研究者総覧

力山 敏樹 (リキヤマ トシキ)

  • 総合医学第2講座 教授
Last Updated :2020/07/29

研究者情報

学位

  • 博士号(東北大学)

学位

    力山 敏樹

ホームページURL

J-Global ID

経歴

  • 東北大学 病院(医科診療部門) 肝・胆・膵外科講師

学歴

  •         - 1990年   東北大学   医学部
  •         - 1990年   東北大学   Faculty of Medicine

所属学協会

  • 日本肝胆膵外科学会   日本外科学会(2007/01-2007/12)   日本消化器外科学会(2007/01-2007/12)   日本消化器病学会(2007/01-2007/12)   日本肝胆膵外科学会(2007/01-2007/12 評議員)   日本胆道学会(2007/01-2007/12)   日本外科学会(2008/01-2009/03)   日本肝臓学会(2007/01-2007/12)   日本肝胆膵外科学会(2008/01-2009/03 評議員)   日本消化器外科学会(2008/01-2009/03)   日本消化器病学会(2008/01-2009/03)   日本胆道学会(2008/01-2009/03)   日本肝臓学会(2008/01-2009/03)   日本外科学会(2010/04-2011/03)   日本肝臓学会(2010/04-2011/03)   日本消化器外科学会(2010/04-2011/03)   日本消化器病学会(2010/04-2011/03)   日本肝胆膵外科学会(2010/04-2011/03 評議員)   日本臨床外科学会(2010/04-2011/03)   日本胆道学会(2010/04-2011/03)   日本膵臓学会(2010/04-2011/03)   日本肝胆膵外科学会   日本外科学会(2007/01-2007/12)   日本消化器外科学会(2007/01-2007/12)   日本消化器病学会(2007/01-2007/12)   日本肝胆膵外科学会(2007/01-2007/12 評議員)   日本胆道学会(2007/01-2007/12)   日本外科学会(2008/01-2009/03)   日本肝臓学会(2007/01-2007/12)   日本肝胆膵外科学会(2008/01-2009/03 評議員)   日本消化器外科学会(2008/01-2009/03)   日本消化器病学会(2008/01-2009/03)   日本胆道学会(2008/01-2009/03)   日本肝臓学会(2008/01-2009/03)   日本外科学会(2010/04-2011/03)   日本肝臓学会(2010/04-2011/03)   日本消化器外科学会(2010/04-2011/03)   日本消化器病学会(2010/04-2011/03)   日本肝胆膵外科学会(2010/04-2011/03 評議員)   日本臨床外科学会(2010/04-2011/03)   日本胆道学会(2010/04-2011/03)   日本膵臓学会(2010/04-2011/03)   

研究活動情報

書籍

  • Disease of the Pancreas-Current Surgical Therapy
    ()
    Springer 2008年
  • Disease of the Pancreas-Current Surgical Therapy
    ()
    Springer 2008年
  • Disease of the Pancreas-Current Surgical Therapy
    ()
    Springer 2008年
  • Disease of the Pancreas-Current Surgical Therapy
    ()
    Springer 2008年

講演・口頭発表等

  • 肝胆膵領域におけるHarmonic FOCUSの使用経験  [通常講演]
    第110回日本外科学会総会 2010年
  • 肝胆膵外科高度技能医を育てるためのシステムと指導医・指導的助手のあり方  [通常講演]
    第22回日本肝胆膵外科学会学術集会 2010年
  • 肝胆膵外科手術における閉創法の工夫  [通常講演]
    第22回日本肝胆膵外科学会学術集会 2010年
  • MDCTによる肝門部胆管癌進展度診断と断端陰性を目指した門脈合併切除ならびにNACRTの意義  [通常講演]
    第65回日本消化器外科学会総会 2010年
  • 肝胆膵領域におけるHarmonic FOCUSの使用経験  [通常講演]
    第160回東北外科集談会 2010年
  • 進行胆嚢癌に対するPD付加の適応と意義  [通常講演]
    第46回日本胆道学会学術集会 2010年
  • MDCT仮想肝切除による術前シミュレーション  [通常講演]
    JDDW2010 2010年
  • 肝胆膵領域におけるHarmonic FOCUSの使用経験  [通常講演]
    第110回日本外科学会総会 2010年
  • 肝胆膵外科高度技能医を育てるためのシステムと指導医・指導的助手のあり方  [通常講演]
    第22回日本肝胆膵外科学会学術集会 2010年
  • 肝胆膵外科手術における閉創法の工夫  [通常講演]
    第22回日本肝胆膵外科学会学術集会 2010年
  • MDCTによる肝門部胆管癌進展度診断と断端陰性を目指した門脈合併切除ならびにNACRTの意義  [通常講演]
    第65回日本消化器外科学会総会 2010年
  • 肝胆膵領域におけるHarmonic FOCUSの使用経験  [通常講演]
    第160回東北外科集談会 2010年
  • 進行胆嚢癌に対するPD付加の適応と意義  [通常講演]
    第46回日本胆道学会学術集会 2010年
  • MDCT仮想肝切除による術前シミュレーション  [通常講演]
    JDDW2010 2010年
  • MDCTによる胆管癌の長軸進展度診断と治療方針  [通常講演]
    第95回日本消化器病学会総会 2009年
  • 肝門部胆管癌の治療戦略と術式選択・切除成績  [通常講演]
    第21回日本肝胆膵外科学会学術集会 2009年
  • 肝門部胆管癌の外科解剖とMDCT仮想肝切除による術前シミュレーション  [通常講演]
    第45回日本胆道学会学術集会 2009年
  • MDCTによる胆管癌の長軸進展度診断と治療方針  [通常講演]
    第95回日本消化器病学会総会 2009年
  • 肝門部胆管癌の治療戦略と術式選択・切除成績  [通常講演]
    第21回日本肝胆膵外科学会学術集会 2009年
  • 肝門部胆管癌の外科解剖とMDCT仮想肝切除による術前シミュレーション  [通常講演]
    第45回日本胆道学会学術集会 2009年
  • 進行肝門部胆管癌の新規治療戦略とMDCT仮想肝切除による術前シミュレーション  [通常講演]
    第108回日本外科学会定期学術集会 2008年
  • 肝門部胆管癌における門脈分岐変異時の胆管形態と術式選択  [通常講演]
    第20回日本肝胆膵外科学会学術集会 2008年
  • 肝門部胆管癌の外科切除成績と新規治療戦略  [通常講演]
    第18回東北肝臓外科研究会 2008年
  • 肝門部胆管癌の外科切除成績と新規治療戦略-断端陰性化を目指して-  [通常講演]
    第63回日本消化器外科学会定期学術集会 2008年
  • MDCTによる肝門部胆管癌血管浸潤診断と門脈合併切除再建の治療成績・意義  [通常講演]
    第44回日本胆道学会学術集会 2008年
  • 進行肝門部胆管癌の新規治療戦略とMDCT仮想肝切除による術前シミュレーション  [通常講演]
    第108回日本外科学会定期学術集会 2008年
  • 肝門部胆管癌における門脈分岐変異時の胆管形態と術式選択  [通常講演]
    第20回日本肝胆膵外科学会学術集会 2008年
  • 肝門部胆管癌の外科切除成績と新規治療戦略  [通常講演]
    第18回東北肝臓外科研究会 2008年
  • 肝門部胆管癌の外科切除成績と新規治療戦略-断端陰性化を目指して-  [通常講演]
    第63回日本消化器外科学会定期学術集会 2008年
  • MDCTによる肝門部胆管癌血管浸潤診断と門脈合併切除再建の治療成績・意義  [通常講演]
    第44回日本胆道学会学術集会 2008年
  • 高度進行胆道癌に対するネオアジュバント放射線化学療法  [通常講演]
    第182回 日本消化器病学会東北支部例会 2007年
  • the present situation of laparoscopic surgery for pancreatic disease in our institution  [通常講演]
    1st the Asian-Pacific Hepato-Pancreato-Biliary Association 2007年 ポスター発表
  • 中下部胆管癌の切除成績と適正切除範囲 治療成績向上のためには?  [通常講演]
    第107回日本外科学会定期学術集会 2007年
  • 中下部胆管癌の切除成績-治療成績向上のためには?  [通常講演]
    第19回日本肝胆膵外科学会学術集会 2007年 ポスター発表
  • 胆管癌に対する拡大手術の適応と限界 治療成績向上のためには?  [通常講演]
    第62回日本消化器外科学会定期学術総会 2007年
  • 肝門部胆管癌の外科切除成績と治療方針  [通常講演]
    第43回日本胆道学会学術集会 2007年
  • 高度進行胆道癌に対するネオアジュバント放射線化学療法  [通常講演]
    第182回 日本消化器病学会東北支部例会 2007年
  • the present situation of laparoscopic surgery for pancreatic disease in our institution  [通常講演]
    1st the Asian-Pacific Hepato-Pancreato-Biliary Association 2007年 ポスター発表
  • 中下部胆管癌の切除成績と適正切除範囲 治療成績向上のためには?  [通常講演]
    第107回日本外科学会定期学術集会 2007年
  • 中下部胆管癌の切除成績-治療成績向上のためには?  [通常講演]
    第19回日本肝胆膵外科学会学術集会 2007年 ポスター発表
  • 胆管癌に対する拡大手術の適応と限界 治療成績向上のためには?  [通常講演]
    第62回日本消化器外科学会定期学術総会 2007年
  • 肝門部胆管癌の外科切除成績と治療方針  [通常講演]
    第43回日本胆道学会学術集会 2007年
  • 術前および病理組織学的に肝内胆管癌との鑑別に苦慮した膵癌肝転移症例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 胆嚢癌,胆管癌同時性重複発癌を来した拡張型膵胆管合流異常症の根治切除の1例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 胆摘後に偶然発見された胆嚢癌症例の検討  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年
  • 肝門部胆管癌根治術後に膵内胆管癌の異時性発生をきたした1例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 肝門部胆管癌における門脈分岐変異時の胆管形態と術式選択  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年
  • 高度進行胆嚢癌に対してGemcitabine+Capecitabine併用療法(GemCap療法)を施行した1例  [通常講演]
    第151回 東北外科集談会 2006年
  • 非B非C型肝細胞癌に関する臨床的検討  [通常講演]
    第42回 肝日本肝癌研究会 2006年
  • 胆嚢癌の手術術式の検討  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • 切除不能胆管癌に対する集学的治療-その後の経口化学療法  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • 肝門部胆管癌術後補助化学療法の可能性  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • MUCIN-PRODUCING BILIARY TUMORS:COMPARISON WITH INTRADUCTAL PAPILLARY CHOLANGIOCARICNOMA.  [通常講演]
    International Hepato Pancreato Biliary Association(IHPBA) 2006年 ポスター発表
  • ss胆嚢癌の予後規定因子  [通常講演]
    第42回 日本胆道学会学術集会 2006年
  • 胆道癌にネオアジュバント放射線化学療法を施行した1例  [通常講演]
    第42回 日本胆道学会学術集会 2006年 ポスター発表
  • 胆管内乳頭状腫瘍(Intraducdtal papillary neoplasm of the bile duct, IPN-B)の診断と手術成績  [通常講演]
    第42回 日本胆道学会学術集会 2006年
  • 拡張型膵管胆道合流異常の胆嚢癌・胆管癌同時重複発癌の1根治切除例  [通常講演]
    第29回 膵・胆管合流異常究会 2006年
  • 肝門部胆管癌の成績向上を目指して:アジュバント療法の現状と今後  [通常講演]
    第44回 日本癌治治療学会 2006年
  • 術前および病理組織学的に肝内胆管癌との鑑別に苦慮した膵癌肝転移症例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 胆嚢癌,胆管癌同時性重複発癌を来した拡張型膵胆管合流異常症の根治切除の1例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 胆摘後に偶然発見された胆嚢癌症例の検討  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年
  • 肝門部胆管癌根治術後に膵内胆管癌の異時性発生をきたした1例  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年 ポスター発表
  • 肝門部胆管癌における門脈分岐変異時の胆管形態と術式選択  [通常講演]
    第18回 日本肝胆膵外科関連会議 2006年
  • 高度進行胆嚢癌に対してGemcitabine+Capecitabine併用療法(GemCap療法)を施行した1例  [通常講演]
    第151回 東北外科集談会 2006年
  • 非B非C型肝細胞癌に関する臨床的検討  [通常講演]
    第42回 肝日本肝癌研究会 2006年
  • 胆嚢癌の手術術式の検討  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • 切除不能胆管癌に対する集学的治療-その後の経口化学療法  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • 肝門部胆管癌術後補助化学療法の可能性  [通常講演]
    第61回 日本消化器外科学会定期学術総会 2006年
  • MUCIN-PRODUCING BILIARY TUMORS:COMPARISON WITH INTRADUCTAL PAPILLARY CHOLANGIOCARICNOMA.  [通常講演]
    International Hepato Pancreato Biliary Association(IHPBA) 2006年 ポスター発表
  • ss胆嚢癌の予後規定因子  [通常講演]
    第42回 日本胆道学会学術集会 2006年
  • 胆道癌にネオアジュバント放射線化学療法を施行した1例  [通常講演]
    第42回 日本胆道学会学術集会 2006年 ポスター発表
  • 胆管内乳頭状腫瘍(Intraducdtal papillary neoplasm of the bile duct, IPN-B)の診断と手術成績  [通常講演]
    第42回 日本胆道学会学術集会 2006年
  • 拡張型膵管胆道合流異常の胆嚢癌・胆管癌同時重複発癌の1根治切除例  [通常講演]
    第29回 膵・胆管合流異常究会 2006年
  • 肝門部胆管癌の成績向上を目指して:アジュバント療法の現状と今後  [通常講演]
    第44回 日本癌治治療学会 2006年
  • 大腸癌肝転移に対する肝切除術式選択と術後補助化学療法の意義.  [通常講演]
    第13回 消化器関連学会週間(DDW) 2005年
  • 肝門部胆管癌根治術後に異時性発生をきたした2例  [通常講演]
    第13回 消化器関連学会週間(DDW) 2005年 ポスター発表
  • 大腸癌肝転移に対する肝切除術式選択と術後補助化学療法の意義.  [通常講演]
    第13回 消化器関連学会週間(DDW) 2005年
  • 肝門部胆管癌根治術後に異時性発生をきたした2例  [通常講演]
    第13回 消化器関連学会週間(DDW) 2005年 ポスター発表

MISC

  • Shimpei Maeda, Fuyuhiko Motoi, Tohru Onogawa, Takanori Morikawa, Ottomo Shigeru, Naoaki Sakata, Tatsuyuki Takadate, Takeshi Naitoh, Toshiki Rikiyama, Yu Katayose, Shinichi Egawa, Michiaki Unno INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY 16 (5) 539 -545 2011年10月 [査読無し][通常論文]
     
    Background We evaluated the efficacy and feasibility of paclitaxel in patients with gemcitabine-refractory pancreatic cancer. We also evaluated the correlation between tumor marker decline and response rate. Methods Thirty patients histologically diagnosed with pancreatic cancer who had undergone paclitaxel treatment as salvage chemotherapy were retrospectively analyzed. Paclitaxel treatment was performed with 80 mg/(m(2) week) for 3 weeks followed by 1 week rest, and this was continued until failure. Tumor marker response was evaluated by measuring levels of carbohydrate antigen 19-9, carcinoembryonic antigen, and DUPAN-2 monthly. Results In total, 272 weekly paclitaxel treatments were performed. The median number of treatments per patient was 8 (range 1-22). The median overall survival from the start of paclitaxel treatment was 6.7 months (range 1.2-18.8). The response rate was 10% (3/30 patients) and the disease control rate was 46.7% (14/30 patients). Although grade 3 and 4 hematological and non-hematological toxicities were seen in 7 and 6 patients, respectively, adverse events were managed by conservative treatment. We found a significant correlation between the disease control rate and tumor marker decline within 2 months of paclitaxel treatment (P = 0.01). Patients with tumor marker decline tended to survive longer. Conclusion Weekly administration of paclitaxel in patients with gemcitabine-refractory pancreatic cancer seems to be well tolerated and can be effective. Paclitaxel treatment should be considered as salvage chemotherapy after gemcitabine failure in patients with good performance status.
  • Shimpei Maeda, Fuyuhiko Motoi, Tohru Onogawa, Takanori Morikawa, Ottomo Shigeru, Naoaki Sakata, Tatsuyuki Takadate, Takeshi Naitoh, Toshiki Rikiyama, Yu Katayose, Shinichi Egawa, Michiaki Unno INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY 16 (5) 539 -545 2011年10月 [査読無し][通常論文]
     
    Background We evaluated the efficacy and feasibility of paclitaxel in patients with gemcitabine-refractory pancreatic cancer. We also evaluated the correlation between tumor marker decline and response rate. Methods Thirty patients histologically diagnosed with pancreatic cancer who had undergone paclitaxel treatment as salvage chemotherapy were retrospectively analyzed. Paclitaxel treatment was performed with 80 mg/(m(2) week) for 3 weeks followed by 1 week rest, and this was continued until failure. Tumor marker response was evaluated by measuring levels of carbohydrate antigen 19-9, carcinoembryonic antigen, and DUPAN-2 monthly. Results In total, 272 weekly paclitaxel treatments were performed. The median number of treatments per patient was 8 (range 1-22). The median overall survival from the start of paclitaxel treatment was 6.7 months (range 1.2-18.8). The response rate was 10% (3/30 patients) and the disease control rate was 46.7% (14/30 patients). Although grade 3 and 4 hematological and non-hematological toxicities were seen in 7 and 6 patients, respectively, adverse events were managed by conservative treatment. We found a significant correlation between the disease control rate and tumor marker decline within 2 months of paclitaxel treatment (P = 0.01). Patients with tumor marker decline tended to survive longer. Conclusion Weekly administration of paclitaxel in patients with gemcitabine-refractory pancreatic cancer seems to be well tolerated and can be effective. Paclitaxel treatment should be considered as salvage chemotherapy after gemcitabine failure in patients with good performance status.
  • Hideo Ohtsuka, Masaya Oikawa, Kyohei Ariake, Toshiki Rikiyama, Fuyuhiko Motoi, Yu Katayose, Michiaki Unno, Alfred C. Johnson INTERNATIONAL JOURNAL OF CANCER 129 (7) 1599 -1610 2011年10月 [査読無し][通常論文]
     
    GC-binding factor 2 (GCF2), a transcriptional repressor that decreases the activity of several genes is capable of binding directly to the GC-rich sequence of the EGFR promoter and repressing the transcriptional activity of EGFR. In addition to its function as a transcriptional repressor, GCF2 can directly interact with other proteins such as flightless-1 (Fli-1). Many previous findings pertaining to the function of Fli-1 have suggested a role for fli-1 in providing a direct link between molecules involved in signal transduction pathways and the actin cytoskeleton. We hypothesized that GCF2, together with Fli-1, plays a role in regulating cytoskeleton function, cell migration, and/or morphology. In our study, we observed that GCF2 is crucial for the activation of RhoA, a small GTPase that plays a key role in the regulation of the actin cytoskeleton. RhoA was markedly inactivated as a result of the decreased expression of GCF2. Co-immunoprecipitations were subsequently performed to further investigate the mechanism for the repressive function. We identified dishevelled (Dvl), which is the key mediator for the Wnt pathway, as a binding partner with GCF2. These results strongly suggest that GCF2 plays a role in the Wnt-noncanonical planar cell polarity (PCP) signaling pathway. Consequently, GCF2 may regulate the cytoskeleton or migration via Dvls and RhoA.
  • Naoaki Sakata, Shinichi Egawa, Toshiki Rikiyama, Gumpei Yoshimatsu, Kunihiro Masuda, Hideo Ohtsuka, Shigeru Ottomo, Kei Nakagawa, Hiroki Hayashi, Takanori Morikawa, Tohru Onogawa, Kuniharu Yamamoto, Hiroshi Yoshida, Masanori Akada, Fuyuhiko Motoi, Takeshi Naitoh, Yu Katayose, Michiaki Unno JOURNAL OF GASTROINTESTINAL SURGERY 15 (3) 525 -532 2011年03月 [査読無し][通常論文]
     
    Backgrouns/Aims There are few studies about the assessment of pancreatic function using computed tomography (CT) volumetry. In this study, we examined the correlation between CT volumetry and endocrine parameters (blood glucose and HbA1c) of the pancreas. Methods A total of 68 patients underwent enhanced CT for pancreatic disease from January to December in 2008. In particular, we analyzed the correlation of diabetic status and pancreatic CT parameters at 1 year after pancreatoduodenectomy in 32 patients. CT parameters including volume, volume/body weight, arterial phase density, the arterial phase to portal phase density ratio (A/P ratio) of the pancreas, and size of pancreatic duct were also analyzed. Correlation between CT parameters and diabetic status was analyzed preoperatively and postoperatively by ANOVA test. Results The preoperative diabetic status and parameters correlated well with arterial phase density (p=0.004), A/P ratio, and pancreatic duct size (p < 0.0001). In the patients who underwent pancreatectomy, two out of 25 patients without preoperative diabetes mellitus (DM) had DM, and two out of seven patients with preoperative DM recovered from DM. Postoperative CT parameters correlated with the DM status 1 year after pancreatectomy. Conclusion CT is a useful modality for evaluation of the pancreatic endocrine function and could be used for the prediction of postoperative diabetic outcome.
  • Naoaki Sakata, Shinichi Egawa, Toshiki Rikiyama, Gumpei Yoshimatsu, Kunihiro Masuda, Hideo Ohtsuka, Shigeru Ottomo, Kei Nakagawa, Hiroki Hayashi, Takanori Morikawa, Tohru Onogawa, Kuniharu Yamamoto, Hiroshi Yoshida, Masanori Akada, Fuyuhiko Motoi, Takeshi Naitoh, Yu Katayose, Michiaki Unno JOURNAL OF GASTROINTESTINAL SURGERY 15 (3) 525 -532 2011年03月 [査読無し][通常論文]
     
    Backgrouns/Aims There are few studies about the assessment of pancreatic function using computed tomography (CT) volumetry. In this study, we examined the correlation between CT volumetry and endocrine parameters (blood glucose and HbA1c) of the pancreas. Methods A total of 68 patients underwent enhanced CT for pancreatic disease from January to December in 2008. In particular, we analyzed the correlation of diabetic status and pancreatic CT parameters at 1 year after pancreatoduodenectomy in 32 patients. CT parameters including volume, volume/body weight, arterial phase density, the arterial phase to portal phase density ratio (A/P ratio) of the pancreas, and size of pancreatic duct were also analyzed. Correlation between CT parameters and diabetic status was analyzed preoperatively and postoperatively by ANOVA test. Results The preoperative diabetic status and parameters correlated well with arterial phase density (p=0.004), A/P ratio, and pancreatic duct size (p < 0.0001). In the patients who underwent pancreatectomy, two out of 25 patients without preoperative diabetes mellitus (DM) had DM, and two out of seven patients with preoperative DM recovered from DM. Postoperative CT parameters correlated with the DM status 1 year after pancreatectomy. Conclusion CT is a useful modality for evaluation of the pancreatic endocrine function and could be used for the prediction of postoperative diabetic outcome.
  • Fuyuhiko Motoi, Toshiki Rikiyama, Yu Katayose, Shin-ichi Egawa, Michiaki Unno ANNALS OF SURGICAL ONCOLOGY 18 (2) 371 -379 2011年02月 [査読無し][通常論文]
     
    The purpose of this study was to obtain a comprehensive understanding of the impact of postoperative tumor marker (TM) normalization on survival after pancreatectomy for pancreatic carcinoma. We propose the concept of surgical RECIST based on residual tumor and TM status. A total of consecutive patients with pancreatic carcinoma underwent pancreatectomy between August 1, 1989, and August 1, 2008. Pre- and postoperative TM values were available for 194 patients. The relationship between TM status, survival, and other clinical and demographic data was determined with univariate log-rank tests and Cox proportional hazards analysis. Postoperative TM levels remained elevated in 92 patients (47.4%; partial responders). TM levels normalized in 102 patients (52.6%; complete responders). Lymph node metastases, portal vein resection, absence of retroperitoneal clearance, residual tumor, preoperative high CA19-9, and surgical partial response were associated with decreased survival. Nodal stage (P = 0.0227) and surgical RECIST (P = 0.025) were significant predictors of survival. Partial responders had a significantly lower median survival time (P = 0.0008) and significantly higher frequency of hepatic metastasis (P = 0.0299). Postresection TM normalization is a strong prognostic factor for pancreatic cancer. The efficacy of pancreatic cancer surgery should be evaluated in the context of both local clearance and serum TM kinetics.
  • 【膵癌・胆道癌に対する免疫治療、ワクチン療法の新展開】 膵癌に対するWT1ペプチドワクチン治療の背景 (胆と膵)
    江川新一, 岡田恭穂, 林洋毅, 北村洋, 深瀬耕二, 乙供茂, 大塚英郎, 森川孝則, 水間正道, 坂田直昭, 中川圭, 吉田寛, 元井冬彦, 内藤剛, 力山敏樹, 片寄友, 海野倫明 胆と膵 32 (2) 141 -144 2011年 [査読無し][通常論文]
  • 【肝門部胆管癌の進展度と手術術式】 この症例の術式は? (肝胆膵画像)
    太田岳洋, 清水宏明, 力山敏樹, 梛野正人, 真口宏介 肝胆膵画像 13 (2) 179 -191 2011年 [査読無し][通常論文]
  • 力山敏樹, 吉田寛, 林洋毅, 元井冬彦, 佐瀬友彦, 片寄友, 江川新一, 海野倫明 肝胆膵画像 13 (2) 163 -172 2011年 [査読無し][通常論文]
  • 片寄友, 力山敏樹, 石田和之, 海野倫明 胆道 25 (1) 53 -59 2011年 [査読無し][通常論文]
  • Motoi Fuyuhiko, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Unno Michiaki Nihon Shokakibyo Gakkai Zasshi 108 (10) 1654 -1660 2011年 [査読無し][通常論文]
  • Kawaguchi Kei, Motoi Fuyuhiko, Ohtsuka Hideo, Fukuyama Shoji, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Satoh Masahiro, Asakura Toru, Shimosegawa Toru, Unno Michiaki Case Rep Gastroenterol 5 (2) 288 -294 2011年 [査読無し][通常論文]
  • Ohtsuka Hideo, Oikawa Masaya, Ariake Kyohei, Rikiyama Toshiki, Motoi Fuyuhiko, Katayose Yu, Unno Michiaki, Johnson Alfred C Int J Cancer 129 (7) 1599 -1610 2011年 [査読無し][通常論文]
  • 【膵癌・胆道癌に対する免疫治療、ワクチン療法の新展開】 膵癌に対するWT1ペプチドワクチン治療の背景 (胆と膵)
    江川新一, 岡田恭穂, 林洋毅, 北村洋, 深瀬耕二, 乙供茂, 大塚英郎, 森川孝則, 水間正道, 坂田直昭, 中川圭, 吉田寛, 元井冬彦, 内藤剛, 力山敏樹, 片寄友, 海野倫明 胆と膵 32 (2) 141 -144 2011年 [査読無し][通常論文]
  • Motoi Fuyuhiko, Rikiyama Toshiki, Katayose Yu, Egawa Shin-ichi, Unno Michiaki Ann Surg Oncol 18 (2) 371 -379 2011年 [査読無し][通常論文]
  • 【肝門部胆管癌の進展度と手術術式】 この症例の術式は? (肝胆膵画像)
    太田岳洋, 清水宏明, 力山敏樹, 梛野正人, 真口宏介 肝胆膵画像 13 (2) 179 -191 2011年 [査読無し][通常論文]
  • 力山敏樹, 吉田寛, 林洋毅, 元井冬彦, 佐瀬友彦, 片寄友, 江川新一, 海野倫明 肝胆膵画像 13 (2) 163 -172 2011年 [査読無し][通常論文]
  • 片寄友, 力山敏樹, 石田和之, 海野倫明 胆道 25 (1) 53 -59 2011年 [査読無し][通常論文]
  • Motoi Fuyuhiko, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Unno Michiaki Nihon Shokakibyo Gakkai Zasshi 108 (10) 1654 -1660 2011年 [査読無し][通常論文]
  • Kawaguchi Kei, Motoi Fuyuhiko, Ohtsuka Hideo, Fukuyama Shoji, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Satoh Masahiro, Asakura Toru, Shimosegawa Toru, Unno Michiaki Case Rep Gastroenterol 5 (2) 288 -294 2011年 [査読無し][通常論文]
  • Shinichi Egawa, Fuyuhiko Motoi, Naoaki Sakata, Yo Kitamura, Kei Nakagawa, Hideo Ohtsuka, Hiroki Hayashi, Takanori Morikawa, Noriyuki Omura, Shigeru Ottomo, Hiroshi Yoshida, Toru Onogawa, Kuniharu Yamamoto, Masanori Akada, Toshiki Rikiyama, Yu Katayose, Seiki Matsuno, Michiaki Unno JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES 17 (6) 745 -751 2010年11月 [査読無し][通常論文]
     
    The Frey procedure, the coring out of the pancreatic head and longitudinal pancreaticojejunostomy, is a safe, easy, and reliable method to solve most of the problems associated with chronic pancreatitis. During long-term follow up, unexpected relapse in the pancreatic tail was encountered. The pattern of failure and the rationale for a new procedure to treat or prevent such relapse were investigated. From 1992 to 2008, 71 patients with chronic pancreatitis underwent the Frey procedure at Tohoku University Hospital. The etiology was alcoholic in 92.6% of them, followed in incidence by idiopathic and hereditary chronic pancreatitis. In the primary operation, besides the Frey procedure, combined resection of the pancreatic tail was performed in three patients, and choledochoduodenostomy was performed in one patient. The follow-up rate was 92.9%, with a median period of 46 months. The incidence of early postoperative complications was 18.4%, with one reoperation for gastrointestinal bleeding from the splenic artery. Pain control was achieved in all patients and there was no operative mortality. During the long-term follow up of 62 patients with the Frey procedure, eight patients had relapse of inflammation and required reoperation. Five of these eight patients had a pseudocyst in the pancreatic tail and underwent distal pancreatectomy (DP). Relapse occurred in alcoholic middle-aged male patients, and in the patients with hereditary and idiopathic pancreatitis. Frey-DP and Frey-spleen-preserving DP (SPDP) procedures can be performed safely and effectively to treat the relapse and to prevent relapse in the pancreatic tail.
  • Shinichi Egawa, Fuyuhiko Motoi, Naoaki Sakata, Yo Kitamura, Kei Nakagawa, Hideo Ohtsuka, Hiroki Hayashi, Takanori Morikawa, Noriyuki Omura, Shigeru Ottomo, Hiroshi Yoshida, Toru Onogawa, Kuniharu Yamamoto, Masanori Akada, Toshiki Rikiyama, Yu Katayose, Seiki Matsuno, Michiaki Unno JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES 17 (6) 745 -751 2010年11月 [査読無し][通常論文]
     
    The Frey procedure, the coring out of the pancreatic head and longitudinal pancreaticojejunostomy, is a safe, easy, and reliable method to solve most of the problems associated with chronic pancreatitis. During long-term follow up, unexpected relapse in the pancreatic tail was encountered. The pattern of failure and the rationale for a new procedure to treat or prevent such relapse were investigated. From 1992 to 2008, 71 patients with chronic pancreatitis underwent the Frey procedure at Tohoku University Hospital. The etiology was alcoholic in 92.6% of them, followed in incidence by idiopathic and hereditary chronic pancreatitis. In the primary operation, besides the Frey procedure, combined resection of the pancreatic tail was performed in three patients, and choledochoduodenostomy was performed in one patient. The follow-up rate was 92.9%, with a median period of 46 months. The incidence of early postoperative complications was 18.4%, with one reoperation for gastrointestinal bleeding from the splenic artery. Pain control was achieved in all patients and there was no operative mortality. During the long-term follow up of 62 patients with the Frey procedure, eight patients had relapse of inflammation and required reoperation. Five of these eight patients had a pseudocyst in the pancreatic tail and underwent distal pancreatectomy (DP). Relapse occurred in alcoholic middle-aged male patients, and in the patients with hereditary and idiopathic pancreatitis. Frey-DP and Frey-spleen-preserving DP (SPDP) procedures can be performed safely and effectively to treat the relapse and to prevent relapse in the pancreatic tail.
  • Michiaki Unno, Yu Katayose, Toshiki Rikiyama, Hiroshi Yoshida, Kuniharu Yamamoto, Takanori Morikawa, Hiroki Hayashi, Fuyuhiko Motoi, Shinichi Egawa JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES 17 (4) 463 -469 2010年07月 [査読無し][通常論文]
     
    Hilar cholangiocarcinoma and intrahepatic cholangiocarcinoma involving the hepatic hilus are defined as "perihilar cholangiocarcinoma". The principle of surgical treatment is hemi-hepatectomy or trisectionectomy of the liver, caudate lobectomy, and resection of the extrahepatic bile duct for complete resection of the tumor. The aim of this study was to review the outcomes of major hepatectomy for perihilar cholangiocarcinoma. Using the Kaplan-Meier method and the Cox proportional hazards model, we analyzed the results in 125 patients with perihilar cholangiocarcinoma who had undergone major hepatectomy. Right hepatectomy, right trisectionectomy, left hepatectomy, and left trisectionectomy were performed in 66, 8, 49, and 2 patients, respectively. Curative resection was achieved in 79 patients (63.2%). Mortality and morbidity rates were 8.0 and 48.7%, respectively. The overall 1-, 3-, and 5-year survival rates of all patients were 73.2, 36.7, and 34.7%, respectively. The median survival was 26.8 months. Multivariate analysis showed that the independent prognostic factors for overall survival were gender, histopathological grading, curative resection, and American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC) pT. Major hepatectomy for perihilar cholangiocarcinoma was acceptable and showed satisfactory outcomes. For long-term survival in these patients, the surgeon should aim for complete resection of the tumor with negative margins.
  • Michiaki Unno, Yu Katayose, Toshiki Rikiyama, Hiroshi Yoshida, Kuniharu Yamamoto, Takanori Morikawa, Hiroki Hayashi, Fuyuhiko Motoi, Shinichi Egawa JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES 17 (4) 463 -469 2010年07月 [査読無し][通常論文]
     
    Hilar cholangiocarcinoma and intrahepatic cholangiocarcinoma involving the hepatic hilus are defined as "perihilar cholangiocarcinoma". The principle of surgical treatment is hemi-hepatectomy or trisectionectomy of the liver, caudate lobectomy, and resection of the extrahepatic bile duct for complete resection of the tumor. The aim of this study was to review the outcomes of major hepatectomy for perihilar cholangiocarcinoma. Using the Kaplan-Meier method and the Cox proportional hazards model, we analyzed the results in 125 patients with perihilar cholangiocarcinoma who had undergone major hepatectomy. Right hepatectomy, right trisectionectomy, left hepatectomy, and left trisectionectomy were performed in 66, 8, 49, and 2 patients, respectively. Curative resection was achieved in 79 patients (63.2%). Mortality and morbidity rates were 8.0 and 48.7%, respectively. The overall 1-, 3-, and 5-year survival rates of all patients were 73.2, 36.7, and 34.7%, respectively. The median survival was 26.8 months. Multivariate analysis showed that the independent prognostic factors for overall survival were gender, histopathological grading, curative resection, and American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC) pT. Major hepatectomy for perihilar cholangiocarcinoma was acceptable and showed satisfactory outcomes. For long-term survival in these patients, the surgeon should aim for complete resection of the tumor with negative margins.
  • 【膵癌治療法の進歩】 Stage IV局所進行膵癌の治療戦略 術前治療(NAC)とR0切除を目的とした後腹膜一括切除(en-bloc dissection:EBD) (消化器内科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 消化器内科 50 (3) 288 -296 2010年 [査読無し][通常論文]
  • 森川孝則, 片寄友, 力山敏樹, 元井冬彦, 小野川徹, 前田晋平, 高舘達之, 吉田寛, 江川新一, 海野倫明 胆道 24 (1) 105 -111 2010年 [査読無し][通常論文]
  • 高舘達之, 山本久仁治, 森川孝則, 小野川徹, 志賀清人, 小林俊光, 元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 胆道 24 (2) 204 -208 2010年 [査読無し][通常論文]
  • 膵切除術後に発症し、弁置換術施行するも救命しえなかったMRSA感染性心内膜炎の1例
    小松弘武, 吉田寛, 小野川徹, 片寄友, 力山敏樹, 元井冬彦, 江川新一, 海野倫明 日本外科感染症学会雑誌 7 (3) 285 -291 2010年 [査読無し][通常論文]
  • 【肝門部の解剖を極める 適切な手術とインターベンション治療のために】 肝門部胆管と門脈の解剖 (胆と膵)
    力山敏樹, 吉田寛, 林洋毅, 元井冬彦, 片寄友, 江川新一, 海野倫明 胆と膵 31 (7) 703 -709 2010年 [査読無し][通常論文]
  • 【必読 炎症性疾患手術】 慢性膵炎に対する外科治療 Frey手術の手技 (手術)
    江川新一, 坂田直昭, 元井冬彦, 力山敏樹, 片寄友, 海野倫明 手術 64 (8) 1131 -1136 2010年 [査読無し][通常論文]
  • 【胆管癌の進展度診断と治療戦略】 胆管癌診療の現状と課題 (日本消化器病学会雑誌)
    久津見弘, 力山敏樹, 祖父尼淳, 味木徹夫, 井岡達也 日本消化器病学会雑誌 107 (7) 1109 -1126 2010年 [査読無し][通常論文]
  • 【進行癌の治療戦略】 膵癌の治療戦略 術前治療とR0切除をめざした後腹膜一括郭清 (外科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 外科 72 (7) 734 -742 2010年 [査読無し][通常論文]
  • 【膵癌の長期生存の条件】 病期群別解析による膵癌切除例の長期生存の条件 (消化器内科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 消化器内科 51 (2) 173 -179 2010年 [査読無し][通常論文]
  • Miura Takayuki, Motoi Fuyuhiko, Ito Kei, Ito Hiromichi, Kanno Atsushi, Satoh Kenichi, Akada Masanori, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Shimosegawa Tohru, Unno Michiaki Nihon Shokakibyo Gakkai Zasshi 107 (10) 1669 -1675 2010年 [査読無し][通常論文]
  • 三浦孝之, 元井冬彦, 伊藤啓, 伊藤広通, 菅野敦, 佐藤賢一, 赤田昌紀, 力山敏樹, 片寄友, 江川新一, 下瀬川徹, 海野倫明 日本消化器病学会雑誌 107 (10) 1669 -1675 2010年 [査読無し][通常論文]
  • 【先天性胆道拡張症、膵・胆管合流異常の常識を見直す】 先天性胆道拡張症、膵・胆管合流異常に対する術後の問題点 術後合併症からみた先天性胆道拡張症手術の問題点 (胆と膵)
    大塚英郎, 吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 胆と膵 31 (11) 1319 -1323 2010年 [査読無し][通常論文]
  • [Long-term survival case after liver resection and postoperative hepatic arterial infusion for multiple liver metastases from rectal cancer].
    Kitamura Yo, Katayose Yu, Miura Koh, Yamamoto Kuniharu, Yoshida Hiroshi, Ottomo Shigeru, Motoi Fuyuhiko, Rikiyama Toshiki, Egawa Shinichi, Sasaki Iwao, Unno Michiaki Gan To Kagaku Ryoho 37 (12) 2641 -2643 2010年 [査読無し][通常論文]
  • 直腸癌術後に早期多発肝転移を来し手術と肝動注療法を施行し長期生存が得られている1例
    北村洋, 片寄友, 三浦康, 山本久仁治, 吉田寛, 乙供茂, 元井冬彦, 力山敏樹, 江川新一, 佐々木巖, 海野倫明 癌と化学療法 37 (12) 2641 -2643 2010年 [査読無し][通常論文]
  • 菅野敦, 佐藤賢一, 廣田衛久, 正宗淳, 高舘達之, 力山敏樹, 海野倫明, 石田和之, 下瀬川徹 胆道 24 (5) 714 -722 2010年 [査読無し][通常論文]
  • 【膵癌治療法の進歩】 Stage IV局所進行膵癌の治療戦略 術前治療(NAC)とR0切除を目的とした後腹膜一括切除(en-bloc dissection:EBD) (消化器内科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 消化器内科 50 (3) 288 -296 2010年 [査読無し][通常論文]
  • 森川孝則, 片寄友, 力山敏樹, 元井冬彦, 小野川徹, 前田晋平, 高舘達之, 吉田寛, 江川新一, 海野倫明 胆道 24 (1) 105 -111 2010年 [査読無し][通常論文]
  • 高舘達之, 山本久仁治, 森川孝則, 小野川徹, 志賀清人, 小林俊光, 元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 胆道 24 (2) 204 -208 2010年 [査読無し][通常論文]
  • 膵切除術後に発症し、弁置換術施行するも救命しえなかったMRSA感染性心内膜炎の1例
    小松弘武, 吉田寛, 小野川徹, 片寄友, 力山敏樹, 元井冬彦, 江川新一, 海野倫明 日本外科感染症学会雑誌 7 (3) 285 -291 2010年 [査読無し][通常論文]
  • 【肝門部の解剖を極める 適切な手術とインターベンション治療のために】 肝門部胆管と門脈の解剖 (胆と膵)
    力山敏樹, 吉田寛, 林洋毅, 元井冬彦, 片寄友, 江川新一, 海野倫明 胆と膵 31 (7) 703 -709 2010年 [査読無し][通常論文]
  • 【必読 炎症性疾患手術】 慢性膵炎に対する外科治療 Frey手術の手技 (手術)
    江川新一, 坂田直昭, 元井冬彦, 力山敏樹, 片寄友, 海野倫明 手術 64 (8) 1131 -1136 2010年 [査読無し][通常論文]
  • 【胆管癌の進展度診断と治療戦略】 胆管癌診療の現状と課題 (日本消化器病学会雑誌)
    久津見弘, 力山敏樹, 祖父尼淳, 味木徹夫, 井岡達也 日本消化器病学会雑誌 107 (7) 1109 -1126 2010年 [査読無し][通常論文]
  • 【進行癌の治療戦略】 膵癌の治療戦略 術前治療とR0切除をめざした後腹膜一括郭清 (外科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 外科 72 (7) 734 -742 2010年 [査読無し][通常論文]
  • 【膵癌の長期生存の条件】 病期群別解析による膵癌切除例の長期生存の条件 (消化器内科)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 消化器内科 51 (2) 173 -179 2010年 [査読無し][通常論文]
  • Miura Takayuki, Motoi Fuyuhiko, Ito Kei, Ito Hiromichi, Kanno Atsushi, Satoh Kenichi, Akada Masanori, Rikiyama Toshiki, Katayose Yu, Egawa Shinichi, Shimosegawa Tohru, Unno Michiaki Nihon Shokakibyo Gakkai Zasshi 107 (10) 1669 -1675 2010年 [査読無し][通常論文]
  • 三浦孝之, 元井冬彦, 伊藤啓, 伊藤広通, 菅野敦, 佐藤賢一, 赤田昌紀, 力山敏樹, 片寄友, 江川新一, 下瀬川徹, 海野倫明 日本消化器病学会雑誌 107 (10) 1669 -1675 2010年 [査読無し][通常論文]
  • 【先天性胆道拡張症、膵・胆管合流異常の常識を見直す】 先天性胆道拡張症、膵・胆管合流異常に対する術後の問題点 術後合併症からみた先天性胆道拡張症手術の問題点 (胆と膵)
    大塚英郎, 吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 胆と膵 31 (11) 1319 -1323 2010年 [査読無し][通常論文]
  • [Long-term survival case after liver resection and postoperative hepatic arterial infusion for multiple liver metastases from rectal cancer].
    Kitamura Yo, Katayose Yu, Miura Koh, Yamamoto Kuniharu, Yoshida Hiroshi, Ottomo Shigeru, Motoi Fuyuhiko, Rikiyama Toshiki, Egawa Shinichi, Sasaki Iwao, Unno Michiaki Gan To Kagaku Ryoho 37 (12) 2641 -2643 2010年 [査読無し][通常論文]
  • 直腸癌術後に早期多発肝転移を来し手術と肝動注療法を施行し長期生存が得られている1例
    北村洋, 片寄友, 三浦康, 山本久仁治, 吉田寛, 乙供茂, 元井冬彦, 力山敏樹, 江川新一, 佐々木巖, 海野倫明 癌と化学療法 37 (12) 2641 -2643 2010年 [査読無し][通常論文]
  • 菅野敦, 佐藤賢一, 廣田衛久, 正宗淳, 高舘達之, 力山敏樹, 海野倫明, 石田和之, 下瀬川徹 胆道 24 (5) 714 -722 2010年 [査読無し][通常論文]
  • Overexpression of Adenovirus-mediated p27(kip1) Lacking the Jab1-binding Region Enhances Cytotoxicity and Inhibits Xenografted Human Cholangiocarcinoma Growth
    Satoru Shiraso, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Tohru Onogawa, Hiroshi Yoshida, Hiroki Hayashi, Hideo Ohtsuka, Fuyuhiko Motoi, Shinichi Egawa, Junya Kato, Michiaki Unno ANTICANCER RESEARCH 29 (6) 2015 -2024 2009年06月 [査読無し][通常論文]
     
    The cyclin-dependent kinase inhibitor (CDK1) p27(kip1) is a negative regulator of cell cycling and has antitumor effects. In our previous study, the recombinant adenovirus expressing wild-type p27(kip1) (Adp27-wt) induced cell cycle arrest and apoptosis, and proved that p27 is a tumor suppressor gene like p53. Another adenovirus vector expressing mutant p27(kip1) (Adp27-mt), which inhibited degradation by the ubiquitin-proteasome system, showed increased protein stability and caused a stronger induction of apoptosis. Recently, the p27(kip1) protein binding with Jab1 (Jun activating binding protein 1) was found to translocate from the nucleus into the cytosol, and then become degraded by the 26S proteasome system. The inhibition of nuclear-cytoplasmic translocation increases the protein stability of p27(kip1) and p27(kip1) with a deletion of the Jab1-binding region (p27-jab-d) is not translocated and not degraded. Therefore, a new recombinant adenovirus (Adp27-jab-d) expressing p27-jab-d was made which was able to induce greater cytotoxicity. Adp27-jab-d inhibited the growth of human cholangiocarcinoma cell line (TFK-1) cells in vitro at 3.3 times (IC50) lower concentration than Adp27-wt. Moreover, in a xenografted severe combined immuno-deficient (SCID) mouse model injected with TFK-1 cells in the subcutaneous tissue, treatment by intratumor injection of Adp27-jab-d once a day for 3 days after the tumor was established, inhibited tumor growth more strongly than Adp27-wt or Adp27-mt and even induced tumor regression. However, the flow cytometric TUNEL assay showed little enhancement of apoptosis. Adp27-jab-d was thought to induce not only apoptosis but also necrosis, which was due to a specific effect of the Adp27-jab-d. Thus, by enhancing the cytotoxicity through inhibiting the translocaton of p27(kip1), p27(kip1) lacking the Jab1-binding region might be useful for cancer therapy. The control protein localization might also be a new target not only for cancer treatment, but also other diseases.
  • Overexpression of Adenovirus-mediated p27(kip1) Lacking the Jab1-binding Region Enhances Cytotoxicity and Inhibits Xenografted Human Cholangiocarcinoma Growth
    Satoru Shiraso, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Tohru Onogawa, Hiroshi Yoshida, Hiroki Hayashi, Hideo Ohtsuka, Fuyuhiko Motoi, Shinichi Egawa, Junya Kato, Michiaki Unno ANTICANCER RESEARCH 29 (6) 2015 -2024 2009年06月 [査読無し][通常論文]
     
    The cyclin-dependent kinase inhibitor (CDK1) p27(kip1) is a negative regulator of cell cycling and has antitumor effects. In our previous study, the recombinant adenovirus expressing wild-type p27(kip1) (Adp27-wt) induced cell cycle arrest and apoptosis, and proved that p27 is a tumor suppressor gene like p53. Another adenovirus vector expressing mutant p27(kip1) (Adp27-mt), which inhibited degradation by the ubiquitin-proteasome system, showed increased protein stability and caused a stronger induction of apoptosis. Recently, the p27(kip1) protein binding with Jab1 (Jun activating binding protein 1) was found to translocate from the nucleus into the cytosol, and then become degraded by the 26S proteasome system. The inhibition of nuclear-cytoplasmic translocation increases the protein stability of p27(kip1) and p27(kip1) with a deletion of the Jab1-binding region (p27-jab-d) is not translocated and not degraded. Therefore, a new recombinant adenovirus (Adp27-jab-d) expressing p27-jab-d was made which was able to induce greater cytotoxicity. Adp27-jab-d inhibited the growth of human cholangiocarcinoma cell line (TFK-1) cells in vitro at 3.3 times (IC50) lower concentration than Adp27-wt. Moreover, in a xenografted severe combined immuno-deficient (SCID) mouse model injected with TFK-1 cells in the subcutaneous tissue, treatment by intratumor injection of Adp27-jab-d once a day for 3 days after the tumor was established, inhibited tumor growth more strongly than Adp27-wt or Adp27-mt and even induced tumor regression. However, the flow cytometric TUNEL assay showed little enhancement of apoptosis. Adp27-jab-d was thought to induce not only apoptosis but also necrosis, which was due to a specific effect of the Adp27-jab-d. Thus, by enhancing the cytotoxicity through inhibiting the translocaton of p27(kip1), p27(kip1) lacking the Jab1-binding region might be useful for cancer therapy. The control protein localization might also be a new target not only for cancer treatment, but also other diseases.
  • Clock Gene Mouse Period2 Overexpression Inhibits Growth of Human Pancreatic Cancer Cells and Has Synergistic Effect with Cisplatin
    Akira Oda, Yu Katayose, Shinichi Yabuuchi, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shirasou, Toru Onogawa, Hideo Ohtsuka, Hiroshi Yoshida, Hiroki Hayashi, Toshiki Rikiyama, Hyunjung Kim, Youngshik Choe, Kyungjin Kim, Hosun Son, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 29 (4) 1201 -1209 2009年04月 [査読無し][通常論文]
     
    Circadian rhythms are the daily oscillations of multiple biological processes regulated by an endogenous clock. The Period2 gene is essential in controlling the circadian rhythm and plays an important role in tumor suppression. We examined whether the overexpression of the mouse Period2 gene (mPer2) in cultured tumor cells from human tissues inhibits cell growth, using the recombinant adenovirus vector AdmPer2. The overexpression of mPer2 in human pancreatic cancer cells (Panc1, Aspc1) reduced cellular proliferation and induced apoptotic cell death. Infection with AdmPer2 also inhibited cell-cycle progression, inducing arrest at the G(2)-M phase. Western blotting analyses confirmed that infection with AdmPer2 reduced Bcl-X(L), Cdc2 and cyclin B1 protein, whereas it increased Bax protein in Aspc1 cells. The overexpression of mPer2 suppressed Cdc2 kinase activity. Moreover, infection with AdmPer2 resulted in dose-dependent synergic cell killing effects with the anticancer agent cisplatin (CDDP) in human pancreatic cancer cells. This synergic effect might be related to the reduction of Bcl-X(L) induced by infection with AdmPer2. Our results suggest that the circadian gene Period2 may play an important role in suppression of cell proliferation in human cancer, and additionally Period2 gene expression level may influence the sensitivity, to cisplatin depending on Bcl-X(L) expression level.
  • ZD1839 (IRESSA (R)) Stabilizes p27(Kip1) and Enhances Radiosensitivity in Cholangiocarcinoma Cell Lines
    Shinichi Yabuuchi, Yu Katayose, Akira Oda, Masamichi Mizuma, Satoru Shirasou, Tsuyoshi Sasaki, Kunhiharu Yamamoto, Masaya Oikawa, Toshiki Rikiyama, Tohru Onogawa, Hiroshi Yoshida, Hideo Ohtuska, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 29 (4) 1169 -1180 2009年04月 [査読無し][通常論文]
     
    The prognosis of cholangiocarcinoma patients is extremely poor despite the aggressive multidisciplinary cancer therapies that have been used clinically (1). Recently, molecular target therapy has attracted attention. Epidermal growth factor receptor (EGFR) tyrosine kinase (TK) is a promising target for anticancer therapy. ZD1839 (IRESSA (R)) is an orally active, selective inhibitor of EGFR-TK. This study examined the effects of ZD1839 in TFK-1 and HuCCT1, the human cholangiocarcinoma cell lines that express EGFR. Somatic mutations in the TK domain of the EGFR gene are associated with the sensitivity of lung cancers to ZD1839 (2). In the analysis of the EGFR sequence, no mutations were found in TFK-1 and HuCCT1. The TFK-1 and HuCCT1 cells showed almost the same sensitivity to ZD1839. It is shown that ZD1839 induced apoptotic cell death of TFK-1 cells as indicated by apoptotic morphological changes and an enhancement of TUNEL-positive cells. ZD1839 produced a dose-dependent inhibition of cellular proliferation in TFK-1. Cell cycle analysis demonstrated that ZD1839 induces G1 arrest. Moreover, concurrent evaluation of the expression of p27(KiP1) protein and Jun activating domain-binding protein 1 (Jab1) with ZD1839 by Western blotting analysis was performed. It was found that ZD1839 activity causes an increase of p27(Kip1) stability that correlates with Jab1 down-regulation. Thus, ZD1839 affects key cellular pathways, controlling cell proliferation and apoptosis. Furthermore, the treatment of TFK-1 with ZD1839 reduced the cell survival after radiation exposure. ZD1839 in combination with radiation produced a dose-dependent and synergic inhibitory effect on cellular proliferation. In conclusion, these results suggest that ZD1839 may have clinical activity against cholangiocarcinoma.
  • Clock Gene Mouse Period2 Overexpression Inhibits Growth of Human Pancreatic Cancer Cells and Has Synergistic Effect with Cisplatin
    Akira Oda, Yu Katayose, Shinichi Yabuuchi, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shirasou, Toru Onogawa, Hideo Ohtsuka, Hiroshi Yoshida, Hiroki Hayashi, Toshiki Rikiyama, Hyunjung Kim, Youngshik Choe, Kyungjin Kim, Hosun Son, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 29 (4) 1201 -1209 2009年04月 [査読無し][通常論文]
     
    Circadian rhythms are the daily oscillations of multiple biological processes regulated by an endogenous clock. The Period2 gene is essential in controlling the circadian rhythm and plays an important role in tumor suppression. We examined whether the overexpression of the mouse Period2 gene (mPer2) in cultured tumor cells from human tissues inhibits cell growth, using the recombinant adenovirus vector AdmPer2. The overexpression of mPer2 in human pancreatic cancer cells (Panc1, Aspc1) reduced cellular proliferation and induced apoptotic cell death. Infection with AdmPer2 also inhibited cell-cycle progression, inducing arrest at the G(2)-M phase. Western blotting analyses confirmed that infection with AdmPer2 reduced Bcl-X(L), Cdc2 and cyclin B1 protein, whereas it increased Bax protein in Aspc1 cells. The overexpression of mPer2 suppressed Cdc2 kinase activity. Moreover, infection with AdmPer2 resulted in dose-dependent synergic cell killing effects with the anticancer agent cisplatin (CDDP) in human pancreatic cancer cells. This synergic effect might be related to the reduction of Bcl-X(L) induced by infection with AdmPer2. Our results suggest that the circadian gene Period2 may play an important role in suppression of cell proliferation in human cancer, and additionally Period2 gene expression level may influence the sensitivity, to cisplatin depending on Bcl-X(L) expression level.
  • ZD1839 (IRESSA (R)) Stabilizes p27(Kip1) and Enhances Radiosensitivity in Cholangiocarcinoma Cell Lines
    Shinichi Yabuuchi, Yu Katayose, Akira Oda, Masamichi Mizuma, Satoru Shirasou, Tsuyoshi Sasaki, Kunhiharu Yamamoto, Masaya Oikawa, Toshiki Rikiyama, Tohru Onogawa, Hiroshi Yoshida, Hideo Ohtuska, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 29 (4) 1169 -1180 2009年04月 [査読無し][通常論文]
     
    The prognosis of cholangiocarcinoma patients is extremely poor despite the aggressive multidisciplinary cancer therapies that have been used clinically (1). Recently, molecular target therapy has attracted attention. Epidermal growth factor receptor (EGFR) tyrosine kinase (TK) is a promising target for anticancer therapy. ZD1839 (IRESSA (R)) is an orally active, selective inhibitor of EGFR-TK. This study examined the effects of ZD1839 in TFK-1 and HuCCT1, the human cholangiocarcinoma cell lines that express EGFR. Somatic mutations in the TK domain of the EGFR gene are associated with the sensitivity of lung cancers to ZD1839 (2). In the analysis of the EGFR sequence, no mutations were found in TFK-1 and HuCCT1. The TFK-1 and HuCCT1 cells showed almost the same sensitivity to ZD1839. It is shown that ZD1839 induced apoptotic cell death of TFK-1 cells as indicated by apoptotic morphological changes and an enhancement of TUNEL-positive cells. ZD1839 produced a dose-dependent inhibition of cellular proliferation in TFK-1. Cell cycle analysis demonstrated that ZD1839 induces G1 arrest. Moreover, concurrent evaluation of the expression of p27(KiP1) protein and Jun activating domain-binding protein 1 (Jab1) with ZD1839 by Western blotting analysis was performed. It was found that ZD1839 activity causes an increase of p27(Kip1) stability that correlates with Jab1 down-regulation. Thus, ZD1839 affects key cellular pathways, controlling cell proliferation and apoptosis. Furthermore, the treatment of TFK-1 with ZD1839 reduced the cell survival after radiation exposure. ZD1839 in combination with radiation produced a dose-dependent and synergic inhibitory effect on cellular proliferation. In conclusion, these results suggest that ZD1839 may have clinical activity against cholangiocarcinoma.
  • 海野倫明, 力山敏樹, 岡上能斗竜, 片寄友 胆道 23 (1) 119 -123 2009年 [査読無し][通常論文]
  • 【新規抗癌剤の導入で膵癌治療はどう変わるか?】 RECIST基準に準じた膵癌切除治療の効果判定 切除完全奏効率からみた術前治療の有効性評価 (癌の臨床)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 癌の臨床 55 (3) 191 -197 2009年 [査読無し][通常論文]
  • 江川新一, 北村洋, 坂田直昭, 乙供茂, 阿部永, 赤田昌紀, 元井冬彦, 力山敏樹, 片寄友, 海野倫明 日本消化器外科学会雑誌 42 (5) 466 -472 2009年 [査読無し][通常論文]
  • 【肝胆膵手術〜教えるポイント・教わるポイント】 教えるポイント・教わるポイント 標準的膵頭十二指腸切除(切除後の再建について) 膵空腸粘膜吻合(no stent法)を中心に (手術)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 手術 63 (7) 1035 -1040 2009年 [査読無し][通常論文]
  • 力山敏樹, 林洋毅, 片寄友, 海野倫明 臨床外科 64 (8) 1039 -1048 2009年 [査読無し][通常論文]
  • [The possibility of local control of cancer by neoadjuvant chemoradiation therapy with gemcitabine and surgical resection for advanced cholangiocarcinoma].
    Nakagawa Kei, Katayose Yu, Rikiyama Toshiki, Okaue Adoru, Unno Michiaki Gan To Kagaku Ryoho 36 (12) 2009 -2011 2009年 [査読無し][通常論文]
  • 海野倫明, 力山敏樹, 岡上能斗竜, 片寄友 胆道 23 (1) 119 -123 2009年 [査読無し][通常論文]
  • 【新規抗癌剤の導入で膵癌治療はどう変わるか?】 RECIST基準に準じた膵癌切除治療の効果判定 切除完全奏効率からみた術前治療の有効性評価 (癌の臨床)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 癌の臨床 55 (3) 191 -197 2009年 [査読無し][通常論文]
  • 江川新一, 北村洋, 坂田直昭, 乙供茂, 阿部永, 赤田昌紀, 元井冬彦, 力山敏樹, 片寄友, 海野倫明 日本消化器外科学会雑誌 42 (5) 466 -472 2009年 [査読無し][通常論文]
  • 【肝胆膵手術〜教えるポイント・教わるポイント】 教えるポイント・教わるポイント 標準的膵頭十二指腸切除(切除後の再建について) 膵空腸粘膜吻合(no stent法)を中心に (手術)
    元井冬彦, 力山敏樹, 片寄友, 江川新一, 海野倫明 手術 63 (7) 1035 -1040 2009年 [査読無し][通常論文]
  • 力山敏樹, 林洋毅, 片寄友, 海野倫明 臨床外科 64 (8) 1039 -1048 2009年 [査読無し][通常論文]
  • [The possibility of local control of cancer by neoadjuvant chemoradiation therapy with gemcitabine and surgical resection for advanced cholangiocarcinoma].
    Nakagawa Kei, Katayose Yu, Rikiyama Toshiki, Okaue Adoru, Unno Michiaki Gan To Kagaku Ryoho 36 (12) 2009 -2011 2009年 [査読無し][通常論文]
  • Hiroyuki Nakamura, Yu Katayose, Toshiki Rikiyama, Tohru Onogawa, Kuniharu Yamamoto, Hiroshi Yoshida, Hiroki Hayashi, Hideo Ohtsuka, Yutaka Hayashi, Shin-Ichi Egawa, Michiaki Unno JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY 15 (5) 554 -559 2008年09月 [査読無し][通常論文]
     
    We report a case of advanced bile duct carcinoma arising in a 15-year-old female with pancreaticobiliary maljunction and congenital biliary cystic disease. Pancreaticoduodenectomy and partial resection of the liver was performed. Surgical and histopathological findings indicated advanced tubular adenocarcinoma, classified as final stage IVb according to the General rules for surgical and pathological studies on cancer of the biliary tract proposed by the Japanese Society of Biliary Surgery, 5th edition, and stage IV according to the American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC), 6th edition. She underwent chemotherapy with gemcitabine HCl after discharge. She died of cachexia 14 months after the surgery. Although it is well known that biliary malignancies arise frequently in patients with pancreaticobiliary maljunction, it is uncommon for advanced bile duct carcinoma to occur in a 15-year-old female. We should pay attention to the possibility of biliary malignancy in patients with pancreaticobiliary maljunction and congenital biliary cystic disease, even when the patients are juveniles.
  • Naoaki Sakata, Shinichi Egawa, Fuyuhiko Motoi, Yukio Mikami, Masaharu Ishida, Takeshi Aoki, Shigeru Ottomo, Shoji Fukuyama, Toshiki Rikiyama, Yu Katayose, Masafumi Goto, Michiaki Unno JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY 15 (5) 488 -492 2008年09月 [査読無し][通常論文]
     
    Background/Purpose. This study was designed to establish institutional indications for pancreatic islet transplantation by examining patients with total pancreatectomy as candidates for islet allotransplantation. Methods. In 12 patients who underwent total pancreatectomy, we compared pre-and postoperative plasma glucose level, body mass index, HbA1c, and daily insulin use; we examined candidacy for islet allotransplantation based on the guidelines of Japan's islet transplantation registry. Results. Eight of the 12 patients with total pancreatectomy were operated for intraductal papillary mucinous neoplasm. At our institution, the 5-year survival of patients with intraductal papillary mucinous neoplasm was far better (76.3%) than that of patients with pancreatic cancer. Postoperatively, plasma glucose level, HbA1c, and daily insulin use were increased in all patients with total pancreatectomy. Of the 12 patients treated with total pancreatectomy, 4 (intraductal papillary mucinous neoplasm, n = 2; islet cell tumor, n = 1; and acute pancreatitis due to arteriovenous malformation, n = 1) showed deteriorated diabetic control and therefore were considered to be candidates for islet allotransplantation according to the guidelines. Conclusions. Islet allotransplantation could be indicated for patients with favorable postoperative survival who have had a total pancreatectomy for either benign or neoplastic disease.
  • Up-regulated p27(Kip1) Reduces Matrix Metalloproteinase-9 and Inhibits Invasion of Human Breast Cancer Cells
    Masamichi Mizuma, Yu Katayose, Kuniharu Yamamoto, Satoru Shiraso, Tsuyoshi Sasaki, Shinichi Yabuuchi, Akira Oda, Kunihiro Masuda, Toshiki Rikiyama, Tohru Onogawa, Hideo Ohtsuka, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 28 (5A) 2669 -2677 2008年09月 [査読無し][通常論文]
     
    Background: p27(Kip1) is a cyclin-dependent kinase inhibitor which has been reported to be associated with invasion, metastasis and angiogenesis in malignant tumors, but its mechanism of action remains unknown. Here, it was examined whether p27(Kip1) has an inhibitory effect on cancer cell invasion and correlates with matrix metalloproteinase expression (MMPs). Material and methods: The human breast cancer cell line MDA-MB-231 and MDA-MB-231 transfected p27(Kip1) MDA-MB-p27 were used for the invasion assay, Western blotting and real-time quantitative RT-PCR. Results: In the invasion assay, the invasion of MDA-MB-p27 was significantly less than that of the parent cell line. In Western blotting analyses, the protein level of MMP-9 was also reduced in MDA-MB-p27. Furthermore, the activity of MMP-9 in cell culture supernatants was lower in MDA-MB-p27 as compared with enzyme-linked immunosorbent assays. In real-time quantitative RT-PCR, the mRNA level of MMP9 was lower in MDA-MB-p27 cells. Conclusion: Upregulation of p27(Kip1) remarkably inhibited the invasion of the breast cancer cells, in part due to the reduced expression of MMP-9. This is the first report of p27(Kip1) modulating MMP9 and indicating that p27(Kip1) might play a key role in tumor cell invasion.
  • Koji Fukase, Hideo Ohtsuka, Tohru Onogawa, Hiroshi Oshio, Takayuki Ii, Mitsuhisa Mutoh, Yu Katayose, Toshiki Rikiyama, Masaya Oikawa, Fuyuhiko Motoi, Shinichi Egawa, Takaaki Abe, Michiaki Unno CANCER SCIENCE 99 (9) 1785 -1792 2008年09月 [査読無し][通常論文]
     
    Although some kinds of bile acids have been implicated in colorectal cancer development, the mechanism of cancer progression remains unexplored in hepatobiliary cancer. From our personal results using complementary DNA microarray, we found that chenodeoxycholic acid (CDCA) induced Snail expression in human carcinoma cell lines derived from hepatocellular carcinoma and cholangiocarcinoma. Snail expression plays an important role in the regulation of E-cadherin and in the acquisition of invasive potential in many types of human cancers including hepatocellular carcinoma. We found that CDCA and lithocholic acid (LCA) induced Snail expression in a concentration-dependent manner and down-regulated E-cadherin expression in hepatocellular carcinoma and cholangiocarcinoma cell lines. Moreover, Snail short interference RNA (siRNA) treatment reduced the down-regulation of E-cadherin by CDCA or LCA. Luciferase analysis demonstrated that the promoter region from -111 to -24 relative to the transcriptional start site was necessary for this induction and, at least in part, nuclear factor Y (NF-Y) and stimulating protein 1 (Sp1) might be an inducer of Snail expression in response to bile acids. In addition, using an in vitro wound healing assay and invasion assay, we observed that CDCA and LCA induced cell migration and invasion. These results suggest that bile acids repress E-cadherin through the induction of transcription factor Snail and increase cancer invasiveness in human hepatocellular carcinoma and cholangiocarcinoma. Inhibition of this bile acid-stimulated pathway may prove useful as an adjuvant in the therapy of hepatocellular carcinoma.
  • Naoaki Sakata, Shinichi Egawa, Fuyuhiko Motoi, Yukio Mikami, Masaharu Ishida, Takeshi Aoki, Shigeru Ottomo, Shoji Fukuyama, Toshiki Rikiyama, Yu Katayose, Masafumi Goto, Michiaki Unno JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY 15 (5) 488 -492 2008年09月 [査読無し][通常論文]
     
    Background/Purpose. This study was designed to establish institutional indications for pancreatic islet transplantation by examining patients with total pancreatectomy as candidates for islet allotransplantation. Methods. In 12 patients who underwent total pancreatectomy, we compared pre-and postoperative plasma glucose level, body mass index, HbA1c, and daily insulin use; we examined candidacy for islet allotransplantation based on the guidelines of Japan's islet transplantation registry. Results. Eight of the 12 patients with total pancreatectomy were operated for intraductal papillary mucinous neoplasm. At our institution, the 5-year survival of patients with intraductal papillary mucinous neoplasm was far better (76.3%) than that of patients with pancreatic cancer. Postoperatively, plasma glucose level, HbA1c, and daily insulin use were increased in all patients with total pancreatectomy. Of the 12 patients treated with total pancreatectomy, 4 (intraductal papillary mucinous neoplasm, n = 2; islet cell tumor, n = 1; and acute pancreatitis due to arteriovenous malformation, n = 1) showed deteriorated diabetic control and therefore were considered to be candidates for islet allotransplantation according to the guidelines. Conclusions. Islet allotransplantation could be indicated for patients with favorable postoperative survival who have had a total pancreatectomy for either benign or neoplastic disease.
  • Up-regulated p27(Kip1) Reduces Matrix Metalloproteinase-9 and Inhibits Invasion of Human Breast Cancer Cells
    Masamichi Mizuma, Yu Katayose, Kuniharu Yamamoto, Satoru Shiraso, Tsuyoshi Sasaki, Shinichi Yabuuchi, Akira Oda, Kunihiro Masuda, Toshiki Rikiyama, Tohru Onogawa, Hideo Ohtsuka, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno ANTICANCER RESEARCH 28 (5A) 2669 -2677 2008年09月 [査読無し][通常論文]
     
    Background: p27(Kip1) is a cyclin-dependent kinase inhibitor which has been reported to be associated with invasion, metastasis and angiogenesis in malignant tumors, but its mechanism of action remains unknown. Here, it was examined whether p27(Kip1) has an inhibitory effect on cancer cell invasion and correlates with matrix metalloproteinase expression (MMPs). Material and methods: The human breast cancer cell line MDA-MB-231 and MDA-MB-231 transfected p27(Kip1) MDA-MB-p27 were used for the invasion assay, Western blotting and real-time quantitative RT-PCR. Results: In the invasion assay, the invasion of MDA-MB-p27 was significantly less than that of the parent cell line. In Western blotting analyses, the protein level of MMP-9 was also reduced in MDA-MB-p27. Furthermore, the activity of MMP-9 in cell culture supernatants was lower in MDA-MB-p27 as compared with enzyme-linked immunosorbent assays. In real-time quantitative RT-PCR, the mRNA level of MMP9 was lower in MDA-MB-p27 cells. Conclusion: Upregulation of p27(Kip1) remarkably inhibited the invasion of the breast cancer cells, in part due to the reduced expression of MMP-9. This is the first report of p27(Kip1) modulating MMP9 and indicating that p27(Kip1) might play a key role in tumor cell invasion.
  • Koji Fukase, Hideo Ohtsuka, Tohru Onogawa, Hiroshi Oshio, Takayuki Ii, Mitsuhisa Mutoh, Yu Katayose, Toshiki Rikiyama, Masaya Oikawa, Fuyuhiko Motoi, Shinichi Egawa, Takaaki Abe, Michiaki Unno CANCER SCIENCE 99 (9) 1785 -1792 2008年09月 [査読無し][通常論文]
     
    Although some kinds of bile acids have been implicated in colorectal cancer development, the mechanism of cancer progression remains unexplored in hepatobiliary cancer. From our personal results using complementary DNA microarray, we found that chenodeoxycholic acid (CDCA) induced Snail expression in human carcinoma cell lines derived from hepatocellular carcinoma and cholangiocarcinoma. Snail expression plays an important role in the regulation of E-cadherin and in the acquisition of invasive potential in many types of human cancers including hepatocellular carcinoma. We found that CDCA and lithocholic acid (LCA) induced Snail expression in a concentration-dependent manner and down-regulated E-cadherin expression in hepatocellular carcinoma and cholangiocarcinoma cell lines. Moreover, Snail short interference RNA (siRNA) treatment reduced the down-regulation of E-cadherin by CDCA or LCA. Luciferase analysis demonstrated that the promoter region from -111 to -24 relative to the transcriptional start site was necessary for this induction and, at least in part, nuclear factor Y (NF-Y) and stimulating protein 1 (Sp1) might be an inducer of Snail expression in response to bile acids. In addition, using an in vitro wound healing assay and invasion assay, we observed that CDCA and LCA induced cell migration and invasion. These results suggest that bile acids repress E-cadherin through the induction of transcription factor Snail and increase cancer invasiveness in human hepatocellular carcinoma and cholangiocarcinoma. Inhibition of this bile acid-stimulated pathway may prove useful as an adjuvant in the therapy of hepatocellular carcinoma.
  • Hiroshi Oshio, Takaaki Abe, Tohru Onogawa, Hideo Ohtsuka, Takeaki Sato, Takayuki Ii, Kouji Fukase, Mitsuhisa Muto, Yu Katayose, Masaya Oikawa, Toshiki Rikiyama, Shinichi Egawa, Michiaki Unno JOURNAL OF GASTROENTEROLOGY 43 (7) 538 -549 2008年07月 [査読無し][通常論文]
     
    Background. Evidence is accumulating that bile acids are involved in colon cancer development, but their molecular mechanisms remain unexplored. Bile acid has been reported to be associated with induction of the cyclooxygenase-2 (COX-2) gene. Because the human liver-specific organic anion transporter-2 (LST2/OATP8/OATP1B3) is expressed in gastrointestinal cancers and might transport bile acids to the intracellular space, we studied the molecular mechanisms by which bile acids induce the transcription of COX-2, and the role of LST-2 in colonic cell lines. Methods. Transcriptional activity of COX-2 was measured using a human COX-2 promoter-luciferase assay under various concentrations of bile acids. Electrophoresis mobility shift assays (EMSAs) for peroxisome proliferator-activated receptor (PPAR) alpha and cyclic AMP responsive element (CRE) were performed. Results. The COX-2 promoter was induced by lithocholic acid (LCA), deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA). Deletion and site-directed mutation analyses showed that CRE is the responsive element for LCA. An adenovirus expression system revealed that LST-2 is responsible for induction of COX-2. By EMSA using oligonucleotides of CRE, we observed formation of a specific protein-DNA complex, which was inhibited by a specific antibody against PPARa and CRE. A PPAR alpha-specific agonist induced transcription of COX2. Conclusion. These results indicate that COX-2 is transcriptionally activated by the addition of LCA, CDCA, and DCA and that LST-2 plays an important role by transporting bile acid to the intracellular space. Moreover, LCA-dependent COX-2 gene activation consists of a transcriptional complex including PPARa and CRE-binding protein. Thus, this induction of COX-2 may participate in carcinogenesis and progression of colorectal cancer cells.
  • Hiroshi Oshio, Takaaki Abe, Tohru Onogawa, Hideo Ohtsuka, Takeaki Sato, Takayuki Ii, Kouji Fukase, Mitsuhisa Muto, Yu Katayose, Masaya Oikawa, Toshiki Rikiyama, Shinichi Egawa, Michiaki Unno JOURNAL OF GASTROENTEROLOGY 43 (7) 538 -549 2008年07月 [査読無し][通常論文]
     
    Background. Evidence is accumulating that bile acids are involved in colon cancer development, but their molecular mechanisms remain unexplored. Bile acid has been reported to be associated with induction of the cyclooxygenase-2 (COX-2) gene. Because the human liver-specific organic anion transporter-2 (LST2/OATP8/OATP1B3) is expressed in gastrointestinal cancers and might transport bile acids to the intracellular space, we studied the molecular mechanisms by which bile acids induce the transcription of COX-2, and the role of LST-2 in colonic cell lines. Methods. Transcriptional activity of COX-2 was measured using a human COX-2 promoter-luciferase assay under various concentrations of bile acids. Electrophoresis mobility shift assays (EMSAs) for peroxisome proliferator-activated receptor (PPAR) alpha and cyclic AMP responsive element (CRE) were performed. Results. The COX-2 promoter was induced by lithocholic acid (LCA), deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA). Deletion and site-directed mutation analyses showed that CRE is the responsive element for LCA. An adenovirus expression system revealed that LST-2 is responsible for induction of COX-2. By EMSA using oligonucleotides of CRE, we observed formation of a specific protein-DNA complex, which was inhibited by a specific antibody against PPARa and CRE. A PPAR alpha-specific agonist induced transcription of COX2. Conclusion. These results indicate that COX-2 is transcriptionally activated by the addition of LCA, CDCA, and DCA and that LST-2 plays an important role by transporting bile acid to the intracellular space. Moreover, LCA-dependent COX-2 gene activation consists of a transcriptional complex including PPARa and CRE-binding protein. Thus, this induction of COX-2 may participate in carcinogenesis and progression of colorectal cancer cells.
  • 【知っておくべきPoor Risk患者の周術期管理】 糖尿病患者の周術期管理 (外科治療)
    吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 外科治療 98 (4) 362 -366 2008年 [査読無し][通常論文]
  • 【いわゆる粘液産生胆管腫瘍をめぐって】 胆管内乳頭状腫瘍と膵IPMNの比較 (胆と膵)
    岡上能斗竜, 片寄友, 力山敏樹, 小野川徹, 石田和之, 江川新一, 海野倫明 胆と膵 29 (6) 523 -527 2008年 [査読無し][通常論文]
  • 【肝内胆管癌 2008,up-to-date】 放射線化学および補助療法の進歩 肝内胆管癌に対する放射線療法の治療成績 (肝・胆・膵)
    吉田寛, 片寄友, 力山敏樹, 元井冬彦, 江川新一, 海野倫明 肝・胆・膵 57 (1) 143 -147 2008年 [査読無し][通常論文]
  • 【縫合・吻合手技 安全・確実な技術を習得するために】 肝胆膵 膵頭十二指腸切除術の再建 吻合法を中心に (消化器外科)
    江川新一, 元井冬彦, 乙供茂, 阿部永, 岡田恭穂, 力山敏樹, 片寄友, 海野倫明 消化器外科 31 (8) 1255 -1261 2008年 [査読無し][通常論文]
  • 【肝内胆管癌の病態特性からみた外科治療の適応と限界】 腫瘤形成型肝内胆管癌の手術適応 (消化器科)
    吉田寛, 片寄友, 力山敏樹, 元井冬彦, 有明恭平, 江川新一, 海野倫明 消化器科 47 (3) 284 -289 2008年 [査読無し][通常論文]
  • 【先天性胆道拡張症 その発生から長期予後まで】 成人の先天性胆道拡張症術後長期成績からみた肝内結石 (胆と膵)
    大塚英郎, 吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 胆と膵 29 (10) 921 -925 2008年 [査読無し][通常論文]
  • 【知っておくべきPoor Risk患者の周術期管理】 糖尿病患者の周術期管理 (外科治療)
    吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 外科治療 98 (4) 362 -366 2008年 [査読無し][通常論文]
  • Nakamura Hiroyuki, Katayose Yu, Rikiyama Toshiki, Onogawa Tohru, Yamamoto Kuniharu, Yoshida Hiroshi, Hayashi Hiroki, Ohtsuka Hideo, Hayashi Yutaka, Egawa Shin-ichi, Unno Michiaki J Hepatobiliary Pancreat Surg 15 (5) 554 -559 2008年 [査読無し][通常論文]
  • 【いわゆる粘液産生胆管腫瘍をめぐって】 胆管内乳頭状腫瘍と膵IPMNの比較 (胆と膵)
    岡上能斗竜, 片寄友, 力山敏樹, 小野川徹, 石田和之, 江川新一, 海野倫明 胆と膵 29 (6) 523 -527 2008年 [査読無し][通常論文]
  • 【肝内胆管癌 2008,up-to-date】 放射線化学および補助療法の進歩 肝内胆管癌に対する放射線療法の治療成績 (肝・胆・膵)
    吉田寛, 片寄友, 力山敏樹, 元井冬彦, 江川新一, 海野倫明 肝・胆・膵 57 (1) 143 -147 2008年 [査読無し][通常論文]
  • 【縫合・吻合手技 安全・確実な技術を習得するために】 肝胆膵 膵頭十二指腸切除術の再建 吻合法を中心に (消化器外科)
    江川新一, 元井冬彦, 乙供茂, 阿部永, 岡田恭穂, 力山敏樹, 片寄友, 海野倫明 消化器外科 31 (8) 1255 -1261 2008年 [査読無し][通常論文]
  • 【肝内胆管癌の病態特性からみた外科治療の適応と限界】 腫瘤形成型肝内胆管癌の手術適応 (消化器科)
    吉田寛, 片寄友, 力山敏樹, 元井冬彦, 有明恭平, 江川新一, 海野倫明 消化器科 47 (3) 284 -289 2008年 [査読無し][通常論文]
  • 【先天性胆道拡張症 その発生から長期予後まで】 成人の先天性胆道拡張症術後長期成績からみた肝内結石 (胆と膵)
    大塚英郎, 吉田寛, 元井冬彦, 片寄友, 力山敏樹, 江川新一, 海野倫明 胆と膵 29 (10) 921 -925 2008年 [査読無し][通常論文]
  • Tsuyoshi Sasaki, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shiraso, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Masaya Oikawa, Toru Onogawa, Masanori Suzuki, Choon-Taek Lee, Michiaki Unno SURGERY TODAY 37 (12) 1073 -1082 2007年12月 [査読無し][通常論文]
     
    Purpose. To evaluate the anti-tumor effects of a novel adenovirus expressing mutant p27(kip1) (Adp27-mt), which consists of a mutation of Thr-187/Pro-188 to Met-187/Ile-188. Methods. Using the human breast cancer cell lines, MDA-MB-231, ZR-75-1, and MCF-7, we tested Adp27-mt for cell cycle assay, growth inhibition assay, and TdT-mediated dUTP-biotin nick end labeling in a human breast cancer-grafted severe combined immunodeficiency (SCID) mouse model. Results. The mutant p27(kip1) induced stronger apoptosis in the breast cancer cell lines than adenovirus expressing wild-type p27(kip1) (Adp27-wt). Adp27-mt inhibits cell growth significantly; being about 5- and 3.5-fold stronger for IC50 than Adp27-wt in the breast cancer cell lines, MDA-MD-231 and ZR-75-1, respectively. In the human breast cancer-grafted SCID mouse model, Adp27-mt induced tumor regression and antitumor effects significantly better than Adp27-wt. Furthermore, Adp27-mt mainly caused G2/M arrest in the cell cycle progression, whereas Adp27-wt mediated a G1/S arrest 48 h after infection. Conclusions. The mutant p27(kip1) protein induced apoptosis, and inhibited cell growth more efficiently with stronger anti-tumor effects than wild-type p27(kip1). Thus, the recombinant adenovirus expressing mutant p27(kip1) could be useful in gene therapy against breast cancer.
  • Tsuyoshi Sasaki, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shiraso, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Masaya Oikawa, Toru Onogawa, Masanori Suzuki, Choon-Taek Lee, Michiaki Unno SURGERY TODAY 37 (12) 1073 -1082 2007年12月 [査読無し][通常論文]
     
    Purpose. To evaluate the anti-tumor effects of a novel adenovirus expressing mutant p27(kip1) (Adp27-mt), which consists of a mutation of Thr-187/Pro-188 to Met-187/Ile-188. Methods. Using the human breast cancer cell lines, MDA-MB-231, ZR-75-1, and MCF-7, we tested Adp27-mt for cell cycle assay, growth inhibition assay, and TdT-mediated dUTP-biotin nick end labeling in a human breast cancer-grafted severe combined immunodeficiency (SCID) mouse model. Results. The mutant p27(kip1) induced stronger apoptosis in the breast cancer cell lines than adenovirus expressing wild-type p27(kip1) (Adp27-wt). Adp27-mt inhibits cell growth significantly; being about 5- and 3.5-fold stronger for IC50 than Adp27-wt in the breast cancer cell lines, MDA-MD-231 and ZR-75-1, respectively. In the human breast cancer-grafted SCID mouse model, Adp27-mt induced tumor regression and antitumor effects significantly better than Adp27-wt. Furthermore, Adp27-mt mainly caused G2/M arrest in the cell cycle progression, whereas Adp27-wt mediated a G1/S arrest 48 h after infection. Conclusions. The mutant p27(kip1) protein induced apoptosis, and inhibited cell growth more efficiently with stronger anti-tumor effects than wild-type p27(kip1). Thus, the recombinant adenovirus expressing mutant p27(kip1) could be useful in gene therapy against breast cancer.
  • Tsuyoshi Sasaki, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shiraso, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Masaya Oikawa, Toru Onogawa, Masanori Suzuki, Choon-Taek Lee, Michiaki Unno SURGERY TODAY 37 (12) 1073 -1082 2007年12月 [査読無し][通常論文]
     
    Purpose. To evaluate the anti-tumor effects of a novel adenovirus expressing mutant p27(kip1) (Adp27-mt), which consists of a mutation of Thr-187/Pro-188 to Met-187/Ile-188. Methods. Using the human breast cancer cell lines, MDA-MB-231, ZR-75-1, and MCF-7, we tested Adp27-mt for cell cycle assay, growth inhibition assay, and TdT-mediated dUTP-biotin nick end labeling in a human breast cancer-grafted severe combined immunodeficiency (SCID) mouse model. Results. The mutant p27(kip1) induced stronger apoptosis in the breast cancer cell lines than adenovirus expressing wild-type p27(kip1) (Adp27-wt). Adp27-mt inhibits cell growth significantly; being about 5- and 3.5-fold stronger for IC50 than Adp27-wt in the breast cancer cell lines, MDA-MD-231 and ZR-75-1, respectively. In the human breast cancer-grafted SCID mouse model, Adp27-mt induced tumor regression and antitumor effects significantly better than Adp27-wt. Furthermore, Adp27-mt mainly caused G2/M arrest in the cell cycle progression, whereas Adp27-wt mediated a G1/S arrest 48 h after infection. Conclusions. The mutant p27(kip1) protein induced apoptosis, and inhibited cell growth more efficiently with stronger anti-tumor effects than wild-type p27(kip1). Thus, the recombinant adenovirus expressing mutant p27(kip1) could be useful in gene therapy against breast cancer.
  • Tsuyoshi Sasaki, Yu Katayose, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shiraso, Shinichi Yabuuchi, Akira Oda, Toshiki Rikiyama, Masaya Oikawa, Toru Onogawa, Masanori Suzuki, Choon-Taek Lee, Michiaki Unno SURGERY TODAY 37 (12) 1073 -1082 2007年12月 [査読無し][通常論文]
     
    Purpose. To evaluate the anti-tumor effects of a novel adenovirus expressing mutant p27(kip1) (Adp27-mt), which consists of a mutation of Thr-187/Pro-188 to Met-187/Ile-188. Methods. Using the human breast cancer cell lines, MDA-MB-231, ZR-75-1, and MCF-7, we tested Adp27-mt for cell cycle assay, growth inhibition assay, and TdT-mediated dUTP-biotin nick end labeling in a human breast cancer-grafted severe combined immunodeficiency (SCID) mouse model. Results. The mutant p27(kip1) induced stronger apoptosis in the breast cancer cell lines than adenovirus expressing wild-type p27(kip1) (Adp27-wt). Adp27-mt inhibits cell growth significantly; being about 5- and 3.5-fold stronger for IC50 than Adp27-wt in the breast cancer cell lines, MDA-MD-231 and ZR-75-1, respectively. In the human breast cancer-grafted SCID mouse model, Adp27-mt induced tumor regression and antitumor effects significantly better than Adp27-wt. Furthermore, Adp27-mt mainly caused G2/M arrest in the cell cycle progression, whereas Adp27-wt mediated a G1/S arrest 48 h after infection. Conclusions. The mutant p27(kip1) protein induced apoptosis, and inhibited cell growth more efficiently with stronger anti-tumor effects than wild-type p27(kip1). Thus, the recombinant adenovirus expressing mutant p27(kip1) could be useful in gene therapy against breast cancer.
  • Mitsuhisa Muto, Tohru Onogawa, Takashi Suzuki, Takanori Ishida, Toshiki Rikiyama, Yu Katayose, Noriaki Ohuchi, Hironobu Sasano, Takaaki Abe, Michiaki Unno CANCER SCIENCE 98 (10) 1570 -1576 2007年10月 [査読無し][通常論文]
     
    Human liver-specific organic anion transporter-2 (LST-2/OATP8/SLCO1B3) has been demonstrated to be expressed in various gastrointestinal carcinomas and also to play pivotal roles in the uptake of a wide variety of both endogenous and exogenous anionic compounds, including bile acids, conjugated steroids and hormones, into hepatocytes in the human liver. However, the biological significance of LST-2 in human carcinomas remains unknown. In the present study, we examined the expression of LST-2 in 102 cases of breast carcinoma using immunohistochemistry and correlated the findings with various clinicopathological parameters in order to examine the possible biological and clinical significance of LST-2. LST-2 immunoreactivity was detected in 51 cases (50.0%); of these 51 positive cases, LST-2 immunoreactivity was inversely correlated with tumor size (P = 0.0289). In addition, LST-2 immunoreactivity was significantly associated with a decreased risk of recurrence and improved prognosis by both univariate (P = 0.02 and P = 0.01) and multivariate (P = 0.03 and P = 0.01) analyses. In the estrogen receptor-positive groups, the LST-2-positive patients showed good prognoses. Considering that LST-2 transports estrone-3-sulfate, these results suggest that LST-2 overexpression is associated with a hormone-dependent growth mechanism of the breast cancer. The results of our present study demonstrate that LST-2 immunoreactivity is a potent prognostic factor in human breast cancer.
  • Mitsuhisa Muto, Tohru Onogawa, Takashi Suzuki, Takanori Ishida, Toshiki Rikiyama, Yu Katayose, Noriaki Ohuchi, Hironobu Sasano, Takaaki Abe, Michiaki Unno CANCER SCIENCE 98 (10) 1570 -1576 2007年10月 [査読無し][通常論文]
     
    Human liver-specific organic anion transporter-2 (LST-2/OATP8/SLCO1B3) has been demonstrated to be expressed in various gastrointestinal carcinomas and also to play pivotal roles in the uptake of a wide variety of both endogenous and exogenous anionic compounds, including bile acids, conjugated steroids and hormones, into hepatocytes in the human liver. However, the biological significance of LST-2 in human carcinomas remains unknown. In the present study, we examined the expression of LST-2 in 102 cases of breast carcinoma using immunohistochemistry and correlated the findings with various clinicopathological parameters in order to examine the possible biological and clinical significance of LST-2. LST-2 immunoreactivity was detected in 51 cases (50.0%); of these 51 positive cases, LST-2 immunoreactivity was inversely correlated with tumor size (P = 0.0289). In addition, LST-2 immunoreactivity was significantly associated with a decreased risk of recurrence and improved prognosis by both univariate (P = 0.02 and P = 0.01) and multivariate (P = 0.03 and P = 0.01) analyses. In the estrogen receptor-positive groups, the LST-2-positive patients showed good prognoses. Considering that LST-2 transports estrone-3-sulfate, these results suggest that LST-2 overexpression is associated with a hormone-dependent growth mechanism of the breast cancer. The results of our present study demonstrate that LST-2 immunoreactivity is a potent prognostic factor in human breast cancer.
  • Michiaki Unno, Tadayuki Okumoto, Yu Katayose, Toshiki Rikiyama, Akihiro Sato, Fuyuhiko Motoi, Masaya Oikawa, Shinichi Egawa, Tadashi Ishibashi JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY 14 (5) 434 -440 2007年09月 [査読無し][通常論文]
     
    Backgroun/Purpose: Hilar cholangiocarcinoma is the one of the most difficult carcinomas to diagnose because of the localization of the main tumor at the hepatic hilus, and because of the complex anatomy of the biliary, artery, and portal systems. To perform a curative operation, it is important to evaluate the extent of carcinoma and the resectability. Hilar cholangiocarcinoma often extends along the axis of the bile duct. Percutaneous transhepatic cholangiogaraphy (PTC) and/or endoscopic retrograde cholangiography (ERC) are usually performed to diagnose the extent of the hilar cholangiocarcinoma. However, computed tomography (CT) was thought not to be useful because its resolution is poor. Now that multidetector row CT (MDCT) and high-performance imaging systems are available, the diagnostic strategy for hilar cholangiocarcinoma has changed. Methods: In this study, we analyzed the preoperative diagnostic imaging of 24 consecutive patients whose hilar cholangiocarcinoma was confirmed by histopathological examination. All patients were submitted to 16-channel MDCT, except for those with an allergy to iodine contrast medium. The data obtained from MDCT were analyzed and checked by both radiologists and surgeons, using multiplanar reconstruction (MPR) images. Results: The accuracy of diagnosis of horizontal spreading was 80.9% and that of vertical spreading was 100%. However, the sensitivity for lymph node metastasis was insufficient. Based on the data from MDCT and other examinations, all patients underwent surgery. Curative operation was performed in 15 patients (62.5%). Conclusions: Our results indicate that 16-channel MDCT is reliable for the diagnosis of hilar cholangiocarcinoma, especially prior to bile duct drainage. Thus, it is important to perform MDCT when patients with obstructive jaundice are encountered.
  • Michiaki Unno, Tadayuki Okumoto, Yu Katayose, Toshiki Rikiyama, Akihiro Sato, Fuyuhiko Motoi, Masaya Oikawa, Shinichi Egawa, Tadashi Ishibashi JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY 14 (5) 434 -440 2007年09月 [査読無し][通常論文]
     
    Backgroun/Purpose: Hilar cholangiocarcinoma is the one of the most difficult carcinomas to diagnose because of the localization of the main tumor at the hepatic hilus, and because of the complex anatomy of the biliary, artery, and portal systems. To perform a curative operation, it is important to evaluate the extent of carcinoma and the resectability. Hilar cholangiocarcinoma often extends along the axis of the bile duct. Percutaneous transhepatic cholangiogaraphy (PTC) and/or endoscopic retrograde cholangiography (ERC) are usually performed to diagnose the extent of the hilar cholangiocarcinoma. However, computed tomography (CT) was thought not to be useful because its resolution is poor. Now that multidetector row CT (MDCT) and high-performance imaging systems are available, the diagnostic strategy for hilar cholangiocarcinoma has changed. Methods: In this study, we analyzed the preoperative diagnostic imaging of 24 consecutive patients whose hilar cholangiocarcinoma was confirmed by histopathological examination. All patients were submitted to 16-channel MDCT, except for those with an allergy to iodine contrast medium. The data obtained from MDCT were analyzed and checked by both radiologists and surgeons, using multiplanar reconstruction (MPR) images. Results: The accuracy of diagnosis of horizontal spreading was 80.9% and that of vertical spreading was 100%. However, the sensitivity for lymph node metastasis was insufficient. Based on the data from MDCT and other examinations, all patients underwent surgery. Curative operation was performed in 15 patients (62.5%). Conclusions: Our results indicate that 16-channel MDCT is reliable for the diagnosis of hilar cholangiocarcinoma, especially prior to bile duct drainage. Thus, it is important to perform MDCT when patients with obstructive jaundice are encountered.
  • 【クリティカルケアに必要な分子生物学の基礎知識】 侵襲に対する生体反応の制御因子 シグナル伝達 (Surgery Frontier)
    吉田寛, 片寄友, 力山敏樹, 小野川徹, 山本久仁治, 海野倫明 Surgery Frontier 14 (1) 27 -32 2007年 [査読無し][通常論文]
  • 佐藤龍一郎, 及川昌也, 片寄友, 力山敏樹, 山本久仁治, 林洋毅, 佐々木巖, 海野倫明 日本消化器外科学会雑誌 40 (4) 427 -32 2007年 [査読無し][通常論文]
  • 【知っておくべき胆嚢癌の診療方針】 診断 胆嚢癌の術前進展度診断法における最近の進歩 (外科)
    吉田寛, 片寄友, 力山敏樹, 朝倉徹, 菅野敦, 江川新一, 海野倫明 外科 69 (11) 1248 -1254 2007年 [査読無し][通常論文]
  • 【クリティカルケアに必要な分子生物学の基礎知識】 侵襲に対する生体反応の制御因子 シグナル伝達 (Surgery Frontier)
    吉田寛, 片寄友, 力山敏樹, 小野川徹, 山本久仁治, 海野倫明 Surgery Frontier 14 (1) 27 -32 2007年 [査読無し][通常論文]
  • 佐藤龍一郎, 及川昌也, 片寄友, 力山敏樹, 山本久仁治, 林洋毅, 佐々木巖, 海野倫明 日本消化器外科学会雑誌 40 (4) 427 -32 2007年 [査読無し][通常論文]
  • 【知っておくべき胆嚢癌の診療方針】 診断 胆嚢癌の術前進展度診断法における最近の進歩 (外科)
    吉田寛, 片寄友, 力山敏樹, 朝倉徹, 菅野敦, 江川新一, 海野倫明 外科 69 (11) 1248 -1254 2007年 [査読無し][通常論文]
  • H Ohtsuka, T Abe, T Onogawa, N Kondo, T Sato, H Oshio, H Mizutamari, T Mikkaichi, M Oikawa, T Rikiyama, Y Katayose, M Unno JOURNAL OF GASTROENTEROLOGY 41 (4) 369 -377 2006年04月 [査読無し][通常論文]
     
    Background. We isolated the human liver-specific organic anion transporter gene, LST-2 (OATP8/SLCO1B3), which is exclusively expressed in the basolateral membrane of the hepatocytes. In this study, we analyzed the transcriptional regulation of the LST-2 gene in hepatocyte-derived cells and the effect of bile acid. Methods. Transcriptional activity of the LST-2 gene was measured using a human LST-2 promoter-luciferase reporter plasmid under various concentrations of bile acids. Electrophoresis mobility shift assays of farnesoid X receptor (FXR), hepatocyte nuclear factor (HNF) 1 alpha, and HNF3 beta were performed. Results. Luciferase analysis showed that the 5'-flanking region from -180 to -20bp is responsible for LST-2 transcriptional activity. By site-directed mutation analysis, it was revealed that the consensus binding sites for FXR, HNF1 alpha, and HNF3 beta play important roles in the transcriptional activity of the LST-2 gene. By electrophoresis mobility shift assay, we observed specific protein-DNA complexes of FXR, HNF1 alpha, and HNF-3 beta. Luciferase activity was increased fivefold when chenodeoxycholate or deoxycholate were added. Northern blot analyses revealed that the expression of LST-2 was increased by addition of chenodeoxycholate or deoxycholate in a dose-dependent manner. Conclusions. This study demonstrated that the transcription of the LST-2 gene is regulated by three transcription factors, FXR, HNF1 alpha, and HNF3 beta. HNF1 alpha and HNF3 beta might contribute to its liver-specific expression, and FXR might play a role in its transcriptional activation by bile acids.
  • H Ohtsuka, T Abe, T Onogawa, N Kondo, T Sato, H Oshio, H Mizutamari, T Mikkaichi, M Oikawa, T Rikiyama, Y Katayose, M Unno JOURNAL OF GASTROENTEROLOGY 41 (4) 369 -377 2006年04月 [査読無し][通常論文]
     
    Background. We isolated the human liver-specific organic anion transporter gene, LST-2 (OATP8/SLCO1B3), which is exclusively expressed in the basolateral membrane of the hepatocytes. In this study, we analyzed the transcriptional regulation of the LST-2 gene in hepatocyte-derived cells and the effect of bile acid. Methods. Transcriptional activity of the LST-2 gene was measured using a human LST-2 promoter-luciferase reporter plasmid under various concentrations of bile acids. Electrophoresis mobility shift assays of farnesoid X receptor (FXR), hepatocyte nuclear factor (HNF) 1 alpha, and HNF3 beta were performed. Results. Luciferase analysis showed that the 5'-flanking region from -180 to -20bp is responsible for LST-2 transcriptional activity. By site-directed mutation analysis, it was revealed that the consensus binding sites for FXR, HNF1 alpha, and HNF3 beta play important roles in the transcriptional activity of the LST-2 gene. By electrophoresis mobility shift assay, we observed specific protein-DNA complexes of FXR, HNF1 alpha, and HNF-3 beta. Luciferase activity was increased fivefold when chenodeoxycholate or deoxycholate were added. Northern blot analyses revealed that the expression of LST-2 was increased by addition of chenodeoxycholate or deoxycholate in a dose-dependent manner. Conclusions. This study demonstrated that the transcription of the LST-2 gene is regulated by three transcription factors, FXR, HNF1 alpha, and HNF3 beta. HNF1 alpha and HNF3 beta might contribute to its liver-specific expression, and FXR might play a role in its transcriptional activation by bile acids.
  • [Indication and significance of hepatopancreatoduodenectomy for gallbladder carcinoma] (Nippon Rinsho)
    Rikiyama Toshiki, Hayashi Hiroki, Katayose Yu, Oikawa Masaya, Unno Michiaki Nippon Rinsho 64 Suppl 1 578 -582 2006年 [査読無し][通常論文]
  • [Multimodal therapy for unresectable upper and hilar bile duct carcinoma] (Nippon Rinsho)
    Katayose Yu, Oda Akira, Oikawa Masaya, Rikiyama Toshiki, Unno Michiaki Nippon Rinsho 64 Suppl 1 547 -550 2006年 [査読無し][通常論文]
  • [Diagnosis of invasion of tumor depth and surgical decision in gallbladder carcinoma] (Nippon Rinsho)
    Unno Michiaki, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Hayashi Hiroki Nippon Rinsho 64 Suppl 1 488 -492 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 特論 胆嚢癌における肝膵合併切除術の意義 (日本臨床)
    力山敏樹, 林洋毅, 片寄友, 及川昌也, 海野倫明 日本臨床 64 (増刊1) 578 -582 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 胆道癌の治療 進行・再発胆道癌の治療/集学的治療 切除不能進行胆管癌の集学的治療 (日本臨床)
    片寄友, 小田聡, 及川昌也, 力山敏樹, 海野倫明 日本臨床 64 (増刊1) 547 -550 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 胆道癌の治療 早期胆道癌の治療/胆嚢癌の外科療法 胆嚢癌の深達度診断と手術 (日本臨床)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅 日本臨床 64 (増刊1) 488 -492 2006年 [査読無し][通常論文]
  • 【胆管癌の診断と治療】 胆管癌に対する化学療法 (外科治療)
    片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 吉田寛, 林洋毅, 小田聡, 海野倫明 外科治療 94 (5) 809 -816 2006年 [査読無し][通常論文]
  • 【転移性肝癌の新たな治療戦略】 大腸癌肝転移に対する肝切除術式選択と術後補助化学療法の位置づけ (消化器科)
    山本久仁治, 片寄友, 力山敏樹, 及川昌也, 小野川徹, 林洋毅, 武藤満完, 海野倫明 消化器科 42 (6) 588 -594 2006年 [査読無し][通常論文]
  • 【粘液産生胆管腫瘍の新展開と問題点】 粘液産生胆管腫瘍外科切除例の検討 (胆と膵)
    小田聡, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 林洋毅, 海野倫明 胆と膵 27 (7) 487 -493 2006年 [査読無し][通常論文]
  • 【胆嚢癌をめぐる最近の話題】 視点 肝胆道癌の転移・浸潤と転写因子Snail (肝・胆・膵)
    深瀬耕二, 阿部高明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 元井冬彦, 江川新一, 海野倫明 肝・胆・膵 53 (2) 263 -270 2006年 [査読無し][通常論文]
  • 武藤満完, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 伊勢秀雄, 海野倫明 胆道 20 (4) 515 -521 2006年 [査読無し][通常論文]
  • 【肝門部の解剖を多角的に見る】 MDCT-cholangiographyから見た肝門部の門脈分岐変異と胆管解剖 (胆と膵)
    力山敏樹, 北見昌広, 片寄友, 及川昌也, 山本久仁治, 小野川徹, 吉田寛, 林洋毅, 海野倫明 胆と膵 27 (11) 827 -833 2006年 [査読無し][通常論文]
  • 【急性胆道炎の処置と手術 診療ガイドラインに基づく戦略】 急性胆管炎に対する緊急開腹ドレナージ (手術)
    海野倫明, 小野川徹, 山本久仁治, 吉田寛, 力山敏樹, 片寄友 手術 60 (12) 1855 -1860 2006年 [査読無し][通常論文]
  • [A case of an elderly patient having advanced hepatocellular carcinoma with tumor thrombus in the inferior vena cava treated with chemo-radio-therapy--intraarterial infusion of weekly high dose 5-FU (WHF)]
    Yabuuchi Shinichi, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Onogawa Toru, Hayashi Hiroki, Muto Mitsuhisa, Unno Michiaki Gan To Kagaku Ryoho 33 (12) 1768 -1770 2006年 [査読無し][通常論文]
  • 下大静脈腫瘍栓(Vv3)を伴う進行肝細胞癌に対して放射線・肝動注化学療法を施行しQOLが改善した1例
    薮内伸一, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 林洋毅, 武藤満完, 海野倫明 癌と化学療法 33 (12) 1768 -1770 2006年 [査読無し][通常論文]
  • [Indication and significance of hepatopancreatoduodenectomy for gallbladder carcinoma] (Nippon Rinsho)
    Rikiyama Toshiki, Hayashi Hiroki, Katayose Yu, Oikawa Masaya, Unno Michiaki Nippon Rinsho 64 Suppl 1 578 -582 2006年 [査読無し][通常論文]
  • [Multimodal therapy for unresectable upper and hilar bile duct carcinoma] (Nippon Rinsho)
    Katayose Yu, Oda Akira, Oikawa Masaya, Rikiyama Toshiki, Unno Michiaki Nippon Rinsho 64 Suppl 1 547 -550 2006年 [査読無し][通常論文]
  • [Diagnosis of invasion of tumor depth and surgical decision in gallbladder carcinoma] (Nippon Rinsho)
    Unno Michiaki, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Hayashi Hiroki Nippon Rinsho 64 Suppl 1 488 -492 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 特論 胆嚢癌における肝膵合併切除術の意義 (日本臨床)
    力山敏樹, 林洋毅, 片寄友, 及川昌也, 海野倫明 日本臨床 64 (増刊1) 578 -582 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 胆道癌の治療 進行・再発胆道癌の治療/集学的治療 切除不能進行胆管癌の集学的治療 (日本臨床)
    片寄友, 小田聡, 及川昌也, 力山敏樹, 海野倫明 日本臨床 64 (増刊1) 547 -550 2006年 [査読無し][通常論文]
  • 【膵癌・胆道癌の診断と治療 最新の研究動向】 胆道癌 胆道癌の治療 早期胆道癌の治療/胆嚢癌の外科療法 胆嚢癌の深達度診断と手術 (日本臨床)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅 日本臨床 64 (増刊1) 488 -492 2006年 [査読無し][通常論文]
  • 【胆管癌の診断と治療】 胆管癌に対する化学療法 (外科治療)
    片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 吉田寛, 林洋毅, 小田聡, 海野倫明 外科治療 94 (5) 809 -816 2006年 [査読無し][通常論文]
  • 【転移性肝癌の新たな治療戦略】 大腸癌肝転移に対する肝切除術式選択と術後補助化学療法の位置づけ (消化器科)
    山本久仁治, 片寄友, 力山敏樹, 及川昌也, 小野川徹, 林洋毅, 武藤満完, 海野倫明 消化器科 42 (6) 588 -594 2006年 [査読無し][通常論文]
  • 【粘液産生胆管腫瘍の新展開と問題点】 粘液産生胆管腫瘍外科切除例の検討 (胆と膵)
    小田聡, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 林洋毅, 海野倫明 胆と膵 27 (7) 487 -493 2006年 [査読無し][通常論文]
  • 【胆嚢癌をめぐる最近の話題】 視点 肝胆道癌の転移・浸潤と転写因子Snail (肝・胆・膵)
    深瀬耕二, 阿部高明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 元井冬彦, 江川新一, 海野倫明 肝・胆・膵 53 (2) 263 -270 2006年 [査読無し][通常論文]
  • 武藤満完, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 伊勢秀雄, 海野倫明 胆道 20 (4) 515 -521 2006年 [査読無し][通常論文]
  • 【肝門部の解剖を多角的に見る】 MDCT-cholangiographyから見た肝門部の門脈分岐変異と胆管解剖 (胆と膵)
    力山敏樹, 北見昌広, 片寄友, 及川昌也, 山本久仁治, 小野川徹, 吉田寛, 林洋毅, 海野倫明 胆と膵 27 (11) 827 -833 2006年 [査読無し][通常論文]
  • 【急性胆道炎の処置と手術 診療ガイドラインに基づく戦略】 急性胆管炎に対する緊急開腹ドレナージ (手術)
    海野倫明, 小野川徹, 山本久仁治, 吉田寛, 力山敏樹, 片寄友 手術 60 (12) 1855 -1860 2006年 [査読無し][通常論文]
  • [A case of an elderly patient having advanced hepatocellular carcinoma with tumor thrombus in the inferior vena cava treated with chemo-radio-therapy--intraarterial infusion of weekly high dose 5-FU (WHF)]
    Yabuuchi Shinichi, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Onogawa Toru, Hayashi Hiroki, Muto Mitsuhisa, Unno Michiaki Gan To Kagaku Ryoho 33 (12) 1768 -1770 2006年 [査読無し][通常論文]
  • 下大静脈腫瘍栓(Vv3)を伴う進行肝細胞癌に対して放射線・肝動注化学療法を施行しQOLが改善した1例
    薮内伸一, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 林洋毅, 武藤満完, 海野倫明 癌と化学療法 33 (12) 1768 -1770 2006年 [査読無し][通常論文]
  • 【どう使うマルチスライスCT(MDCT)】 胆道癌の描出と水平方向進展の診断 (胆と膵)
    力山敏樹, 海野倫明, 片寄友, 及川昌也, 山本久仁治, 小野川徹, 石橋忠司, 森谷卓也, 松野正紀 胆と膵 26 (臨増) 191 -197 2005年 [査読無し][通常論文]
  • 【肝切除術 成功の秘訣】 肝切除術後管理(術後肝不全対策を含めて) (消化器外科)
    及川昌也, 海野倫明, 片寄友, 力山敏樹, 山本久仁治, 小野川徹, 武藤満完, 松野正紀 消化器外科 28 (4) 459 -463 2005年 [査読無し][通常論文]
  • 【胆道疾患の臨床 最近の進歩】 胆道癌 胆嚢癌の手術と遠隔成績 (臨床消化器内科)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 臨床消化器内科 20 (7) 1025 -1030 2005年 [査読無し][通常論文]
  • 片寄友, 海野倫明, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 臨床外科 60 (6) 751 -756 2005年 [査読無し][通常論文]
  • 【再手術 予防・適応・手術手技】 術後胆管狭窄 (手術)
    山本久仁治, 片寄友, 力山敏樹, 及川昌也, 林洋毅, 海野倫明 手術 59 (10) 1507 -1511 2005年 [査読無し][通常論文]
  • 及川昌也, 片寄友, 力山敏樹, 山本久仁治, 林洋毅, 海野倫明 臨床外科 60 (11) 167 -172 2005年 [査読無し][通常論文]
  • [Low-dose cisplatin plus 5-fluorouracil with radiotherapy for unresectable upper and hilar bile duct carcinoma]
    Oda Akira, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Hayashi Hiroki, Unno Michiaki Gan To Kagaku Ryoho 32 (11) 1615 -1617 2005年 [査読無し][通常論文]
  • 大塩博, 片寄友, 力山敏樹, 及川昌也, 林洋毅, 小野川徹, 海野倫明 日本門脈圧亢進症学会雑誌 11 (2) 160 -165 2005年 [査読無し][通常論文]
  • 胆道ステント療法の意義 進行上部・肝門部胆管癌に対する集学的治療
    小田聡, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 海野倫明 癌と化学療法 32 (11) 1615 -1617 2005年 [査読無し][通常論文]
  • 【どう使うマルチスライスCT(MDCT)】 胆道癌の描出と水平方向進展の診断 (胆と膵)
    力山敏樹, 海野倫明, 片寄友, 及川昌也, 山本久仁治, 小野川徹, 石橋忠司, 森谷卓也, 松野正紀 胆と膵 26 (臨増) 191 -197 2005年 [査読無し][通常論文]
  • 【肝切除術 成功の秘訣】 肝切除術後管理(術後肝不全対策を含めて) (消化器外科)
    及川昌也, 海野倫明, 片寄友, 力山敏樹, 山本久仁治, 小野川徹, 武藤満完, 松野正紀 消化器外科 28 (4) 459 -463 2005年 [査読無し][通常論文]
  • 【胆道疾患の臨床 最近の進歩】 胆道癌 胆嚢癌の手術と遠隔成績 (臨床消化器内科)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 臨床消化器内科 20 (7) 1025 -1030 2005年 [査読無し][通常論文]
  • 片寄友, 海野倫明, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 臨床外科 60 (6) 751 -756 2005年 [査読無し][通常論文]
  • 【再手術 予防・適応・手術手技】 術後胆管狭窄 (手術)
    山本久仁治, 片寄友, 力山敏樹, 及川昌也, 林洋毅, 海野倫明 手術 59 (10) 1507 -1511 2005年 [査読無し][通常論文]
  • 及川昌也, 片寄友, 力山敏樹, 山本久仁治, 林洋毅, 海野倫明 臨床外科 60 (11) 167 -172 2005年 [査読無し][通常論文]
  • [Low-dose cisplatin plus 5-fluorouracil with radiotherapy for unresectable upper and hilar bile duct carcinoma]
    Oda Akira, Katayose Yu, Rikiyama Toshiki, Oikawa Masaya, Yamamoto Kuniharu, Hayashi Hiroki, Unno Michiaki Gan To Kagaku Ryoho 32 (11) 1615 -1617 2005年 [査読無し][通常論文]
  • 大塩博, 片寄友, 力山敏樹, 及川昌也, 林洋毅, 小野川徹, 海野倫明 日本門脈圧亢進症学会雑誌 11 (2) 160 -165 2005年 [査読無し][通常論文]
  • 胆道ステント療法の意義 進行上部・肝門部胆管癌に対する集学的治療
    小田聡, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 林洋毅, 海野倫明 癌と化学療法 32 (11) 1615 -1617 2005年 [査読無し][通常論文]
  • Hepatic resection through an anterior approach employing a modified liver hanging maneuver in patients with a massive liver tumor severely oppressing the inferior vena cava
    M Suzuki, M Unno, Y Katayose, H Takeuchi, T Rikiyama, T Onogawa, T Sato, M Mizuma, H Ohtuka, S Mastuno HEPATO-GASTROENTEROLOGY 51 (59) 1459 -1463 2004年09月 [査読無し][通常論文]
     
    For a large hepatic neoplasm existing in the right hepatic lobe, hepatic resection using an anterior approach is required. We have reported an operative procedure for hepatic transection using absorbable polyglycolic acid tape. In patients with suspected tumor invasion of the inferior vena cava, on the other hand, considering the range of the residual tumor while sparing the inferior vena cava as much as possible, combined resection and reconstruction of the inferior vena cava is conducted only if operative curativity is expected. We conducted hepatic transection while maintaining the blood flow of the residual liver by applying the liver hanging maneuver method of Belghiti et al. and polyglycolic acid tape in patients with giant liver tumors of the right hepatic lobe compressing the hepatic inferior vena cava. Strong angled dissecting forceps, were inserted into the, ventral side of the inferior vena cava from the caudal side, and the tip was induced between hepatic veins. Two strips of polyglycolic acid tape were pinched with forceps and strongly ligated on the right and left sides of the cutoff line. Subsequently, hepatic transection was conducted using electrocautery spray coagulation and CUSA without blocking the inflow blood of the residual liver, and the right hepatic lobe was extirpated. This procedure has already been performed in 5 patients suspected of inferior vena cava invasion, and the inferior vena cava was able to be preserved in all the patients.
  • Hepatic resection through an anterior approach employing a modified liver hanging maneuver in patients with a massive liver tumor severely oppressing the inferior vena cava
    M Suzuki, M Unno, Y Katayose, H Takeuchi, T Rikiyama, T Onogawa, T Sato, M Mizuma, H Ohtuka, S Mastuno HEPATO-GASTROENTEROLOGY 51 (59) 1459 -1463 2004年09月 [査読無し][通常論文]
     
    For a large hepatic neoplasm existing in the right hepatic lobe, hepatic resection using an anterior approach is required. We have reported an operative procedure for hepatic transection using absorbable polyglycolic acid tape. In patients with suspected tumor invasion of the inferior vena cava, on the other hand, considering the range of the residual tumor while sparing the inferior vena cava as much as possible, combined resection and reconstruction of the inferior vena cava is conducted only if operative curativity is expected. We conducted hepatic transection while maintaining the blood flow of the residual liver by applying the liver hanging maneuver method of Belghiti et al. and polyglycolic acid tape in patients with giant liver tumors of the right hepatic lobe compressing the hepatic inferior vena cava. Strong angled dissecting forceps, were inserted into the, ventral side of the inferior vena cava from the caudal side, and the tip was induced between hepatic veins. Two strips of polyglycolic acid tape were pinched with forceps and strongly ligated on the right and left sides of the cutoff line. Subsequently, hepatic transection was conducted using electrocautery spray coagulation and CUSA without blocking the inflow blood of the residual liver, and the right hepatic lobe was extirpated. This procedure has already been performed in 5 patients suspected of inferior vena cava invasion, and the inferior vena cava was able to be preserved in all the patients.
  • T Abe, M Unno, H Takeuchi, T Kakita, Y Katayose, T Rikiyama, T Morikawa, M Suzuki, S Matsuno JOURNAL OF GASTROINTESTINAL SURGERY 8 (5) 604 -615 2004年07月 [査読無し][通常論文]
     
    Ischemia-reperfusion injury causes oxidative stress producing reactive oxygen species, which is a serious problem linked to morbidity and mortality in liver surgery. We investigated the effects of edaravone, a new free radical scavenger, on liver oxidative stress in vitro and in vivo. We employed a hypoxia-reoxygenation model of primary cultured hepatocytes using an AnaeroPack (Mitsubishi Gas Chemical Co., Tokyo,japan). Hepatocytes were exposed to 3 or 4 hours of hypoxia and then returned to oxygenation. We analyzed the time course changes of aspartate aminotransferase (AST), phosphatidylcholine hydroperoxide (PCOOH), and adenosine triphosphate (ATP) content in hepatocytes of edaravone-treated groups or nontreated groups after reoxygenation. Edaravone significantly attenuated the elevation of the AST level of the medium and hepatocellular PCOOH and preserved the hepatocellular ATP level. In vivo, male Sprague-Dawley rats were subjected to 45 minutes of hepatic ischemia and 120 minutes of reperfusion. The rats were intravenously injected with vehicle or edaravone (3 mg/kg or 10 mg/kg) before reperfusion and 1 hour after reperfusion. Serum AST levels and hepatic PCOOH and energy charge were significantly improved in both edaravone groups compared with control. In conclusion, edaravone has the ability to eliminate intra-hepatocellular superoxide species and attenuate oxidative liver damage in liver surgery.
  • M Kim, M Sgagias, XY Deng, YJ Jung, T Rikiyama, K Lee, M Ouellette, K Cowan BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 320 (1) 138 -144 2004年07月 [査読無し][通常論文]
     
    The INK4A/ARF locus on chromosome 9 is a tumor suppressor gene frequently mutated in human cancers. In order to study the effects of p14ARF expression in tumor cells, we constructed a recombinant adenovirus containing p14ARF cDNA (Adp14(ARF)). Adp14(ARF) infection of U2OS osteosarcoma cells which has wild type p53 and mutant p14ARF revealed high levels of p14 (ARF) expression within 24 h. In addition, Adp14(ARF)-mediated expressing of p14 (ARF) was associated with increased levels of p53, p21, and mdm2 protein. Growth inhibition assays following Adp14(ARF) infection demonstrated that the growth of U2OS cells was inhibited relative to infection with control virus. Furthermore, TUNEL analysis as well as PARP cleavage assays demonstrated that Adp14(ARF) infection was associated with increased apoptosis in U2OS cell line and that it was associated with Adp14(ARF) induced overexpression of Fas and Fas-L. Addition of Fas-L neutralizing antibody NOK-1 decreased Adp14-mediated cell death, indicating that p14 (ARF) induction of the Fas pathway is associated with increased apoptosis. The finding that Adp14(ARF) infection did not induce Fas expression in U2OS/E6 and MCF/E6 cells suggests that wild type p53 expression may be necessary for Adp14(ARF)- mediated induction of Fas. The observation that overexpression of p53 by Adp53 infection in MCF-7 does not induce increased Fas protein levels nor apoptotic cell death suggests that p53 overexpression is required but not sufficient enough for apoptosis. These studies suggest there are other mechanisms other than induction of p53 in ARF-mediated apoptosis and gene therapy using Adp14(ARF) may be a promising treatment option for human cancers containing wild type p53 and mutant or deleted p 14 expression. (C) 2004 Elsevier Inc. All rights reserved.
  • T Abe, M Unno, H Takeuchi, T Kakita, Y Katayose, T Rikiyama, T Morikawa, M Suzuki, S Matsuno JOURNAL OF GASTROINTESTINAL SURGERY 8 (5) 604 -615 2004年07月 [査読無し][通常論文]
     
    Ischemia-reperfusion injury causes oxidative stress producing reactive oxygen species, which is a serious problem linked to morbidity and mortality in liver surgery. We investigated the effects of edaravone, a new free radical scavenger, on liver oxidative stress in vitro and in vivo. We employed a hypoxia-reoxygenation model of primary cultured hepatocytes using an AnaeroPack (Mitsubishi Gas Chemical Co., Tokyo,japan). Hepatocytes were exposed to 3 or 4 hours of hypoxia and then returned to oxygenation. We analyzed the time course changes of aspartate aminotransferase (AST), phosphatidylcholine hydroperoxide (PCOOH), and adenosine triphosphate (ATP) content in hepatocytes of edaravone-treated groups or nontreated groups after reoxygenation. Edaravone significantly attenuated the elevation of the AST level of the medium and hepatocellular PCOOH and preserved the hepatocellular ATP level. In vivo, male Sprague-Dawley rats were subjected to 45 minutes of hepatic ischemia and 120 minutes of reperfusion. The rats were intravenously injected with vehicle or edaravone (3 mg/kg or 10 mg/kg) before reperfusion and 1 hour after reperfusion. Serum AST levels and hepatic PCOOH and energy charge were significantly improved in both edaravone groups compared with control. In conclusion, edaravone has the ability to eliminate intra-hepatocellular superoxide species and attenuate oxidative liver damage in liver surgery.
  • M Kim, M Sgagias, XY Deng, YJ Jung, T Rikiyama, K Lee, M Ouellette, K Cowan BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 320 (1) 138 -144 2004年07月 [査読無し][通常論文]
     
    The INK4A/ARF locus on chromosome 9 is a tumor suppressor gene frequently mutated in human cancers. In order to study the effects of p14ARF expression in tumor cells, we constructed a recombinant adenovirus containing p14ARF cDNA (Adp14(ARF)). Adp14(ARF) infection of U2OS osteosarcoma cells which has wild type p53 and mutant p14ARF revealed high levels of p14 (ARF) expression within 24 h. In addition, Adp14(ARF)-mediated expressing of p14 (ARF) was associated with increased levels of p53, p21, and mdm2 protein. Growth inhibition assays following Adp14(ARF) infection demonstrated that the growth of U2OS cells was inhibited relative to infection with control virus. Furthermore, TUNEL analysis as well as PARP cleavage assays demonstrated that Adp14(ARF) infection was associated with increased apoptosis in U2OS cell line and that it was associated with Adp14(ARF) induced overexpression of Fas and Fas-L. Addition of Fas-L neutralizing antibody NOK-1 decreased Adp14-mediated cell death, indicating that p14 (ARF) induction of the Fas pathway is associated with increased apoptosis. The finding that Adp14(ARF) infection did not induce Fas expression in U2OS/E6 and MCF/E6 cells suggests that wild type p53 expression may be necessary for Adp14(ARF)- mediated induction of Fas. The observation that overexpression of p53 by Adp53 infection in MCF-7 does not induce increased Fas protein levels nor apoptotic cell death suggests that p53 overexpression is required but not sufficient enough for apoptosis. These studies suggest there are other mechanisms other than induction of p53 in ARF-mediated apoptosis and gene therapy using Adp14(ARF) may be a promising treatment option for human cancers containing wild type p53 and mutant or deleted p 14 expression. (C) 2004 Elsevier Inc. All rights reserved.
  • Sasaki, I, C Shibata, Y Funayama, K Fukushima, KI Takahashi, H Ogawa, T Ueno, A Hashimoto, M Nagao, K Watanabe, S Haneda, K Shiiba, T Rikiyama, H Naito DISEASES OF THE COLON & RECTUM 47 (6) 940 -943 2004年06月 [査読無し][通常論文]
     
    Although side-to-side isoperistaltic anastomosis is a useful strictureplasty technique when long segments of intestinal stenosis complicate Crohn's disease, concerns have been raised regarding disease recurrence adjacent to the anastomosis. We performed side-to-side isoperistaltic anastomosis without spatulated intestinal ends as a method of reconstruction after intestinal resection for Crohn's disease; both intestinal ends were transversely closed like a Heineke-Mikulicz-type strictureplasty. With this procedure, the luminal diameter proximal and distal to the anastomosis became wider than the original diameter of the intestine. This new procedure, which we refer to as the "modified side-to-side isoperistaltic anastomosis with double Heineke-Mikulicz procedure" could become an alternative operation after intestinal resection in persons with Crohn's disease, although long-term outcome analysis is necessary.
  • Sasaki, I, C Shibata, Y Funayama, K Fukushima, KI Takahashi, H Ogawa, T Ueno, A Hashimoto, M Nagao, K Watanabe, S Haneda, K Shiiba, T Rikiyama, H Naito DISEASES OF THE COLON & RECTUM 47 (6) 940 -943 2004年06月 [査読無し][通常論文]
     
    Although side-to-side isoperistaltic anastomosis is a useful strictureplasty technique when long segments of intestinal stenosis complicate Crohn's disease, concerns have been raised regarding disease recurrence adjacent to the anastomosis. We performed side-to-side isoperistaltic anastomosis without spatulated intestinal ends as a method of reconstruction after intestinal resection for Crohn's disease; both intestinal ends were transversely closed like a Heineke-Mikulicz-type strictureplasty. With this procedure, the luminal diameter proximal and distal to the anastomosis became wider than the original diameter of the intestine. This new procedure, which we refer to as the "modified side-to-side isoperistaltic anastomosis with double Heineke-Mikulicz procedure" could become an alternative operation after intestinal resection in persons with Crohn's disease, although long-term outcome analysis is necessary.
  • 片寄友, 海野倫明, 力山敏樹, 柿田徹也, 小野川徹, 白相悟, 水間正道, 大塚英郎, 佐藤武揚, 松野正紀 日本消化器外科学会雑誌 37 (3) 301 -306 2004年 [査読無し][通常論文]
  • 【はじめての消化器外科手術】 Hassab手術 (手術)
    力山敏樹, 海野倫明, 片寄友, 松野正紀 手術 58 (6) 1067 -1071 2004年 [査読無し][通常論文]
  • 画像上多隔壁胆嚢との鑑別が困難であった胆嚢腺筋症の1例
    武藤満完, 海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 胆と膵 25 (7) 455 -458 2004年 [査読無し][通常論文]
  • 【胆道疾患診療の新しい展開】 新しい検査法とその特徴 multidetector-row CT マルチスライスCTによる胆道癌診断 (肝・胆・膵)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 石橋忠司, 松野正紀 肝・胆・膵 49 (3) 309 -314 2004年 [査読無し][通常論文]
  • 深瀬耕二, 海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 水間正道, 松野正紀 Journal of Microwave Surgery 22 91 -94 2004年 [査読無し][通常論文]
  • 片寄友, 海野倫明, 力山敏樹, 柿田徹也, 小野川徹, 白相悟, 水間正道, 大塚英郎, 佐藤武揚, 松野正紀 日本消化器外科学会雑誌 37 (3) 301 -306 2004年 [査読無し][通常論文]
  • 【はじめての消化器外科手術】 Hassab手術 (手術)
    力山敏樹, 海野倫明, 片寄友, 松野正紀 手術 58 (6) 1067 -1071 2004年 [査読無し][通常論文]
  • 画像上多隔壁胆嚢との鑑別が困難であった胆嚢腺筋症の1例
    武藤満完, 海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 松野正紀 胆と膵 25 (7) 455 -458 2004年 [査読無し][通常論文]
  • 【胆道疾患診療の新しい展開】 新しい検査法とその特徴 multidetector-row CT マルチスライスCTによる胆道癌診断 (肝・胆・膵)
    海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 小野川徹, 石橋忠司, 松野正紀 肝・胆・膵 49 (3) 309 -314 2004年 [査読無し][通常論文]
  • 深瀬耕二, 海野倫明, 片寄友, 力山敏樹, 及川昌也, 山本久仁治, 水間正道, 松野正紀 Journal of Microwave Surgery 22 91 -94 2004年 [査読無し][通常論文]
  • T Rikiyama, J Curtis, M Oikawa, DB Zimonjic, N Popescu, BA Murphy, MA Wilson, AC Johnson BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION 1629 (1-3) 15 -25 2003年10月 [査読無し][通常論文]
     
    GC-binding factor 2 (GCF2) is a transcriptional repressor that decreases activity of the epidermal growth factor receptor (EGFR) and other genes. We have mapped the gene for GCF2 by fluorescence in situ hybridization (FISH) to chromosome 2q37. Sequence analysis of the GCF2 gene and cDNA showed that the gene consists of eight exons and introns and spans 73 kbp of DNA. Northern blot analysis showed that GCF2 mRNA was differentially expressed in many human tissues and cell lines. GCF2 mRNA was expressed as a 4.2 kb mRNA in most human tissues with the highest expression level in peripheral blood leukocytes and lowest expression in brain and testis. Additional transcripts of 6.6, 2.9 and 2.4 kb were found in some tissues but the only transcript detected in cancer cell lines was 4.2 kb with high levels found in seven Burkitts' lymphoma cell lines. Western blot analysis showed that GCF2 protein is present at high levels in Burkitts' lymphoma and several other cancer cell lines. GCF2 was found in both nuclear and cytoplasmic compartments in cells. Deletion mutants of GCF2 revealed that amino acids 429-528 are required for both DNA binding and repression of the EGFR promoter. Furthermore, GCF2 was able to substantially decrease activator protein 2 (AP2) enhancement of the EGFR promoter. Thus, GCF2 is a transcriptional repressor overexpressed in cancer cell lines with a role in regulating expression of the EGFR. Published by Elsevier B.V.
  • T Rikiyama, J Curtis, M Oikawa, DB Zimonjic, N Popescu, BA Murphy, MA Wilson, AC Johnson BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION 1629 (1-3) 15 -25 2003年10月 [査読無し][通常論文]
     
    GC-binding factor 2 (GCF2) is a transcriptional repressor that decreases activity of the epidermal growth factor receptor (EGFR) and other genes. We have mapped the gene for GCF2 by fluorescence in situ hybridization (FISH) to chromosome 2q37. Sequence analysis of the GCF2 gene and cDNA showed that the gene consists of eight exons and introns and spans 73 kbp of DNA. Northern blot analysis showed that GCF2 mRNA was differentially expressed in many human tissues and cell lines. GCF2 mRNA was expressed as a 4.2 kb mRNA in most human tissues with the highest expression level in peripheral blood leukocytes and lowest expression in brain and testis. Additional transcripts of 6.6, 2.9 and 2.4 kb were found in some tissues but the only transcript detected in cancer cell lines was 4.2 kb with high levels found in seven Burkitts' lymphoma cell lines. Western blot analysis showed that GCF2 protein is present at high levels in Burkitts' lymphoma and several other cancer cell lines. GCF2 was found in both nuclear and cytoplasmic compartments in cells. Deletion mutants of GCF2 revealed that amino acids 429-528 are required for both DNA binding and repression of the EGFR promoter. Furthermore, GCF2 was able to substantially decrease activator protein 2 (AP2) enhancement of the EGFR promoter. Thus, GCF2 is a transcriptional repressor overexpressed in cancer cell lines with a role in regulating expression of the EGFR. Published by Elsevier B.V.
  • Analysis of the epidermal growth factor receptor promoter: The effect of nuclear factor-kappa B
    H Nishi, G Neta, KH Nishi, LM Akers, T Rikiyama, KN Proctor, BA Murphy, AC Johnson INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 11 (1) 49 -55 2003年01月 [査読無し][通常論文]
     
    The epidermal growth factor receptor gene is highly regulated and responsive to extracellular stimuli that control cell growth. We have identified five putative nuclear factor-kappaB (NF-kappaB) binding sites within the epidermal growth factor receptor (EGFR) promoter region by sequence analysis. We have analyzed the potential role of NF-kappaB family members in the regulation of the EGFR transcription. Electrophoretic mobility shift analysis demonstrated that the p50 and p49, subunit proteins of the NF-kappaB, bound to the EGFR promoter at four out of five of these sites. However, it was found that NF-kappaB could not transactivate the EGFR by cotransfection experiments with each NF-kappaB subunit, using p50, p65 and c-Rel and an EGFR promoter luciferase reporter. Treatment of cells with tumor necrosis factor (TNF)-alpha, which could degrade the I-kappaB and then result in translocation of NF-kappaB to nucleus, did not enhance EGFR promoter reporter gene transcription. Also, TNF-alpha did not induce EGFR expression at the protein level. These results indicate that even though purified NF-kappaB can bind to the putative sites, there is no evidence that NF-kappaB transactivates the EGFR promoter region.
  • 消化器外科手術アトラス 総胆管結石症に対する腹腔鏡下胆管切開術 (消化器外科)
    徳村弘実, 鹿郷昌之, 原田伸彦, 豊島隆, 力山敏樹, 山本久仁治 消化器外科 26 (2) 131 -141 2003年 [査読無し][通常論文]
  • 術前MDCTのMPR画像で直接膵浸潤が確認された中・下部胆管癌の1切除例
    大塩博, 鈴木正徳, 海野倫明, 片寄友, 力山敏樹, 竹内丙午, 柿田徹也, 小野川徹, 水間正道, 白相悟, 松野正紀 胆と膵 24 (6) 465 -469 2003年 [査読無し][通常論文]
  • 【消化器疾患に対するinterventional radiology(IVR)】 胆道 切除不能肝門部胆管癌に対するexpandable metallic biliary stenting(EMBS)治療の工夫 (外科)
    柿田徹也, 海野倫明, 片寄友, 力山敏樹, 松野正紀 外科 65 (10) 1177 -1182 2003年 [査読無し][通常論文]
  • 【肝病態生理研究のあゆみ】 ヒト肝細胞におけるLiver-Specific Organic Anion Transporter LST-2の転写調節機構 (薬理と治療)
    大塚英郎, 海野倫明, 片寄友, 力山敏樹, 小野川徹, 佐藤武揚, 大塩博, 松野正紀, 阿部高明 薬理と治療 31 (Suppl.1) S89-S93 2003年 [査読無し][通常論文]
  • Analysis of the epidermal growth factor receptor promoter: The effect of nuclear factor-kappa B
    H Nishi, G Neta, KH Nishi, LM Akers, T Rikiyama, KN Proctor, BA Murphy, AC Johnson INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 11 (1) 49 -55 2003年01月 [査読無し][通常論文]
     
    The epidermal growth factor receptor gene is highly regulated and responsive to extracellular stimuli that control cell growth. We have identified five putative nuclear factor-kappaB (NF-kappaB) binding sites within the epidermal growth factor receptor (EGFR) promoter region by sequence analysis. We have analyzed the potential role of NF-kappaB family members in the regulation of the EGFR transcription. Electrophoretic mobility shift analysis demonstrated that the p50 and p49, subunit proteins of the NF-kappaB, bound to the EGFR promoter at four out of five of these sites. However, it was found that NF-kappaB could not transactivate the EGFR by cotransfection experiments with each NF-kappaB subunit, using p50, p65 and c-Rel and an EGFR promoter luciferase reporter. Treatment of cells with tumor necrosis factor (TNF)-alpha, which could degrade the I-kappaB and then result in translocation of NF-kappaB to nucleus, did not enhance EGFR promoter reporter gene transcription. Also, TNF-alpha did not induce EGFR expression at the protein level. These results indicate that even though purified NF-kappaB can bind to the putative sites, there is no evidence that NF-kappaB transactivates the EGFR promoter region.
  • 消化器外科手術アトラス 総胆管結石症に対する腹腔鏡下胆管切開術 (消化器外科)
    徳村弘実, 鹿郷昌之, 原田伸彦, 豊島隆, 力山敏樹, 山本久仁治 消化器外科 26 (2) 131 -141 2003年 [査読無し][通常論文]
  • 術前MDCTのMPR画像で直接膵浸潤が確認された中・下部胆管癌の1切除例
    大塩博, 鈴木正徳, 海野倫明, 片寄友, 力山敏樹, 竹内丙午, 柿田徹也, 小野川徹, 水間正道, 白相悟, 松野正紀 胆と膵 24 (6) 465 -469 2003年 [査読無し][通常論文]
  • 【消化器疾患に対するinterventional radiology(IVR)】 胆道 切除不能肝門部胆管癌に対するexpandable metallic biliary stenting(EMBS)治療の工夫 (外科)
    柿田徹也, 海野倫明, 片寄友, 力山敏樹, 松野正紀 外科 65 (10) 1177 -1182 2003年 [査読無し][通常論文]
  • 【肝病態生理研究のあゆみ】 ヒト肝細胞におけるLiver-Specific Organic Anion Transporter LST-2の転写調節機構 (薬理と治療)
    大塚英郎, 海野倫明, 片寄友, 力山敏樹, 小野川徹, 佐藤武揚, 大塩博, 松野正紀, 阿部高明 薬理と治療 31 (Suppl.1) S89-S93 2003年 [査読無し][通常論文]
  • [S4 S5 subsegmentectomy of the liver for gallbladder carcinoma]
    Unno Michiaki, Suzuki Masanori, Katayose Yu, Takeuchi Heigo, Rikiyama Toshiki, Matsuno Seiki Nippon Geka Gakkai Zasshi 103 (8) 543 -548 2002年 [査読無し][通常論文]
  • Deng Xiyun, Kim Min, Vandier Didier, Jung Yun-jin, Rikiyama Toshiki, Sgagias Magda K, Goldsmith Merrill, Cowan Kenneth H Biochem Biophys Res Commun 296 (4) 792 -798 2002年 [査読無し][通常論文]
  • [Laparoscopic biliary surgery] (Nippon Geka Gakkai Zasshi)
    Tokumura Hiromi, Rikiyama Toshiki, Harada Nobuhiko, Kakyo Masayuki, Yamamoto Kuniharu Nippon Geka Gakkai Zasshi 103 (10) 737 -741 2002年 [査読無し][通常論文]
  • [S4 S5 subsegmentectomy of the liver for gallbladder carcinoma]
    Unno Michiaki, Suzuki Masanori, Katayose Yu, Takeuchi Heigo, Rikiyama Toshiki, Matsuno Seiki Nippon Geka Gakkai Zasshi 103 (8) 543 -548 2002年 [査読無し][通常論文]
  • Deng Xiyun, Kim Min, Vandier Didier, Jung Yun-jin, Rikiyama Toshiki, Sgagias Magda K, Goldsmith Merrill, Cowan Kenneth H Biochem Biophys Res Commun 296 (4) 792 -798 2002年 [査読無し][通常論文]
  • [Laparoscopic biliary surgery] (Nippon Geka Gakkai Zasshi)
    Tokumura Hiromi, Rikiyama Toshiki, Harada Nobuhiko, Kakyo Masayuki, Yamamoto Kuniharu Nippon Geka Gakkai Zasshi 103 (10) 737 -741 2002年 [査読無し][通常論文]

委員歴

  • 2010年 - 2010年   日本肝胆膵外科学会   評議員   日本肝胆膵外科学会
  • 2007年 - 2008年   日本肝胆膵外科学会   評議員   日本肝胆膵外科学会
  • 2006年 - 2007年   日本肝胆膵外科学会   評議員   日本肝胆膵外科学会


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