ITOU Tetsuya

写真a

Affiliation

School of Medicine, Department of Surgery, Surgical Oncology and Science

Job title

Assistant Professor
To the head of this page.▲

Affiliation 【 display / non-display 】

  • Sapporo Medical University   医学部消化器・総合、乳腺・内分泌外科   助教  

To the head of this page.▲
 

Papers 【 display / non-display 】

  • Clinical feasibility of laparoscopic lateral pelvic lymph node dissection following total mesorectal excision for advanced rectal cancer

    Tomohisa Furuhata, Kenji Okita, Toshihiko Nishidate, Tatsuya Ito, Hiroshi Yamaguchi, Tomomi Ueki, Emi Akizuki, Makoto Meguro, Tadashi Ogawa, Kazuharu Kukita, Yasutoshi Kimura, Toru Mizuguchi, Koichi Hirata

    SURGERY TODAY ( SPRINGER )  45 ( 3 ) 310 - 314  2015.03  [Refereed]

    　View Summary

    Purpose To evaluate the technical feasibility, safety and oncological outcomes of laparoscopic lateral pelvic lymph node dissection in patients with advanced low rectal cancer. Methods Laparoscopic lateral pelvic lymph node dissection was performed in 18 patients from November 2009 to September 2012. The data regarding the patient demographics, surgical outcomes and short-term oncological outcomes were analyzed. Results In all 18 patients, the procedures were completed without conversion to open surgery. The mean length of the operation was 603.7 min (473-746 min). The mean number of harvested lateral pelvic lymph nodes was 16.9 (7-27), and five patients (27.8 %) had lymph node metastases. The postoperative mortality and morbidity rates were 0 and 16.7 %, respectively. Three patients developed Grade 2 urinary retention. No local recurrence had developed after a mean follow-up period of 23.6 months. Conclusion Laparoscopic lateral pelvic lymph node dissection is technically feasible, safe and oncologically acceptable within the limitations of the short-term follow-up period.

    DOI PubMed

  • Targeting tight junctions during epithelial to mesenchymal transition in human pancreatic cancer.

    Daisuke Kyuno, Hiroshi Yamaguchi, Tatsuya Ito, Tsuyoshi Kono, Yasutoshi Kimura, Masafumi Imamura, Takumi Konno, Koichi Hirata, Norimasa Sawada, Takashi Kojima

    World journal of gastroenterology ( 31 )  20 ( 31 ) 10813 - 24  2014.08  [Refereed]  [International journal]

    　View Summary

    Pancreatic cancer continues to be a leading cause of cancer-related death worldwide and there is an urgent need to develop novel diagnostic and therapeutic strategies to reduce the mortality of patients with this disease. In pancreatic cancer, some tight junction proteins, including claudins, are abnormally regulated and therefore are promising molecular targets for diagnosis, prognosis and therapy. Claudin-4 and -18 are overexpressed in human pancreatic cancer and its precursor lesions. Claudin-4 is a high affinity receptor of Clostridium perfringens enterotoxin (CPE). The cytotoxic effects of CPE and monoclonal antibodies against claudin-4 are useful as novel therapeutic tools for pancreatic cancer. Claudin-18 could be a putative marker and therapeutic target with prognostic implications for patients with pancreatic cancer. Claudin-1, -7, tricellulin and marvelD3 are involved in epithelial to mesenchymal transition (EMT) of pancreatic cancer cells and thus might be useful as biomarkers during disease. Protein kinase C is closely related to EMT of pancreatic cancer and regulates tight junctions of normal human pancreatic duct epithelial cells and the cancer cells. This review focuses on the regulation of tight junctions via protein kinase C during EMT in human pancreatic cancer for the purpose of developing new diagnostic and therapeutic modalities for pancreatic cancer.

    DOI PubMed

  • Tight junctions in human pancreatic duct epithelial cells.

    Takashi Kojima, Hiroshi Yamaguchi, Tatsuya Ito, Daisuke Kyuno, Tsuyoshi Kono, Takumi Konno, Norimasa Sawada

    Tissue barriers ( 4 )  1 ( 4 ) e24894  2013.10  [Refereed]  [International journal]

    　View Summary

    Tight junctions of the pancreatic duct are essential regulators of physiologic secretion of the pancreas and disruption of the pancreatic ductal barrier is known to contribute to the pathogenesis of pancreatitis and progression of pancreatic cancer. Various inflammatory mediators and carcinogens can trigger tight junction disassembly and disruption of the pancreatic barrier, however signaling events that mediates such barrier dysfunctions remain poorly understood. This review focuses on structure and regulation of tight junctions in normal pancreatic epithelial cells and mechanisms of junctional disruption during pancreatic inflammation and cancer. We will pay special attention to a novel model of human telomerase reverse transcriptase-transfected human pancreatic ductal epithelial cells and will describe the roles of major signaling molecules such as protein kinase C and c-Jun N-terminal kinase in formation and disassembly of the pancreatic ductal barrier.

    DOI PubMed

  • Protein kinase Cα inhibitor protects against downregulation of claudin-1 during epithelial-mesenchymal transition of pancreatic cancer.

    Daisuke Kyuno, Takashi Kojima, Hiroshi Yamaguchi, Tatsuya Ito, Yasutoshi Kimura, Masafumi Imamura, Akira Takasawa, Masaki Murata, Satoshi Tanaka, Koichi Hirata, Norimasa Sawada

    Carcinogenesis ( 6 )  34 ( 6 ) 1232 - 43  2013.06  [Refereed]  [International journal]

    　View Summary

    Protein kinase Cα (PKCα) is highly expressed in pancreatic cancer. However, the effects of PKCα on Snail and claudin-1, which play crucial roles in epithelial cell polarity during epithelial-mesenchymal transition (EMT), remain unclear. In this study, we investigated the mechanisms of regulation of Snail and claudin-1 via a PKCα signal pathway during EMT in pancreatic cancer cells and in normal human pancreatic duct epithelial cells (HPDEs). By immunostaining, overexpression of PKCα and downregulation of claudin-1 were observed in poorly differentiated human pancreatic cancer tissues and the pancreatic cancer cell line PANC-1. Treatment with the PKCα inhibitor Gö6976 transcriptionally decreased Snail and increased claudin-1 in PANC-1 cells. The PKCα inhibitor prevented upregulation of Snail and downregulation of claudin-1 during EMT induced by transforming growth factor-β1 (TGF-β1) treatment and under hypoxia in PANC-1 cells. The effects of the PKCα inhibitor were in part regulated via an extracellular signal-regulated kinase (ERK) signaling pathway. The PKCα inhibitor also prevented downregulation of the barrier function and fence function during EMT in well-differentiated pancreatic cancer cell line HPAC. In normal HPDEs, the PKCα inhibitor transcriptionally induced not only claudin-1 but also claudin-4, -7 and occludin without a change of Snail. Treatment with the PKCα inhibitor in normal HPDEs prevented downregulation of claudin-1 and occludin by TGF-β1 treatment and enhanced upregulation of claudin-1, -4, -7 and occludin under hypoxia. These findings suggest that PKCα regulates claudin-1 via Snail- and mitogen-activated protein kinase/ERK-dependent pathways during EMT in pancreatic cancer. Thus, PKCα inhibitors may be potential therapeutic agents against the malignancy of human pancreatic cancer cells.

    DOI PubMed

  • [Case report; a case of ileus due to ileal stenosis caused by oral intake of calcium polystyrene sulfonate].

    Kato S, Ono Y, Takagi T, Yoshida J, Hirakawa M, Ito T, Nakanishi K, Ogino J, Hasegawa T

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine ( 1 )  102   150 - 152  2013.01  [Refereed]

    PubMed

display all >>

To the head of this page.▲

Misc 【 display / non-display 】

display all >>

To the head of this page.▲