Shuichi Kaneko

Kanazawa Medical University, Kanazawa, Ishikawa, Japan

Are you Shuichi Kaneko?

Claim your profile

Publications (519)2337.82 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The prevention of relapse and infection complications during remission maintenance therapy is required to improve the prognosis of patients with microscopic polyangiitis (MPA) showing rapidly progressive glomerulonephritis (RPGN). The clinicopathological characteristics of patients with ANCA-positive MPA were examined to determine the risk factors for relapse or infectious complications after remission induction therapy. Patients and methods: The study population consisted of 52 patients diagnosed as ANCA-positive MPA showing RPGN from 2002 to 2012, after publication of the Japanese guideline for RPGN. The clinicopathological findings were examined between the presence and absence of relapse or infectious complications. Results: The value of vasculitis damage index (VDI) was high for the relapse group and VDI value was identified as the leading factor associated with relapse [hazard ratio (HR) 3.36, 95 % confidence interval (CI) 1.58-7.12, P < 0.01]. On the other hand, the values of Birmingham Vasculitis Activity Score, clinical grade category of RPGN at diagnosis, and VDI at remission were high in the infectious group. Furthermore, clinical grade category of RPGN was the leading factor associated with infectious complications (HR 5.30, 95 % CI 1.41-19.9, P = 0.01). Conclusion: The disease activity at diagnosis and severity of organ damage at remission were associated with relapse and infectious complications during remission maintenance therapy and infectious complication affected kidney survival and all-cause mortality in patients with ANCA-positive MPA exhibiting RPGN.
    Clinical and Experimental Nephrology 11/2015; DOI:10.1007/s10157-015-1199-7 · 2.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Renal coloboma syndrome (RCS) is characterized by renal anomalies and optic nerve colobomas. PAX2 mutations contribute to RCS. However, approximately half of the patients with RCS have no mutation in PAX2 gene. Methods: To investigate the incidence and effects of mutations of PAX2 and 25 candidate genes, patient genes were screened using next-generation sequence analysis, and candidate mutations were confirmed using Sanger sequencing. The correlation between mutations and clinical manifestation was evaluated. Result: Thirty patients, including 26 patients (two families of five and two, 19 sporadic cases) with RCS, and 4 optic nerve coloboma only control cases were evaluated in the present study. Six PAX2 mutations in 21 probands [28%; two in family cohorts (n = 5 and n = 2) and in 4 out of 19 patients with sporadic disease] including four novel mutations were confirmed using Sanger sequencing. Moreover, four other sequence variants (CHD7, SALL4, KIF26B, and SIX4) were also confirmed, including a potentially pathogenic novel KIF26B mutation. Kidney function and proteinuria were more severe in patients with PAX2 mutations than in those without the mutation. Moreover, the coloboma score was significantly higher in patients with PAX2 gene mutations. Three out of five patients with PAX2 mutations had focal segmental glomerulosclerosis (FSGS) diagnosed from kidney biopsies. Conclusion: The results of this study identify several new mutations of PAX2, and sequence variants in four additional genes, including a novel potentially pathogenic mutation in KIF26B, which may play a role in the pathogenesis of RCS.
    PLoS ONE 11/2015; 10(11):e0142843. DOI:10.1371/journal.pone.0142843 · 3.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Here, we report a fluorescent probe based on a macrocyclic peptide scaffold that specifically stains EpCAM-expressing MCF7 cells. The 14-mer macrocyclic peptide binding to the extracellular domain of EpCAM with a dissociation constant in the low nM range (1.7 nM) was discovered using the random non-standard peptide-integrated discovery system. Notably, this probe containing a fluorescence tag is less than 3000 Da in total and able to visualize nearly every live cell under high cell-density conditions, which was not achieved by the conventional mAb staining method. This suggests that the molecular probe based on the compact macrocyclic scaffold has great potentials as an imaging tool for the EpCAM biomarker as well as a delivery vehicle for drug conjugates.
    Journal of Molecular Evolution 11/2015; DOI:10.1007/s00239-015-9710-z · 1.68 Impact Factor
  • Source
    Kaori Kuroda · Yumie Takeshita · Shuichi Kaneko · Toshinari Takamura ·
    [Show abstract] [Hide abstract]
    ABSTRACT: A bent cannula tip and agglutination (arrow) in a 6-mm-long Quick-set® cannula.
    Journal of Diabetes Investigstion 11/2015; 6(6):739-40. DOI:10.1111/jdi.12357 · 1.83 Impact Factor

  • [Show abstract] [Hide abstract]
    ABSTRACT: Significant associations of HLA-DP alleles with chronic hepatitis B (CHB) infection are evident in Asian and Arabian populations, including Japanese, Han Chinese, Korean, and Saudi Arabian populations. Here, significant associations between CHB infection and five DPB1 alleles (two susceptibility alleles, DPB1(*) 05:01 and (*) 09:01, and three protective alleles, DPB1(*) 02:01, (*) 04:01, and (*) 04:02) were confirmed in a population comprising of 2582 Japanese individuals. Furthermore, odds ratios for CHB were higher for those with both DPB1 susceptibility alleles than for those with only one susceptibility allele; therefore, effects of susceptibility alleles were additive for risk of CHB infection. Similarly, protective alleles showed an additive effect on protection from CHB infection. Moreover, heterozygotes of any protective allele showed stronger association with CHB than did homozygotes, suggesting that heterozygotes may bind a greater variety of hepatitis B-derived peptides, and thus present these peptides more efficiently to T-cell receptors than homozygotes. Notably, compound heterozygote of the protective allele (any one of DPB1*02:01, *04:01, and *04:02) and the susceptible allele DPB1*05:01 was significantly associated with protection against CHB infection, which indicates that one protective HLA-DPB1 molecule can provide dominant protection. Identification of the HLA-DPB1 genotypes associated with susceptibility to and protection from CHB infection is essential for future analysis of the mechanisms responsible for immune recognition of hepatitis B virus antigens by HLA-DPB1 molecules.
    Tissue Antigens 10/2015; DOI:10.1111/tan.12684 · 2.14 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: In the current American Joint Committee on Cancer/International Union Against Cancer staging system (seventh edition) for intrahepatic cholangiocarcinoma (ICC), tumor size was excluded, and periductal invasion was added as a new tumor classification-defining factor. The objective of the current report was to propose a new staging system for ICC that would be better for stratifying the survival of patients based on data from the nationwide Liver Cancer Study Group of Japan database. Methods: Of 756 patients who underwent surgical resection for ICC between 2000 and 2005, multivariate analyses of the clinicopathologic factors of 419 patients who had complete data sets were performed to elucidate relevant factors for inclusion in a new tumor classification and staging system. Results: Overall survival data were best stratified using a cutoff value of 2 cm using a minimal P value approach to discriminate patient survival. The 5-year survival rate of 15 patients who had ICC measuring ≤2 cm in greatest dimension without lymph node metastasis or vascular invasion was 100%, and this cohort was defined as T1. Multivariate analysis of prognostic factors for 267 patients with lymph node-negative and metastasis-negative (N0M0) disease indicated that the number of tumors, the presence arterial invasion, and the presence major biliary invasion were independent and significant prognostic factors. The proposed new system, which included tumor number, tumor size, arterial invasion, and major biliary invasion for tumor classification, provided good stratification of overall patient survival according to disease stage. Macroscopic periductal invasion was associated with major biliary invasion and an inferior prognosis. Conclusions: The proposed new staging system, which includes a tumor cutoff size of 2 cm and major biliary invasion, may be useful for assigning patients to surgery. Cancer 2015. © 2015 American Cancer Society.
    Cancer 10/2015; DOI:10.1002/cncr.29686 · 4.89 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Although sorafenib is a standard drug for advanced hepatocellular carcinoma (HCC), little is known about a patient's clinical course after treatment. We investigated the effect of post-progression survival (PPS) and progression-free survival (PFS) on overall survival (OS) in patients whose advanced HCC was treated by sorafenib. Methods: We searched in the PubMed database for reports with survival data of patients with HCC treated with sorafenib monotherapy, and selected reports with ≥ 20 patients each that provided data for both OS and PFS or time to progression (TTP). Median PPS (mPPS) was defined as the period obtained by subtracting median PFS or TTP (mPFS/TTP) from median OS (mOS). We identified 56 reports with 5803 patients. We investigated the correlation of mOS and either mPPS or mPFS/TTP using weighted linear regression. Results: Median PPS correlated with mOS (r = 0.834) very strongly, whereas mPFS/TTP did not correlate with mOS as highly as PPS did (r = 0.546). When we stratified survival data by Child-Pugh classification, a significantly greater average percentage of mPPS to mOS was seen in Child-Pugh class A (54.4 ± 17.6 %) than in Child-Pugh class B (32.0 ± 11.6 %) (P = 0.015). Conclusions: PPS highly correlated with OS, and its importance should be more emphasized for advanced HCC patients treated after sorafenib therapy, whereas we need to take more care in interpreting the results of PFS to evaluate treatment efficacy in clinical trial of advanced HCC. This article is protected by copyright. All rights reserved.
    Hepatology Research 10/2015; DOI:10.1111/hepr.12601 · 2.74 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Various sleep abnormalities, such as delayed sleep onset, frequent awakening and daytime sleepiness, deteriorate the quality of life in patients with chronic kidney disease (CKD), including those on haemodialysis (HD). Although there are some candidate causative molecules in the central nervous system, the contribution of peripheral blood cells (PBCs) remains unclear. In this study, we performed polysomnographic analysis in CKD patients and used PBCs to examine the expression of genes related to sleep and wakefulness states. Methods: Polysomnographic analysis was performed in 9 CKD patients and 6 controls. Genes related to sleep and wakefulness were evaluated by RNA microarray in 19 subjects, including CKD patients and control subjects. Results: Polysomnographic analysis revealed that the duration of the rapid eye movement (REM)/non-REM phases during total sleep time was different between CKD patients and healthy controls. In mRNA microarray evaluation, hierarchical clustering analysis showed different patterns of sleep-related gene expression in HD patients. mRNA expression levels of GABA receptor (GABBR2), noradrenaline receptor (ADRA1A), dopamine receptor (DRD1) and histamine receptor (HRH1) showed an inverse correlation with renal function. Moreover, the mRNA expression of orexin and its receptor (HCRTR1 and HCRTR2) was also inversely correlated with renal function. Conclusion: These data indicate that the expression of sleep-related genes in PBCs of CKD patients may be associated with sleep abnormalities.
    Clinical and Experimental Nephrology 09/2015; DOI:10.1007/s10157-015-1150-y · 2.02 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Some observational studies have shown the relationships between hyperuricemia and chronic kidney disease (CKD); however, the threshold of serum uric acid (SUA) for deterioration of kidney function and the association between SUA and kidney injury by baseline kidney function remains unclear. This study aimed to clarify the relationships between SUA and reduced kidney function. Methods: We analyzed a historical cohort of male Japanese individuals who underwent medical checkup between 1998 and 2007. Participants with baseline data and who were followed up for at least one year were included and stratified according to baseline kidney function. Kidney function was classified as normal [estimated glomerular filtration rate (eGFR) ≥ 90 ml/min/1.73 m2] or mildly reduced (eGFR 60-89 ml/min/1.73 m2). The outcome measured was kidney impairment defined as a decrease in eGFR to < 60 ml/min/1.73 m2. Associations between SUA and risk for outcome and eGFR slopes were assessed. Results: A total of 41632 subjects with mean age 45.4 years were included. During a mean follow-up of four years, 3186 (7.6%) subjects developed kidney dysfunction. Subjects with SUA ≥ 6.0 mg/dL had a significantly increased risk for kidney impairment compared with subjects with SUA of 4-4.9 mg/dL. SUA threshold levels were different according to baseline kidney function; SUA ≥ 7.0 and ≥ 6.0 mg/dL for normal and mildly reduced kidney function, respectively. Approximately the same trends were observed for eGFR slopes. Conclusion: In the general population, hyperuricemia appears to be a risk factor for kidney impairment in males. For participants with mild kidney dysfunction, even a slight elevation of SUA can be a risk factor.
    PLoS ONE 09/2015; 10(9):e0137449. DOI:10.1371/journal.pone.0137449 · 3.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Multidrug resistance-associated protein 3 (MRP3) is a carrier-type transport protein belonging to the ABC transporters. In this study, we investigated the safety and immunogenicity of a MRP3-derived peptide (MRP3765) as a vaccine and characterized the MRP3-specific T cell responses induced. Twelve hepatocellular carcinoma (HCC) patients treated with hepatic arterial infusion chemotherapy (HAIC) were enrolled. The MRP3-derived peptide was emulsified in incomplete Freund's adjuvant and administered via subcutaneous immunization three times weekly. No serious adverse drug reactions to the peptide vaccine were observed, and the vaccination was well tolerated. The vaccination induced MRP3-specific immunity in 72.7% of the patients. In a phenotypic analysis, the largest post-vaccinated increase in MRP3-specific T cells was due to an increase in cells with the effector memory phenotype. Among the 12 patients, one patient showed a partial response, nine showed a stable disease, and two showed a progressive disease. The median overall survival time was 14.0 months. In conclusion, the safety, effects of immune boosting, and possible prolongation of overall survival by the MRP3-derived peptide demonstrate the potential of the peptide to provide clinical benefit in HCC patients. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Cancer letters 09/2015; 369(1). DOI:10.1016/j.canlet.2015.08.020 · 5.62 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A 60-year-old male with end-stage kidney disease due to autosomal polycystic kidney disease began maintenance hemodialysis in 2005. A brain CT scan showed dilatation of left vertebral artery, basilar artery, bilateral post cerebral artery, and middle cerebral artery. At the time, he was diagnosed as vertebrobasilar dolichoectasia. He was once admitted to our hospital for ischemic stroke. After discharge, he was treated with anticoagulant agent from 2010 to 2012 without any new stroke events. In March, 2012, he was admitted to our hospital for an evaluation of diplopia and left hemiplegia. Brain MRI showed acute ischemia of bilateral pons and right temporal lobe. He was once recovered with urokinase and argatroban, but 3 months after admission, he died with sudden hypotension and impaired consciousness. Autopsy revealed that subarachnoid hemorrhage due to the rupture of basilar artery aneurysm was responsible for this event.
    08/2015; DOI:10.1007/s13730-015-0190-1
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims/IntroductionTo investigate the clinical and anthropometrical parameters that are associated with non-exercise activity thermogenesis (NEAT) that is composed with basal energy expenditure (BEE) and diet-induced thermogenesis (DIT) in patients with diabetes.Materials and Methods Body composition was assessed using bioelectrical impedance, and BEE and DIT were measured using indirect calorimetry in 40 Japanese patients with diabetes.ResultsBEE correlated positively with bodyweight, BMI, fat mass, and fat-free mass and correlated negatively with age in both males and females. In multivariate logistic regression analysis, BEE correlated positively with both fat mass and fat-free mass independently of gender and age. In addition, DIT correlated positively with body weight, BMI, fat mass, and fat-free mass and correlated negatively with age in females, but not males. Fat-free mass contributed to DIT at least partly, and an aging-related decrease in DIT was observed. The best anthropometric parameter that reflected fat mass and fat-free mass was hip circumference (HC) and calf circumference (CC), respectively, in both males and females. Indeed, both HC (males, β=0.600, p<0.001; females, β=0.752, p<0.001) and CC (males, β=0.810, p=0.012; females, β=0.821, p=0.002) were correlated with BEE independently of age and gender. In addition, CC (β=0.653, p=0.009) but not HC was correlated with DIT significantly only in females, independently of age.ConclusionsHC reflects fat mass and was positively associated with BEE but not with DIT. In contrast, CC reflects fat-free mass and was positively associated with BEE in both males and females and with DIT in females.This article is protected by copyright. All rights reserved.
    08/2015; DOI:10.1111/jdi.12421
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We determined the feasibility of substituting sitagliptin or mitiglinide for bolus insulin injection therapy in patients with type 2 diabetes. 60 patients with type 2 diabetes were enrolled and randomized to switch from mealtime dosing of a rapid-acting insulin analog to either sitagliptin or mitiglinide for 16 weeks. Body weight, body mass index, and waist circumference decreased significantly in both groups at the end of the study. Mitiglinide significantly increased fasting plasma glucose (FPG) levels at the end of the study from 146.5±36.3 to 168.0±38.8 mg/dL, whereas sitagliptin did not affect FPG. Glycated hemoglobin (HbA1c) and 1,5-anhydroglucitol increased significantly in both groups. The C peptide immunoreactivity (CPR) responses after arginine were diminished in both groups. γ-GTP and triglycerides increased, and high-density lipoprotein cholesterol and adiponectin decreased, in the sitagliptin group, but not in the mitiglinide group. Mean Diabetes Treatment Satisfaction Questionnaire scores improved significantly in both groups. Patients whose mean total daily doses of rapid-acting insulin analog were 16.6 and 17.8 units were switched to sitagliptin and mitiglinide, respectively, without a change in the HbA1c level. Total insulin doses/body weight predicted changes in HbA1c only in the sitagliptin group, but not in the mitiglinide group. Use of >0.27 IU/kg of a rapid-acting insulin analog predicted an increase in HbA1c after switching to sitagliptin. The CPR index (CPI) was also a predictor for a change in HbA1c in the sitagliptin group, but not in the mitiglinide group; patients with a CPI<1.4 developed a worse HbA1c after switching to sitagliptin. Sitagliptin may predominantly act on FPG, whereas mitiglinide may act on postprandial plasma glucose to achieve glycemic control after switching from a bolus insulin regimen. Additional therapy to sitagliptin or mitiglinide is clearly required to obtain equivalent glycemic control in patients using a higher dose of insulin. (UMIN 000007051).
    08/2015; 3(1):e000122. DOI:10.1136/bmjdrc-2015-000122
  • [Show abstract] [Hide abstract]
    ABSTRACT: This paper studies the dynamics of the hepatitis B virus (HBV) model and the therapy regimens of HBV disease. First, we propose a new mathematical model of HBV with drug resistance, and then analyze its qualitative and dynamical properties. Combining the clinical data and theoretical analysis, we demonstrate that our model is biologically plausible and also computationally viable. Second, we demonstrate that the intermittent antiviral therapy regimen is one of the possible strategies to treat this kind of complex disease. There are two main advantages of this regimen, i.e. it not only may delay the development of drug resistance, but also may reduce the duration of on-treatment time compared with the long-term continuous medication. Moreover, such an intermittent antiviral therapy can reduce the adverse side effects. Our theoretical model and computational results provide qualitative insight into the progression of HBV, and also a possible new therapy for HBV disease.
    International Journal of Bifurcation and Chaos 06/2015; 25(07):1540011. DOI:10.1142/S0218127415400118 · 1.08 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Differentially regulated microRNAs (miRNAs) are associated with hepatic fibrosis, but their potential usefulness for blocking hepatic fibrosis has not been fully exploited. We examined the expression of miRNAs in the liver of a transgenic mouse model in which platelet-derived growth factor C (PDGF-C) is overexpressed (Pdgf-c Tg), resulting in hepatic fibrosis and steatosis and the eventual development of hepatocellular carcinoma (HCC). Robust induction of miR-214 correlated with fibrogenesis in the liver of Pdgf-c Tg, Atherogenic high fat diet induced NASH mouse, patients with chronic hepatitis B and chronic hepatitis C. Pdgf-c Tg mice were injected with LNA-antimiR-214 via the tail vein using Invivofectamine® 2.0. and the degree of hepatic fibrosis and tumor incidence were evaluated. Pdgf-c Tg mice treated with LNA-antimiR-214 showed a marked reduction in fibrosis, and tumor incidence compared with saline- or LNA-miR-control-injected control mice. In vitro, LNA-antimiR-214 significantly ameliorated the TGF-β1-induced pro-fibrotic gene expression in Lx-2 cells. MiR-214 targets a negative regulator of EGFR signaling, Mig-6. Mimic-miR-214 decreased the expression of Mig-6 and increased the levels of EGF-mediated p-EGFR (Y1173 and Y845) and p-Met (Tyr1234/1235) in Huh-7 cells. Conversely, LNA-antimiR-214 repressed these genes expression. In conclusions, miR-214 appears to participate in the development of hepatic fibrosis by modulating EGFR and TGF-β signaling pathways. LNA-anti-miR-214 may be a potentially therapy in the prevention of hepatic fibrosis.
    Cancer Science 06/2015; DOI:10.1111/cas.12730 · 3.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hepatocellular carcinoma is composed of a subset of cells with enhanced tumorigenicity and chemoresistance that are called cancer stem (or stem-like) cells. We explored the role of chromodomain-helicase-DNA-binding protein 4, which is encoded by the CHD4 gene and is known to epigenetically control gene regulation and DNA damage responses in EpCAM(+) liver cancer stem cells. Gene and protein expression profiles were determined by microarray and immunohistochemistry in 245 and 144 hepatocellular carcinoma patients, respectively. The relationship between gene/protein expression and prognosis was examined. The functional role of chromodomain-helicase-DNA-binding protein 4 was evaluated in primary hepatocellular carcinoma cells and in cell lines in vitro and in vivo. Chromodomain helicase DNA-binding protein 4 was abundantly expressed in EpCAM(+) hepatocellular carcinoma with expression of hepatic stem cell markers and poor prognosis in two independent cohorts. In cell lines, CHD4 knockdown increased chemosensitivity and CHD4 overexpression induced epirubicin chemoresistance. To inhibit the functions of chromodomain-helicase-DNA-binding protein 4 that are mediated through histone deacetylase and poly (ADP-ribose) polymerase, we evaluated the effect of the histone deacetylase inhibitor suberohydroxamic acid and the poly (ADP-ribose) polymerase inhibitor AG-014699. Treatment with either suberohydroxamic acid or AG-014699 reduced the number of EpCAM(+) liver cancer stem cells in vitro, and suberohydroxamic acid and AG-014699 in combination successfully inhibited tumor growth in a mouse xenograft model. Chromodomain-helicase-DNA-binding protein 4 plays a pivotal role in chemoresistance and the maintenance of stemness in liver cancer stem cells and is therefore a good target for the eradication of hepatocellular carcinoma. Copyright © 2015. Published by Elsevier B.V.
    Journal of Hepatology 06/2015; DOI:10.1016/j.jhep.2015.06.009 · 11.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A 43-year-old woman who had received anticoagulant therapy for atrial fibrillation for 2 years was admitted to our hospital with hematemesis. Endoscopy revealed a huge submucosal hematoma in the antrum of the stomach. Repeat endoscopy on day 6 showed that the submucosal hematoma had developed into a giant ulcer. Gastric mucosal biopsy and general examination confirmed a diagnosis of AL amyloidosis due to multiple myeloma. Although patients with cardiac involvement of AL amyloidosis often require anticoagulant therapy, gastrointestinal bleeding may occur. Therefore, the potential benefits of anticoagulation must be carefully weighed against the risk of hemorrhage.
    Nippon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology 06/2015; 112(6):1023-9. DOI:10.11405/nisshoshi.112.1023
  • [Show abstract] [Hide abstract]
    ABSTRACT: Human telomerase reverse transcriptase (hTERT) is a catalytic enzyme required for telomere elongation. In this study, we investigated the safety and immunogenicity of an hTERT-derived peptide (hTERT461) as a vaccine and characterized the hTERT-specific T cell responses induced. Fourteen hepatocellular carcinoma (HCC) patients were enrolled in the study. The hTERT-derived peptide was emulsified in incomplete Freund's adjuvant and administered via subcutaneous immunization three times biweekly. The maximum toxicity observed was grade 2 according to the common terminology criteria and mainly consisted of skin reactions at the site of vaccination. The vaccination induced hTERT-specific immunity in 71.4% patients and 57.1% patients administered hTERT461 peptide-specific T cells could prevent HCC recurrence after vaccination. In phenotypic analysis, the post-vaccinated increase in hTERT-specific T cells was due to an increase in cells with the effector memory phenotype, with the potential to produce multiple cytokines. Seven hTERT-specific T cell receptors were obtained from the vaccinated patients, showing their cytotoxic activities to hTERT-derived peptide-bearing cells. In conclusion, the safety and effects of immune boosting by hTERT461 peptide have shown the potential of the peptide to provide clinical benefits in HCC patients. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Cancer letters 05/2015; 364(2). DOI:10.1016/j.canlet.2015.04.031 · 5.62 Impact Factor
  • Shinji Kitajima · Shuichi Kaneko · Takashi Wada ·

    Therapeutic apheresis and dialysis: official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy 05/2015; DOI:10.1111/1744-9987.12309 · 1.71 Impact Factor

Publication Stats

10k Citations
2,337.82 Total Impact Points


  • 1997-2015
    • Kanazawa Medical University
      • • Department of Gastroenterology
      • • Department of Physiology
      • • Department of Internal Medicine (III)
      Kanazawa, Ishikawa, Japan
  • 1987-2015
    • Kanazawa University
      • • Department of Gastroenterology
      • • Department of Disease Control and Homeostasis
      • • Department of Internal Medicine
      • • Department of Laboratory Medicine
      • • School of Medicine
      • • Division of Immunology and Molecular Biology
      Kanazawa, Ishikawa, Japan
  • 2002-2006
    • The University of Tokyo
      • School of Medicine
      Tōkyō, Japan
  • 1994
    • Nippon Kayaku Co., Ltd.
      Edo, Tōkyō, Japan
  • 1989
    • National Institute of Allergy and Infectious Diseases
      • Laboratory of Immunoregulation
      베서스다, Maryland, United States