M Mori

Osaka University, Suika, Ōsaka, Japan

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Publications (808)2636.3 Total impact


  • No preview · Article · Dec 2015
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    ABSTRACT: Background: [(18) F]fluorodeoxyglucose (FDG)-PET has been used to evaluate the response of primary tumours to neoadjuvant therapy for oesophageal cancer. The clinical significance of the number of PET-positive nodes before and after therapy has not been investigated previously. Methods: [(18) F]FDG-PET was performed before and 2-3 weeks after completion of neoadjuvant chemotherapy to identify the number of PET-positive nodes, and these numbers were assessed in relation to metabolic changes in the primary tumour. Results: Of 302 patients in total, 90 had no PET-positive nodes, 83 had one, 59 had two and 70 patients had three or more positive nodes before therapy. After treatment, the numbers were: none in 207 patients, one in 59, two in 20 and three or more in 16 patients. The number of PET-positive nodes after treatment was influenced by both the number of PET-positive nodes before therapy and the response to preoperative therapy, and correlated with the number of metastatic lymph nodes. Overall survival was longer in patients who had no PET-positive nodes after treatment than in those who had one or more. Multivariable analysis identified the numbers of PET-positive nodes before and after chemotherapy as independent prognostic factors, together with clinical response, tumour depth and lymph node involvement. Conclusion: The number of PET-positive nodes after treatment correlated with survival in patients with oesophageal cancer who underwent neoadjuvant chemotherapy.
    No preview · Article · Oct 2015 · British Journal of Surgery
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    ABSTRACT: Functional microRNAs (miRNAs) in exosomes have been recognised as potential stable biomarkers in cancers. The aim of this study is to identify specific miRNAs in exosome as serum biomarkers for the early detection of recurrence in human colorectal cancer (CRC). Serum samples were sequentially obtained from six patients with and without recurrent CRC. The miRNAs were purified from exosomes, and miRNA microarray analysis was performed. The miRNA expression profiles and copy number aberrations were explored using microarray and array CGH analyses in 124 CRC tissues. Then, we validated exosomal miRNAs in 2 serum sample sets (90 and 209 CRC patients) by quantitative real-time RT-PCR. Exosomal miR-17-92a cluster expression level in serum was correlated with the recurrence of CRC. Exosomal miR-19a expression levels in serum were significantly increased in patients with CRC as compared with healthy individuals with gene amplification. The CRC patients with high exosomal miR-19a expression showed poorer prognoses than the low expression group (P<0.001). Abundant expression of exosomal miR-19a in serum was identified as a prognostic biomarker for recurrence in CRC patients.British Journal of Cancer advance online publication, 9 June 2015; doi:10.1038/bjc.2015.201 www.bjcancer.com.
    No preview · Article · Jun 2015 · British Journal of Cancer
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    Preview · Article · Jun 2015 · Annals of Oncology
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    ABSTRACT: Identification of promising biomarkers that predict the prognosis of patients with breast cancer is needed. In this study, we hypothesised that the expression of the epithelial-mesenchymal transition-related biomarker plastin3 (PLS3) in peripheral blood could be a prognostic factor in breast cancer. We examined PLS3 expression in breast cancer cell lines with epithelial and mesenchymal traits and in circulating tumour cells (CTCs) obtained from the peripheral blood of breast cancer patients. We investigated PLS3 expression in the peripheral blood of 594 patients with breast cancer to evaluate the clinical significance of PLS3 expression. Robust PLS3 expression was observed in different breast cancer cell lines (Hs578t, MCF-7, MDA-MB-468, and MDA-MB-231) as well as in a bone marrow derived cancer cell line (BC-M1). In both the training (n=298) and validation (n=296) sets, PLS3 expression was observed in CTCs of patients with breast cancer. PLS3-positive patients showed significantly poorer overall and disease-free survival than PLS3-negative patients (P=0.0001 and 0.003, respectively). Subset analysis revealed that this prognostic biomarker was relevant in patients with stage I-III cancer, particularly in patients with luminal-type and triple-negative-type tumours. These data demonstrated that PLS3 was expressed in CTCs undergoing the epithelial-mesenchymal transition in patients with breast cancer. Furthermore, PLS3 may be an excellent biomarker for identifying groups at risk of recurrence or with a poor prognosis.British Journal of Cancer advance online publication 16 April 2015. doi:10.1038/bjc.2015.132 www.bjcancer.com.
    No preview · Article · Apr 2015 · British Journal of Cancer
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    ABSTRACT: Long-term immunosuppression is associated with an increased risk of cancer. Especially, the immunosuppression in pancreas transplantation is more intensive than that in other organ transplantation because of its strong immunogenicity. Therefore, it suggests that the risk of post-transplant de novo malignancy might increase in pancreas transplantation. However, there have been few studies of de novo malignancy after pancreas transplantation. The aim of this study was to analyze the incidence of de novo malignancy after pancreas transplantation in Japan. Post-transplant patients with de novo malignancy were surveyed and characterized in Japan. Among 107 cases receiving pancreas transplantation in Japan between 2001 and 2010, de novo malignancy developed in 9 cases (8.4%): post-transplant lymphoproliferative disorders in 6 cases, colon cancer in 1 case, renal cancer in 1 case, and brain tumor in 1 case. We clarified the incidence of de novo malignancy after pancreas transplantation in Japan. Copyright © 2015 Elsevier Inc. All rights reserved.
    No preview · Article · Apr 2015 · Transplantation Proceedings
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    ABSTRACT: This study investigated whether an intestinal epithelial culture method can be applied to mouse and human esophageal cultures. The esophagi harvested from 1-day-old mice and adult humans were maintained in collagen gels. A commercially available culture medium for human embryonic stem cells was used for the human esophageal culture. We discovered that the intestinal epithelial culture method can be successfully applied to both mouse and human esophageal cultures. The long-term cultured esophageal organoids were rod-like luminal structures lined with myofibroblasts. We discovered that regeneration of the esophageal mucosal surface can be almost completely achieved in vitro, and the advantage of this method is that organoid cultures may be generated using host-derived fibroblasts as a niche. This method is a promising tool for mouse and human research in intestinal biology, carcinogenesis, and regenerative medicine. © 2015 International Society for Diseases of the Esophagus.
    No preview · Article · Mar 2015 · Diseases of the Esophagus

  • No preview · Conference Paper · Feb 2015
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    ABSTRACT: Background: The MYC oncogene has long been established as a central driver in many types of human cancers including colorectal cancer. However, the realization of MYC-targeting therapies remains elusive; as a result, synthetic lethal therapeutic approaches are alternatively being explored. A synthetic lethal therapeutic approach aims to kill MYC-driven tumors by targeting a certain co-regulator on the MYC pathway. Patients and methods: We analyzed copy number and expression profiles from 130 colorectal cancer tumors together with publicly available datasets to identify co-regulators on the MYC pathway. Candidates were functionally tested by in vitro assays using colorectal cancer and normal fibroblast cell lines. Additionally, survival analyses were carried out on another 159 colorectal cancer patients and public datasets. Results: Our in silico screening identified two MYC co-regulator candidates, AURKA and TPX2, which are interacting mitotic regulators located on chromosome 20q. We found the two candidates showed frequent co-amplification with the MYC locus while expression levels of MYC and the two genes were positively correlated with those of MYC downstream target genes across multiple cancer types. In vitro, the aberrant expression of MYC, AURKA and TPX2 resulted in more aggressive anchorage-independent growth in normal fibroblast cells. Furthermore, knockdown of AURKA or TPX2, or treatment with an AURKA-specific inhibitor effectively suppressed the proliferation of MYC-expressing colorectal cancer cells. Additionally, combined high expression of MYC, AURKA and TPX2 proved to be a poor prognostic indicator of colorectal cancer patient survival. Conclusions: Through bioinformatic analyses and experiments, we proposed TPX2 and AURKA as novel co-regulators on the MYC pathway. Inhibiting the AURKA/TPX2 axis would be a novel synthetic lethal therapeutic approach for MYC-driven cancers.
    Full-text · Article · Jan 2015 · Annals of Oncology

  • No preview · Article · Nov 2014 · European Journal of Cancer
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    ABSTRACT: Purpose: Recent advances in laparoscopic surgical technology have made it possible to perform advanced high-level surgery, such as lymph node dissection for malignancy. Grasping the anatomy during such procedures is important for a safe operation. We have developed a new image information system that provides three-dimensional (3D) reconstructed CT images synchronized with the motion of the laparoscope. This study assesses this new navigation system. Methods: Enhanced CT using a custom-made software program can provide 3D angiography images reconstructed as a laparoscopic view. A motion sensor mounted on the laparoscope can detect the direction angle of the laparoscope. The real-time rendered 3D CT images are synchronized with the laparoscopic video images according to the motion of the scope. These 3D CT images are projected on another monitor close to the laparoscopic video monitor. Lymph node dissection can be performed with the help of the real-time navigation system that provides a detailed 3D view of the vasculature. Results: Ten laparoscopic gastrectomies were performed using this navigation system. Real-time intraoperative navigation of the vasculature was available, allowing for an excellent surgical outcome. No complications occurred in this series. Conclusion: Our intraoperative navigation system allows for safe laparoscopic gastric lymph node dissection.
    No preview · Article · Aug 2014 · Surgery Today

  • No preview · Article · Jul 2014
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    ABSTRACT: Background: Cancer stem cells (CSCs) are responsible for treatment failure. However, their identification and roles in resistance are not well established in head and neck squamous cell carcinoma (HNSCC). Methods: Three HNSCC cell lines (FaDu, Detroit562 and BICR6) were treated with cisplatin or radiation. Cell surface antigens were analysed by LyoPlate, a novel cell surface antigen array. The expression levels of antigens highly expressed after treatments were further compared between cisplatin-resistant Detroit562 cells and its parental line. Association of the candidate antigen with CSCs properties, namely sphere formation and in vivo tumourigenicity, was also examined. Results: CD10, CD15s, CD146 and CD282 were upregulated across the treated cell lines, while the increased expression of CD10 was prominent in the cisplatin-resistant cell line. Isolation mediated by FACS revealed that the CD10-positive subpopulation was more refractory to cisplatin, fluorouracil and radiation than the CD10-negative subpopulation. It also showed an increased ability to form spheres in vitro and tumours in vivo. Moreover, the CD10-positive subpopulation expressed the CSC marker OCT3/4 at a higher level than that in the CD10-negative subpopulation. Conclusions: CD10 is associated with therapeutic resistance and CSC-like properties of HNSCC. CD10 may serve as a target molecule in the treatment of refractory HNSCC.
    Preview · Article · May 2014 · British Journal of Cancer
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    ABSTRACT: In Japan, absolute shortage of donors still continues even after the law allowing organ transplantation from deceased donors came into force in 1997. With the passage of the waiting period after registration for pancreas transplantation (PTx), both deaths and serious cases of diabetic complications necessitating withdrawal of the registration have undoubtedly increased. Therefore, so-called "marginal donor" (MD) has been considered as a potential solution for shortage of donors in Japan. The aim of the present study is to evaluate feasibility of MD in terms of post-PTx outcomes using data from Japan Organ Transplantation Network. A total of 148 PTx were performed from deceased donors in Japan from 2000 to 2012. MD was defined as follows: (1) >45 years old; (2) hemodynamically unstable at harvest using a high-dose dopamine or more than 2 vasopressors; or (3) non-heart-beating status. Postoperative outcomes after PTx were compared between the MD group and the non-MD group. Among the 148 PTx donors, 108 donors (73.0%) satisfied the criteria of MD. Early graft loss of pancreas graft during 3 months post-transplant was observed in 15 patients (10.1%), and the marginality (MD vs non-MD) was not significantly correlated with the early loss of pancreas graft. The overall patient survival of the MD group (1, 3, 5 years: 94.7%, 94.7%, 94.7%) was not significantly different from that of the non-MD group (1, 3, 5 years: 95.0%, 95.0%, 95.0%). Pancreas graft survival in the MD group (1, 3, 5 years: 80.9%, 73.2%, 66.0%) seemed to be slightly lower than that in the non-MD group (1, 3, 5 years: 92.5%, 85.2%, 77.4%), but no statistically significant differences were found between the 2 groups. These results suggest the feasibility of the use of MD for PTx.
    No preview · Article · Apr 2014 · Transplantation Proceedings
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    ABSTRACT: Background: We previously conducted gene expression microarray analyses to identify novel indicators for colorectal cancer (CRC) metastasis and prognosis from which we identified PVT-1 as a candidate gene. PVT-1, which encodes a long noncoding RNA, mapped to chromosome 8q24 whose copy-number amplification is one of the most frequent events in a wide variety of malignant diseases. However, PVT-1 molecular mechanism of action remains unclear. Methods: We conducted cell proliferation and invasion assays using colorectal cancer cell lines transfected with PVT-1siRNA or negative control siRNA. Gene expression microarray analyses on these cell lines were also carried out to investigate the molecular function of PVT-1. Further, we investigated the impact of PVT-1 expression on the prognosis of 164 colorectal cancer patients by qRT–PCR. Results: CRC cells transfected with PVT-1 siRNA exhibited significant loss of their proliferation and invasion capabilities. In these cells, the TGF-β signalling pathway and apoptotic signals were significantly activated. In addition, univariate and multivariate analysis revealed that PVT-1 expression level was an independent risk factor for overall survival of colorectal cancer patients. Conclusion: PVT-1, which maps to 8q24, generates antiapoptotic activity in CRC, and abnormal expression of PVT-1 was a prognostic indicator for CRC patients.
    Full-text · Article · Nov 2013 · British Journal of Cancer

  • No preview · Article · Oct 2013 · International Journal of Radiation OncologyBiologyPhysics
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    ABSTRACT: Several studies have examined the clinical significance of metabolic response in primary tumours by [(18) F]fluorodeoxyglucose positron emission tomography ((18) F-FDG-PET) in patients with oesophageal cancer who undergo neoadjuvant therapy. The relevance of the metabolic response in lymph nodes is unclear. Consecutive patients with oesophageal cancer who underwent neoadjuvant chemotherapy followed by surgery were studied. (18) F-FDG-PET was performed before and 2-3 weeks after completion of neoadjuvant chemotherapy, assessing FDG uptake in primary tumours and lymph nodes considered to be metastatic. Before therapy, 156 (73·9 per cent) of 211 patients had PET-positive nodes, of whom 89 (57.1 per cent) had no evidence of metabolic activity in these lymph nodes following chemotherapy. There was a significant relationship between post-treatment lymph node status assessed by FDG-PET and numbers of pathologically confirmed metastatic lymph nodes. Patients with post-treatment PET-positive nodes had shorter survival than those without (5-year survival rate 25 versus 62·6 per cent; P < 0·001). There was no difference in survival between patients with PET-positive nodes before but not after therapy and patients who had PET-negative nodes throughout (5-year survival rate 59 versus 71 per cent respectively; P = 0·207). Multivariable analysis identified post-treatment nodal status assessed by FDG-PET and tumour depth as independent prognostic factors. Identification of PET-positive lymph nodes after completion of chemotherapy is a predictor of poor prognosis of patients with oesophageal cancer scheduled for surgery. FDG-PET lymph node status after neoadjuvant chemotherapy is more important than that before chemotherapy.
    No preview · Article · Oct 2013 · British Journal of Surgery
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    ABSTRACT: Background: The TP53 pathway is frequently inactivated in human cancers. PICT1 (also known as GLTSCR2) is a novel regulator of the MDM2-TP53 pathway via its interaction with the ribosomal protein RPL11 in the nucleolus. However, the clinical significance of PICT1 in gastric cancer remains unknown. Methods: To evaluate PICT1 function, we used shRNA to inhibit PICT1 expression in gastric cancer cells that expressed wild-type TP53. PICT1 expression and TP53 mutation status were quantified in 110 cases of primary gastric cancer to explore the impact of PICT1 expression levels on gastric cancer. Results: Deficiency of PICT1 significantly impaired cell proliferation and colony formation via TP53-mediated cell cycle arrest. Following induction of PICT1 deficiency, RPL11 translocated out of the nucleolus. Of the 110 gastric cancer samples tested, 70 (63.6%) and 40 (36.4%) tumours expressed wild-type and mutant TP53, respectively. In gastric cancer patients with wild-type TP53 tumours, patients with relatively low PICT1 expression levels had a better prognosis compared with high expression level patients (P=0.046). Conclusion: The findings suggest that PICT1 has a crucial role in gastric cancer progression by regulating the MDM2-TP53 pathway through RPL11. Clinically, PICT1 expression is a novel prognostic parameter in gastric cancer patients with wild-type TP53 tumours.
    Full-text · Article · Sep 2013 · British Journal of Cancer
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    ABSTRACT: Background: Paired related homoeobox 1 (PRRX1) has been identified as a new epithelial-mesenchymal transition (EMT) inducer in breast cancer. However, the function of PRRX1 in colorectal cancer (CRC) has not been elucidated. Methods: We utilised ectopic PRRX1-expressing cell lines to analyse the function of PRRX1 in CRC. The clinical significance of PRRX1 was also examined on three independent CRC case sets. Results: PRRX1 induced EMT and the stem-like phenotype in CRC cells. In contrast to studies of breast cancer, abundant expression of PRRX1 was significantly associated with metastasis and poor prognosis in CRC. Conclusion: PRRX1 is an indicator of metastasis and poor prognosis in CRC cases. Further investigation is required to uncover the signalling network regulating PRRX1.
    Full-text · Article · Jun 2013 · British Journal of Cancer
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    ABSTRACT: Background: Gemcitabine-based chemotherapy is the standard treatment for pancreatic cancer. However, the issue of resistance remains unresolved. The aim of this study was to identify microRNAs (miRNAs) that govern the resistance to gemcitabine in pancreatic cancer. Methods: miRNA microarray analysis using gemcitabine-resistant clones of MiaPaCa2 (MiaPaCa2-RGs), PSN1 (PSN1-RGs), and their parental cells (MiaPaCa2-P, PSN1-P) was conducted. Changes in the anti-cancer effects of gemcitabine were studied after gain/loss-of-function analysis of the candidate miRNA. Further assessment of the putative target gene was performed in vitro and in 66 pancreatic cancer clinical samples. Results: miR-320c expression was significantly higher in MiaPaCa2-RGs and PSN1-RGs than in their parental cells. miR-320c induced resistance to gemcitabine in MiaPaCa2. Further experiments showed that miR-320c-related resistance to gemcitabine was mediated through SMARCC1, a core subunit of the switch/sucrose nonfermentable (SWI/SNF) chromatin remodeling complex. In addition, clinical examination revealed that only SMARCC1-positive patients benefited from gemcitabine therapy with regard to survival after recurrence (P=0.0463). Conclusion: The results indicate that miR-320c regulates the resistance of pancreatic cancer cells to gemcitabine through SMARCC1, suggesting that miR-320c/SMARCC1 could be suitable for prediction of the clinical response and potential therapeutic target in pancreatic cancer patients on gemcitabine-based therapy.
    Preview · Article · Jun 2013 · British Journal of Cancer

Publication Stats

19k Citations
2,636.30 Total Impact Points

Institutions

  • 2009-2015
    • Osaka University
      • • Division of Gastroenterological Surgery
      • • Department of Surgery
      Suika, Ōsaka, Japan
  • 2009-2012
    • Osaka City University
      • Department of Gastroenterological Surgery
      Ōsaka, Ōsaka, Japan
  • 1985-2012
    • Kyushu University
      • • Department of Surgery and Science
      • • Division of Surgery
      • • Medical Institute of Bioregulation - MIB Hospital
      • • Department of Surgery and Oncology
      Hukuoka, Fukuoka, Japan
  • 1980-2012
    • Gunma University
      • • Department of Medicine and Molecular Science
      • • School of Medicine
      • • Institute for Molecular and Cellular Regulation
      Maebashi, Gunma, Japan
  • 2007-2011
    • Sojo University
      Kumamoto, Kumamoto Prefecture, Japan
  • 2008
    • Japan Science and Technology Agency (JST)
      Edo, Tōkyō, Japan
  • 1993-2006
    • Oita University
      • • Department of Anesthesiology
      • • Faculty of Medicine
      Ōita, Ōita, Japan
  • 2005
    • Hitachi Medical Corporation
      Edo, Tōkyō, Japan
  • 2004
    • Okayama Prefectural University
      Okayama, Okayama, Japan
  • 1986-2003
    • Hitachi, Ltd.
      Edo, Tōkyō, Japan
  • 1986-2002
    • Kumamoto University
      • • Department of Molecular Genetics
      • • School of Medicine
      Kumamoto, Kumamoto Prefecture, Japan
  • 1993-2001
    • Dana-Farber Cancer Institute
      • Division of Molecular and Cellular Oncology
      Boston, Massachusetts, United States
  • 1979-2001
    • Sapporo Medical University
      • • Department of Pathology II
      • • Department of Clinical Pathology
      • • Division of Internal Medicine II
      Sapporo, Hokkaidō, Japan
    • Chiba University Hospital
      Tiba, Chiba, Japan
  • 1998-2000
    • Saitama Cancer Center
      Saitama, Saitama, Japan
  • 1999
    • University of Massachusetts Medical School
      • Department of Medicine
      Worcester, MA, United States
    • Thomas Jefferson University
      Philadelphia, Pennsylvania, United States
  • 1988-1999
    • Jichi Medical University
      • • Division of Hematology
      • • Department of Pediatrics
      Totigi, Tochigi, Japan
  • 1997
    • Saiseikai Maebashi Hospital
      Edo, Tōkyō, Japan
  • 1996-1997
    • The University of Tokyo
      • Faculty & Graduate School of Medicine
      白山, Tōkyō, Japan
  • 1988-1997
    • Keio University
      • School of Medicine
      Edo, Tokyo, Japan
  • 1995
    • Ina Research Inc.
      Ina, Nagano, Japan
  • 1986-1992
    • National Cancer Center, Japan
      Edo, Tōkyō, Japan
  • 1991
    • Harvard Medical School
      Boston, Massachusetts, United States
    • The University of Tokushima
      • Institute for Enzyme Research
      Tokushima-shi, Tokushima-ken, Japan
  • 1990
    • Kurume University
      Куруме, Fukuoka, Japan
  • 1987
    • Hokkaido University
      • Faculty of Science
      Sapporo, Hokkaidō, Japan
    • Chiba University
      Tiba, Chiba, Japan
  • 1984
    • Kagoshima University
      • School of Medicine
      Kagosima, Kagoshima, Japan
  • 1968-1971
    • Osaka Dental University
      Ōsaka, Ōsaka, Japan