Researchers Database

NAITO Itaru

    Graduate School of Medical Sciences Department of Gastroenterology and Metabolism Professor
Contact: inaitomed.nagoya-cu.ac.jp
Last Updated :2025/07/02

Researcher Information

J-Global ID

Research Interests

  • IgG4関連硬化性胆管炎   IgG4関連疾患   胆管狭窄   胆管ステント   硬化症胆管炎   自己免疫膵炎   

Research Areas

  • Life sciences / Gastroenterology

Academic & Professional Experience

  • 2023/04 - Today  名古屋市立大学医学部附属みどり市民病院消化器内科教授
  • 2022/10 - 2023/03  名古屋市立大学大学院医学研究科消化器・代謝内科学講師
  • 2019/04 - 2022/09  Nagoya City UniversityGraduate School of Medical Sciences講師
  • 2015/09 - 2019/03  Nagoya City UniversityGraduate School of Medical Sciences講師
  • 2013/04 - 2015/08  Nagoya City UniversityGraduate School of Medical Sciences病院講師
  • 2011/04 - 2013/03  Nagoya City UniversityGraduate School of Medical Sciences助教
  • 2010/04 - 2011/03  Nagoya City UniversityGraduate School of Medical Sciences助教
  • 2007/07 - 2010/03  Nagoya City UniversityGraduate School of Medical Sciences臨床研究医
  • 2001/07 - 2007/06  岐阜県立多治見病院消化器科
  • 1998/04 - 2001/06  共立湖西総合病院内科
  • 1997/04 - 1998/03  Nagoya City University第一内科研修医

Education

  • 1991/04 - 1997/03  Nagoya City University  医学部

Association Memberships

  • THE JAPANESE SOCIETY OF INTERNAL MEDICINE   The Japanese Society of Gastroenterology   JAPAN GASTROENTEROLOGICAL ENDOSCOPY SOCIETY   JAPAN BILIARY ASSOCIATION   JAPAN PANCREAS SOCIETY   The Japan Society of Hepatology   

Published Papers

MISC

Awards & Honors

  • 2024 DEN Best Reviewers Award 2023
  • 2023 DEN Best Reviewers Award 2022
  • 2012 IDEN Best Poster Award
  • 2004 JDDW2004 Best Poster Award

Research Grants & Projects

  • 日本学術振興会:科学研究費助成事業
    Date (from‐to) : 2025/04 -2028/03 
    Author : 内藤 格
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2017/04 -2020/03 
    Author : Yoshida Michihiro
     
    Peritoneal dissemination and malignant ascites in pancreatic ductal adenocarcinoma (PDAC) patients represent a major clinical issue. Lysophosphatidic acid (LPA) is a lipid mediator that modulates the progression of various cancers. Based on the increasing evidence showing that LPA is abundant in malignant ascites, we focused on autotaxin (ATX), which is a secreted enzyme that is important for the production of LPA. This study aimed to elucidate the importance of the ATX-LPA axis in malignant ascites in PDAC and to determine whether ATX works as a molecular target for treating peritoneal dissemination. Many findings obtained through this study demonstrated that ATX in ascites works as a promotor of peritoneal dissemination, and the targeting of ATX must represent a useful and novel therapy for peritoneal dissemination of PDAC.
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2017/04 -2020/03 
    Author : 内藤 格; 吉田 道弘; 加藤 晃久
     
    近年では膵癌に対して複数の化学療法が施行可能になってきているため、化学療法における効果予測因子の確立は急務である。特にゲムシタビン(Gem)療法とナノ化パクリタキセル(nab-PTX)療法の併用療法であるGnP療法が1次治療の化学療法のひとつとなってきているが、GnP療法の効果予測因子は明らかとなっていない。 我々は、GnP療法が施行された膵癌75例の超音波内視鏡下生検(EUS-FNA)病理組織検体を用いてclassⅢβ-tubulin(TUBB3)染色を施行し、TUBB3の発現とGnP療法の治療効果や無増悪生存期間(PFS)との関連性につき検討を行った。この検討にて、病勢制御率(DCR)は、TUBB3陰性群において有意に高値であり、無増悪生存期間(PFS)もTUBB3陰性群において有意に延長し、PFSにおける多変量解析においても、TUBB3発現(hazard ratio, 2.41; p=0.026)が独立した関連因子であることを明らかにした。 この結果により、TUBB3発現がGnP療法の効果予測因子になり得る可能性が示唆されたが、TUBB3発現がGnP療法以外の化学療法の効果予測因子である可能性や膵癌の予後不良因子である可能性もあるため、GnP以外の化学療法におけるTUBB3発現と化学療法の治療効果(PFS、DCR)や予後(OS)との関連性を検討する必要があると考えた。 現在、膵癌に対する1次治療として用いられているオキサリプラチン、イリノテカン塩酸塩、フルオロウラシル、レボホリナートカルシウム併用療法(FOLFIRINOX療法)が施行された膵癌のEUS-FNA病理組織検体も用いてTUBB3染色を施行し、TUBB3発現が膵癌の一般的な化学療法の効果予測因子や、膵癌の予後不良因子ではなく、GnP療法の効果予測因子であることを明らかにしたいと考えている。
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2016/04 -2020/03 
    Author : Miyabe Katsuyuki
     
    We investigated drug resistance mechanism for Fiber Growth Factor Receptor (FGFR) inhibitors on cholangiocarcinoma. In an in-vitro study, we generated a cell line which possessed drug resistance against FGFR inhibitors using a KMCH cell stain harboring the fibroblast growth factor receptor (FGFR) amplifications. Additionally, we are analyzing what mechanisms are associated with drug resistance for FGFR inhibitors using the cell line. In an in-vivo study, Copy Number Variation (CNV) analysis was performed using patients-derived xenografts (PDX) administered FGFR inhibitors (Ponatinib or BGJ398) and possessed drug resistance against the inhibitors. Compared with control PDXs, the drug-resistance PDX had some specific gene aberrations. Furthermore, a total of 22 gene aberrations were detected by the comparison between the PDX and a real human tissue sample administered Ponatinib. We are further investigating the role of detected genes by exome sequence using the PDX samples.
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2014/04 -2018/03 
    Author : NAITOH Itaru
     
    We evaluated the efficacy of fluorescence in situ hybridization (FISH) using transpapillary forceps biopsy specimens in the diagnosis of cholangiocarcinoma (CCA). We evaluated the copy number gains (> 2 copies) of CEP 3, 7, and 17 in patients with CCA and IgG4-related sclerosing cholangitis (IgG4-SC). The complementary use of FISH analysis using transpapillary forceps biopsy specimens improves the diagnostic yield for CCA in the differential diagnosis from IgG4-SC. Furthermore, a CEP 7 copy number gain may be a biomarker of poor prognosis in CCA patients.
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2011/04 -2015/03 
    Author : NAKAZAWA takahiro; OHARA Hirotaka; INAGAKI Hiroshi; HAYSHI Kaduki; NAITOH Itaru
     
    We analyzed the immunoglobulin V heavy chain (VH) gene rearrangement and somatic hypermutation of lymphoid cells infiltrating in AIP (n=3), using obstructive pancreatitis (n=3) as non-autoimmune control. DNA was extracted from the affected inflammatory lesions. After PCR amplification of rearranged VH genes, the clones were subcloned. 100 recombinant clones were randomly picked-up in each case and sequenced. Monoclonal VH rearrangement was not detected in any cases examined. As compared with obstructive pancreatitis, there was no VH family or VH fragment specific to AIP. However, rates of unmutated VH fragments in AIP (25%) were higher than that in obstructive pancreatitis (5.1%) (P=0.0039). Conclusions: Some autoantibodies encoded by germline or less mutated VH genes may fail to be eliminated, and could play a role in the development of AIP.
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)
    Date (from‐to) : 2011 -2012 
    Author : NAITOH Itaru
     
    Our aim was to clarify which of these biopsy specimens and counting method could be a useful tool for supporting the diagnosis of autoimmune pancreatitis(AIP). We retrospectively evaluated biopsy specimens from pancreas, stomach, duodenum, duodenal papilla, colon, liver, bile duct, and minor salivary gland in 36 patients with AIP. The positive IgG4 immunostaining of the duodenal papilla in one high-power field (HPF) showed the highest sensitivity (52%) and accuracy (73%) among the 8 sites. It also showed the highest sensitivity among 4 different counting methods (IgG4 immunostaining in one HPF and 3 HPFs, both IgG4 immunostaining and IgG/IgG4 ratio in one HPF and 3 HPFs), but there were no significant differences with respect to specificity and accuracy. IgG4 immunostaining of swollen duodenal papilla with more than 10 IgG4-positive plasma cells in at least one HPF is useful for supporting the diagnosis of AIP.
  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2010 -2012 
    Author : OHARA Hirotaka; NAKAZAWA Takahiro; ANDOH Tomoaki; HAYASHI Kazuki; NAITOH Itaru; KANEMATSU Takayoshi
     
    Several inflammatory cytokines induced expression of MAdCAM-1 on the vascular endothelial cells of pancreas and increased permeability of endothelium. It was suggested that infiltration of lymphocytes were inhibited by IL-10 because IL-10 inhibited expression of MAdCAM-1. In cerulean-induced pancreatitis model of mice, IL-10-inducing drugs were considered effective against pancreatitis because the increasing of body weight and serum amylase levels of mice ware inhibited by glatiramer acetate which induced expression of IL-10. Consequently, progression of IL-10-inducing drugs are contributable for the therapy of pancreatitis.


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