA in the plasma, and examined its usefulness in case of patients affected with pancreatic/bile duct cancers.
    We obtained plasma DNA from 25 of patients with pancreatic cancers and 33 with bile duct cancers. PCR was performed using primers specific for p53(exon 5-8)and p16(exon 1-2), and mis-matched heteroduplex was examined using MutS-binding reaction. Consequently, we could detect mutated DNA in 18 and 33 patients with pancreatic cancers and bile duct cancers, respectively. Thus, we surmise that detecting mutated DNA in the plasma using MutS is useful for identifying the ptients who are suffered from solid cancers.

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  • 原発性胆汁性肝硬変の肝移植後の再発機序に関する研究

    1996.4 - 1997.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    市田隆文

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    Grant type：Competitive

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  • 原発性胆汁性肝硬変の肝移植後の再発機序に関する研究

    Grant number：08670567

    1996

    System name：科学研究費助成事業 基盤研究(C)

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    市田 隆文, 松田 康伸, 杉村 一仁

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    Grant amount：\1300000 （ Direct Cost: \1300000 ）

    今回の研究に基ずく全国調査ではわが国の成人肝移植レシピエントは83例で54例が海外での脳死肝移植、28例がわが国における生体肝移植で1例が心臓死ドナー肝移植であることが判明した。その中の原発性胆汁性肝硬変症例は脳死肝移植例が10例、生体肝移植例が11例であった。この症例を対象に原発性胆汁性肝硬変の肝移植後の再発機序に関する研究を試みた。以下に今回の研究で明らかになったことを列挙する。
    原発性胆汁性肝硬変症例の肝移植成績として生体肝移植11例は最長3年3ヶ月の観察期間で生存率100%であり、脳死肝移植症例11例中9例が生存し最長8年6ヶ月である(生存率81%)ことが判明した。
    原発性胆汁性肝硬変の原疾患の再発に関する検索では脳死肝移植症例と生体肝移植症例の肝移植後の血中アルカリフォスファターゼ値の再上昇はそれぞれ7例中1例と9例中5例に、抗糸粒体抗体の再陽性化は8例中2例と10例中7例に、IgM値の再上昇は7例中1例と9例中6例にそれぞれ認められた。
    さらに組織学的観察では胆管病変を認めた脳死肝移植例では5例中、1例も認めていないが生体肝移植例では6例中2例に観察された。この原発性胆汁性肝硬変の再発に関してはすでに国際的な論争があるが、本研究では症例数には限りがあるが脳死肝移植に比例して生体肝移植例の方が血清学的マーカーの肝移植後の推移ならびに組織学的検索から再発の可能性が示唆された。しかしながら、術後の肝生検での胆管病変に関して慢性拒絶反応と原発性胆汁性肝硬変との組織学的鑑別が困難であるため、未だ明確な組織学的確診が得られないことも事実である。
    この要因を探るためにHLAのmatchingとHLADNAタイピングを検索中であるが、少なくとも生体肝移植例では親子間のドナー、レシピエントの関連よりHLAクラスIIのmatchingが何らかの要因になっている可能性が考えられた。
    今後、レシピエントリンパ球を用いたHLADNAタイピングの検索が必要と考えている。

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  • 肝細胞増殖因子 (hepatocyte growth factor)による肝再生機構

    1990.1 - 1990.12

    System name：その他の研究制度

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    Grant type：Competitive

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Teaching Experience

  • 臨床検査実習II

    2025
    Institution name：新潟大学

  • 臨床検査実習I

    2025
    Institution name：新潟大学

  • 日本酒学概論V(医歯学・保健学)

    2023
    Institution name：新潟大学

  • 保健学特定研究(検査技術科学)

    2021
    Institution name：新潟大学

  • 病態生理機能学実習

    2021
    Institution name：新潟大学

  • 保健学特別研究(検査技術科学)

    2021
    Institution name：新潟大学

  • 保健学総合

    2021
    Institution name：新潟大学

  • 生体システム機能検査科学特講演習

    2020
    Institution name：新潟大学

  • 生体システム機能検査科学特講

    2020
    Institution name：新潟大学

  • 医療英語ベーシック(検査)

    2020
    Institution name：新潟大学

  • 入門医療英語

    2018
    Institution name：新潟大学

  • 医療安全管理学

    2018
    Institution name：新潟大学

  • 臨床検査管理概論

    2018
    Institution name：新潟大学

  • 医学検査管理総論

    2016
    Institution name：新潟大学

  • 臨床検査実習

    2016
    -
    2024
    Institution name：新潟大学

  • 成人・老年看護学演習Ⅱ

    2016
    Institution name：新潟大学

  • フィジカルアセスメント

    2015
    Institution name：新潟大学

  • 臨床薬理学

    2015
    Institution name：新潟大学

  • 病態生理学

    2015
    Institution name：新潟大学

  • 保健学特別研究(検査技術科学)

    2014
    Institution name：新潟大学

  • 保健学特定研究(検査技術科学)

    2014
    Institution name：新潟大学

  • 疾患と臨床検査

    2011
    Institution name：新潟大学

  • 病気の成り立ちⅡ

    2010
    -
    2016
    Institution name：新潟大学

  • 臨床生体情報検査科学特別研究

    2010
    -
    2013
    Institution name：新潟大学

  • 疾病の予防と治療

    2009
    Institution name：新潟大学

  • 医療英語(検査)

    2008
    Institution name：新潟大学

  • 病態生理機能学特論

    2008
    Institution name：新潟大学

  • 画像検査科学

    2008
    Institution name：新潟大学

  • 画像検査科学実習

    2008
    Institution name：新潟大学

  • 医療と画像技術

    2008
    Institution name：新潟大学

  • 病態解析学概論

    2008
    Institution name：新潟大学

  • 生活習慣と健康

    2008
    Institution name：新潟大学

  • スタディスキルズ (検査)

    2008
    Institution name：新潟大学

  • 病気の成り立ちⅠ

    2008
    Institution name：新潟大学

  • 卒業研究

    2008
    -
    2024
    Institution name：新潟大学

  • 生理機能検査科学実習

    2008
    -
    2021
    Institution name：新潟大学

  • 病態生理機能学実習

    2008
    -
    2018
    Institution name：新潟大学

  • 生体システム機能検査学特講

    2008
    -
    2016
    Institution name：新潟大学

  • 生体システム機能検査学特講演習

    2008
    -
    2014
    Institution name：新潟大学

  • 筋電図検査科学

    2008
    -
    2013
    Institution name：新潟大学

  • 医用写真技術実習

    2008
    -
    2010
    Institution name：新潟大学

  • 疾患と臨床検査Ⅰ

    2008
    -
    2010
    Institution name：新潟大学

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