Updated on 2025/10/04

写真a

 
OUCHIDA Mamoru
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Associate Professor
Position
Associate Professor
External link

Degree

  • Ph.D. ( Kyushu University )

Research Interests

  • Human Genetics

  • 分子生物学

  • Molecular Biology

  • 病態医化学

  • 分子腫瘍学

Research Areas

  • Life Science / Pathological biochemistry

  • Life Science / Medical biochemistry

  • Life Science / Molecular biology

  • Life Science / Cell biology

Education

  • Kyushu University   大学院理学研究科   分子遺伝学

    - 1988

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    Country: Japan

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  • Kyushu University   理学部   生物学科

    - 1983

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    Country: Japan

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Research History

  • Okayama University   学術研究院医歯薬学域 分子腫瘍学   Associate Professor

    2021.4

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  • Okayama University   大学院医歯薬学総合研究科 分子腫瘍学   Associate Professor

    2007.4 - 2021.3

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  • Okayama University   大学院医歯学総合研究科 分子遺伝学講座   Associate Professor (as old post name)

    2001.4 - 2007.3

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  • Okayama University   医学部附属分子細胞医学研究施設   Associate Professor (as old post name)

    1997.4 - 2001.3

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  • Thomas Jefferson University, Cancer Institute

    1993.3 - 1995.2

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  • Saga Medical School

    1989.1 - 1997.3

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Professional Memberships

 

Papers

  • Txn1 mutation is a monogenic cause of chronic kidney disease associated with mitochondrial dysfunction in rats

    Iori Ohmori, Mamoru Ouchida, Yoshiko Hada, Haruhito, A. Uchida, Shinya Toyokuni, Tomoji Mashimo

    BioRxiv   2023.8

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    DOI: 10.1101/2023.08.14.553187

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  • "Input/output cytokines" in epidermal keratinocytes and the involvement in inflammatory skin diseases. Reviewed International journal

    Shin Morizane, Tomoyuki Mukai, Ko Sunagawa, Kota Tachibana, Yoshio Kawakami, Mamoru Ouchida

    Frontiers in immunology   14   1239598 - 1239598   2023

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    Considering the role of epidermal keratinocytes, they occupy more than 90% of the epidermis, form a physical barrier, and also function as innate immune barrier. For example, epidermal keratinocytes are capable of recognizing various cytokines and pathogen-associated molecular pattern, and producing a wide variety of inflammatory cytokines, chemokines, and antimicrobial peptides. Previous basic studies have shown that the immune response of epidermal keratinocytes has a significant impact on inflammatory skin diseases. The purpose of this review is to provide foundation of knowledge on the cytokines which are recognized or produced by epidermal keratinocytes. Since a number of biologics for skin diseases have appeared, it is necessary to fully understand the relationship between epidermal keratinocytes and the cytokines. In this review, the cytokines recognized by epidermal keratinocytes are specifically introduced as "input cytokines", and the produced cytokines as "output cytokines". Furthermore, we also refer to the existence of biologics against those input and output cytokines, and the target skin diseases. These use results demonstrate how important targeted cytokines are in real skin diseases, and enhance our understanding of the cytokines.

    DOI: 10.3389/fimmu.2023.1239598

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  • Thioredoxin deficiency increases oxidative stress and causes bilateral symmetrical degeneration in rat midbrain. Reviewed International journal

    Iori Ohmori, Mamoru Ouchida, Hirohiko Imai, Saeko Ishida, Shinya Toyokuni, Tomoji Mashimo

    Neurobiology of disease   175   105921 - 105921   2022.11

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    Thioredoxin, encoded by Txn1, acts as a critical antioxidant in the defense against oxidative stress by regulating the dithiol/disulfide balance of interacting proteins. The role of thioredoxin in the central nervous system (CNS) is largely unknown. A phenotype-driven study of N-ethyl-N-nitrosourea-mutated rats with wild-running seizures revealed the importance of Txn1 mutations in CNS degeneration. Genetic mapping identified Txn1-F54L in the epileptic rats. The insulin-reducing activity of Txn1-F54L was approximately one-third of that of the wild-type (WT). Bilateral symmetrical vacuolar degeneration in the midbrain, mainly in the thalamus and the inferior colliculus, was observed in the Txn1-F54L rats. The lesions displayed neuronal and oligodendrocytic cell death. Neurons in Txn1-F54L rats showed morphological changes in the mitochondria. Vacuolar degeneration peaked at five weeks of age, and spontaneous repair began at seven weeks. The TUNEL assay showed that fibroblasts derived from homozygotes were susceptible to cell death under oxidative stress. In five-week-old WT rats, energy metabolism in the thalamus was significantly higher than that in the cerebral cortex. In conclusion, in juvenile rats, Txn1 seems to play an essential role in reducing oxidative stress in the midbrains with high energy metabolism.

    DOI: 10.1016/j.nbd.2022.105921

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  • Aberrant serine protease activities in atopic dermatitis Reviewed

    Shin Morizane, Ko Sunagawa, Hayato Nomura, Mamoru Ouchida

    JOURNAL OF DERMATOLOGICAL SCIENCE   107 ( 1 )   2 - 7   2022.7

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  • Novel animal model of combined generalized and focal epilepsy. Reviewed International journal

    Iori Ohmori, Mamoru Ouchida, Masakazu Shinohara, Kiyoka Kobayashi, Saeko Ishida, Tomoji Mashimo

    Epilepsia   63 ( 7 )   e80-e85   2022.5

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    Thioredoxin, encoded by Txn1, is a critical antioxidant that protects against oxidative damage by regulating the dithiol/disulfide balance of interacting proteins. We recently discovered the Adem rat, an epileptic rat harboring the Txn1-F54L mutation, characterized by wild running and vacuolar degeneration in the midbrain. This study aimed to characterize the classification of epilepsy in Adem rats. We performed simultaneous video-electroencephalographic recordings, magnetic resonance imaging, neurotransmitter measurements using gas chromatography-mass spectrometry (GC-MS), and immunohistochemistry. Adem rats exhibited absence, tonic, and focal seizures. The type of epilepsy was classified as combined generalized and focal epilepsy. Neurotransmitters in the midbrain and cortex were measured at 3 weeks of age, when neuronal cell death occurs in the midbrain. The results of GC-MS ruled out the dominance of the excitatory system in the midbrain and cortex of Adem rats. Activation of astrocytes and microglia was more pronounced at 5 weeks of age, at which time epileptic seizures occurred frequently. The underlying pathology in Adem rats remains unknown. However, glial cell activation and inflammation may play a significant role in the occurrence of epilepsy.

    DOI: 10.1111/epi.17295

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  • Multifaceted Analysis of IL-23A- and/or EBI3-Including Cytokines Produced by Psoriatic Keratinocytes Reviewed

    Tachibana K, Tang N, Urakami H, Kajita Ai, Kobashi M, Nomura H, Sasakura M, Sugihara S, FJiang F, Tomonobu N, Sakaguchi M, Ouchida M, Morizane S

    International Journal of Molecular Sciences   22 ( 23 )   10.3390/ijms222312659   2021.11

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  • Txn1 mutation causes epilepsy associated with vacuolar degeneration in the midbrain.

    Iori Ohmori, Mamoru Ouchida, Hirohiko Imai, Saeko Ishida, Shinya Toyokuni, Tomoji Mashimo

    bioRxiv   2021.10

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    Publisher:Cold Spring Harbor Laboratory  

    Abstract

    Thioredoxin (TXN), encoded by Txn1, acts as a critical antioxidant in the defense against oxidative stress by regulating the dithiol/disulfide balance of interacting proteins. The role of TXN in the central nervous system (CNS) is largely unknown. A phenotype-driven study of N-ethyl-N-nitrosourea-mutated rats with running seizures at around five-week of age revealed the relevance of Txn1 mutations to CNS disorders. Genetic mapping identified Txn1-F54L in epileptic rats. The insulin-reducing activity of Txn1-F54L rats was approximately one-third that of the wild-type. Vacuolar degeneration in the midbrain, mainly in the thalamus and the inferior colliculus, was observed in the Txn1-F54L rats. The lesions displayed neuronal and oligodendrocyte cell death. Neurons in Txn1-F54L rats showed morphological changes in the mitochondria. Vacuolar degeneration began at three weeks of age, and spontaneous repair began at seven weeks; a dramatic change from cell death to repair occurred in the midbrain during a restricted period. In conclusion, Txn1 is essential for the development of the midbrain in juvenile rats.

    DOI: 10.1101/2021.10.07.463470

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  • VLX1570 induces apoptosis through the generation of ROS and induction of ER stress on leukemia cell lines. Reviewed International journal

    Nami Kurozumi, Takayuki Tsujioka, Mamoru Ouchida, Kanae Sakakibara, Takako Nakahara, Shin-Ichiro Suemori, Masaki Takeuchi, Akira Kitanaka, Misako Shibakura, Kaoru Tohyama

    Cancer science   112 ( 8 )   3302 - 3313   2021.8

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    A novel proteasome deubiquitinase inhibitor, VLX1570, has been highlighted as a promising therapeutic agent mainly for lymphoid neoplasms and solid tumors. We examined in vitro effects of VLX1570 on eight myeloid and three lymphoid leukemia cell lines. From cell culture studies, 10 out of 11 cell lines except K562 were found to be susceptible to VLX1570 treatment and it inhibited cell growth mainly by apoptosis. Next, to identify the signaling pathways associated with apoptosis, we performed gene expression profiling using HL-60 with or without 50 nmol/L of VLX1570 for 3 hours and demonstrated that VLX1570 induced the genetic pathway involved in "heat shock transcription factor 1 (HSF1) activation", "HSF1 dependent transactivation", and "Regulation of HSF1 mediated heat shock response". VLX1570 increased the amount of high molecular weight polyubiquitinated proteins and the expression of HSP70 as the result of the suppression of ubiquitin proteasome system, the expression of heme oxygenase-1, and the amount of phosphorylation in JNK and p38 associated with the generation of reactive oxygen species (ROS) induced apoptosis and the amount of phosphorylation in eIF2α, inducing the expression of ATF4 and endoplasmic reticulum (ER) stress dependent apoptosis protein, CHOP, and the amount of phosphorylation slightly in IRE1α, leading to increased expression of XBP-1s in leukemia cell lines. In the present study, we demonstrate that VLX1570 induces apoptosis and exerts a potential anti-leukemic effect through the generation of ROS and induction of ER stress in leukemia cell lines.

    DOI: 10.1111/cas.14982

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  • Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats. Reviewed International journal

    Iori Ohmori, Kiyoka Kobayashi, Mamoru Ouchida

    Neurochemistry international   141   104859 - 104859   2020.12

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    This study aimed to examine the effects of Cacna1a mutation on the phenotype of Scn1a-associated epilepsy in rats. We used rats with an N1417H missense mutation in the Scn1a gene and others with an M251K mutation in the Cacna1a gene. Scn1a/Cacna1a double mutant rats were generated by mating both Scn1a and Cacna1a mutants. We investigated general health and the epileptic phenotype in all these genotypes. The onset threshold of hyperthermia-induced seizures was examined at 5 weeks and spontaneous seizures were monitored using video-EEG recordings from 6 to 12 weeks of age. Scn1a/Cacna1a double mutants showed significantly reduced threshold for hyperthermia-sensitive seizures onset compared with the Scn1a mutants and had absence seizures having 6-7 c/s spike-wave bursts with changes in the spike-wave pattern, whereas Cacna1a mutants had regular 6-7 c/s spike-wave bursts. In Scn1a/Cacna1a double mutants, 6-7 c/s spike-wave bursts were accompanied with eyelid myoclonia and continuously shifting generalized clonic seizures, which were not observed in either Scn1a or Cacna1a mutants. Although a curvature of the spine was observed in rats of all these genotypes, the degree of curvature was more pronounced in Scn1a/Cacna1a double mutants, followed by Cacna1a and Scn1a mutants. Our results indicate that Cacna1a and Scn1a mutations mutually alter their original phenotypes in rats. The phenotype of absence seizures with eyelid myoclonia, generalized clonic seizures, and of spine curvature in the Scn1a/Cacna1a double mutants were similar to that observed in patients with Dravet syndrome.

    DOI: 10.1016/j.neuint.2020.104859

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  • Development of a novel analgesic for neuropathic pain targeting brain-derived neurotrophic factor. Reviewed International journal

    Kae Ikeda, Keita Hazama, Yoshitaro Itano, Mamoru Ouchida, Hideki Nakatsuka

    Biochemical and biophysical research communications   531 ( 3 )   390 - 395   2020.10

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    Effective treatment of neuropathic pain is challenging as its underlying mechanism remains largely unknown. Recently, the participation of brain-derived neurotrophic factor (BDNF) in neuropathic pain has been attracting increased attention. BDNF binds to a member of the tyrosine kinase receptor family, the TrkB receptor, that is specific for BDNF and is the transmembrane receptor on the posterior horn of spinal cord. In the present study, we purified two proteins that included the BDNF-binding domain of TrkB (eTrkB) and eTrkB coupled with a liposomal outer surface (liposomal eTrkB) in order to inhibit the BDNF-TrkB pathway in neuropathic pain. Results of the pull-down assay showed that eTrkB was bound to BDNF. We investigated the neuropathic pain suppression effect of this purified protein by its intrathecal administration in a rat neuropathic pain model. Mechanical and thermal hyperalgesia induced by L5 lumbar nerve ligation was markedly suppressed by treatment with eTrkB protein. Furthermore, we showed a prolonged algetic inhibition by liposomal eTrkB protein treatment. In conclusion, this study suggests that eTrkB, which sequesters endogenous BDNF and inhibits the BDNF-TrkB pathway, may prove to be a novel analgesic to treat neuropathic pain.

    DOI: 10.1016/j.bbrc.2020.07.109

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  • Analysis of All 34 Exons of the SPINK5 Gene in Japanese Atopic Dermatitis Patients. Reviewed

    Shin Morizane, Mamoru Ouchida, Ko Sunagawa, Saeko Sugimoto, Mina Kobashi, Satoru Sugihara, Hayato Nomura, Kazuhide Tsuji, Atsushi Sato, Yoshihiro Miura, Hiroaki Hattori, Kotaro Tada, Wook-Kang Huh, Akemi Seno, Keiji Iwatsuki

    Acta medica Okayama   72 ( 3 )   275 - 282   2018.6

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    Lympho-epithelial Kazal-type-related inhibitor (LEKTI) is a large multidomain serine protease inhibitor that is expressed in epidermal keratinocytes. Nonsense mutations of the SPINK5 gene, which codes for LEKTI, cause Netherton syndrome, which is characterized by hair abnormality, ichthyosis, and atopy. A single nucleotide polymorphism (SNP) of SPINK5, p.K420E, is reported to be associated with the pathogenesis of atopic dermatitis (AD). We studied all 34 exons of the SPINK5 gene in Japanese 57 AD patients and 50 normal healthy controls. We detected nine nonsynonymous variants, including p.K420E; these variants had already been registered in the SNP database. Among them, p.R654H (n=1) was found as a heterozygous mutation in the AD patients, but not in the control. No new mutation was detected. We next compared the data of the AD patients with data from the Human Genetic Variation Database provided by Kyoto University; a significant difference was found in the frequency of the p.S368N genotype distribution. PolyPhen-2 and SIFT, two algorithms for predicting the functional effects of amino acid substitutions, showed significant scores for p.R654H. Therefore, R654H might be a risk factor for epidermal barrier dysfunction in some Japanese AD patients.

    DOI: 10.18926/AMO/56073

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  • Novel analgesics targeting brain-derived neurotrophic factor for neuropathic pain. Reviewed

    Hazama K, Ikeda K, Tsuge M, Itano Y, Ouchida M, Nakatsuka H

    Kawasaki Medical Journal.   44 ( 2 )   41 - 52   2018

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  • Human RAD 17 Polymorphism at Codon 546 Is Associated with the Risk of Colorectal Cancer. Reviewed

    Yukiko Yasuda, Akiko Sakai, Sachio Ito, Kaori Sasai, Hiromasa Yamamoto, Nagahide Matsubara, Mamoru Ouchida, Hiroshi Katayama, Kenji Shimizu

    Acta medica Okayama   71 ( 1 )   59 - 68   2017.2

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    DOI: 10.18926/AMO/54826

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  • A case of Dravet syndrome with cortical myoclonus indicated by jerk-locked back-averaging of electroencephalogram data. Reviewed International journal

    Yoshinori Kobayashi, Yoshiyuki Hanaoka, Tomoyuki Akiayma, Iori Ohmori, Mamoru Ouchida, Toshiyuki Yamamoto, Makio Oka, Harumi Yoshinaga, Katsuhiro Kobayashi

    Brain & development   39 ( 1 )   75 - 79   2017.1

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    DOI: 10.1016/j.braindev.2016.07.005

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  • Development of a novel analgesic for cancer pain targeting brain-derived neurotrophic factor. Reviewed

    Tsuge M, Hazama K, Kanzaki H, Itano Y, Maeshima K, Ouchida M, Nakatsuka H

    Kawasaki Medical Journal.   43   107 - 120   2017

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  • Genetic alterations in lung adenocarcinoma with a micropapillary component. Reviewed International journal

    Masashi Furukawa, Shinichi Toyooka, Kouichi Ichimura, Hiromasa Yamamoto, Junichi Soh, Shinsuke Hashida, Mamoru Ouchida, Kazuhiko Shien, Hiroaki Asano, Kazunori Tsukuda, Shinichiro Miyoshi

    Molecular and clinical oncology   4 ( 2 )   195 - 200   2016.2

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    Pulmonary adenocarcinoma (PA) with a micropapillary component (PA-MPC) is known as an aggressive subtype of PA. The molecular profiles of PA-MPC have not been well characterized. the pathological reports of patients who underwent surgical resection for lung cancer between April, 2004 and May, 2012 were reviewed. Of the 674 patients diagnosed with PA, 28 were found to have MPC. A total of 138 resected PAs without MPC were selected in the same period to serve as age-, gender- and smoking status-matched controls to the PA-MPC group. Mutational status was determined by the following two methods: SNaPshot assay based on multiplex polymerase chain reaction (PCR), primer extension and capillary electrophoresis that was designed to assess 38 somatic mutations in 8 genes [AKT1, BRAF, endothelial growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), mitogen-activated protein kinase kinase 1, neuroblastoma RAS viral oncogene homolog, phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA) and phosphatase and tensin homolog]; and a PCR-based sizing assay that assesses EGFR exon 19 (deletions), EGFR exon 20 (insertions) and human epidermal growth factor receptor 2 exon 20 (insertions). echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase fusion gene (EML4-ALK) was screened by ALK immunohistochemistry and confirmed using the reverse transcription PCR assay and the break-apart fluorescence in situ hybridization assay. Regarding genetic alterations, 13 (46.4%) of the 28 PA-MPCs harbored mutually exclusive mutations: 9 (32.1%) EGFR mutations, 1 (3.6%) KRAS mutation and 3 (10.7%) EML4-ALK fusion genes. PAs without MPC harbored 42 (30.4%) EGFR mutations, 17 (12.3%) KRAS mutations, 3 (2.2%) EML4-ALK fusion genes and 1 (0.7%) PIK3CA mutation. EML4-ALK fusion genes appeared to occur significantly more frequently in PA-MPCs compared with PAs without MPC (P=0.027). Although the sample size was small, our study suggests that the molecular pathogenesis of PA-MPC may be different from that of other adenocarcinomas.

    DOI: 10.3892/mco.2015.690

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  • Five-aza-2'-deoxycytidine-induced hypomethylation of cholesterol 25-hydroxylase gene is responsible for cell death of myelodysplasia/leukemia cells. Reviewed International journal

    Takayuki Tsujioka, Akira Yokoi, Yoshitaro Itano, Kentaro Takahashi, Mamoru Ouchida, Shuichiro Okamoto, Toshinori Kondo, Shin-ichiro Suemori, Yumi Tohyama, Kaoru Tohyama

    Scientific reports   5   16709 - 16709   2015.11

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    DNA methyltransferase inhibitors (DNMT inhibitors) are administered for high-risk MDS, but their action mechanisms are not fully understood. Hence, we performed a genome-wide DNA methylation assay and focused on cholesterol 25-hydroxylase (CH25H) among the genes whose expression was up-regulated and whose promoter region was hypomethylated after decitabine (DAC) treatment in vitro. CH25H catalyzes hydroxylation of cholesterol and produces 25-hydroxycholesterol (25-OHC). Although CH25H mRNA expression level was originally low in MDS/leukemia cell lines, exposure to DNMT inhibitors enhanced CH25H mRNA expression. The promoter region of CH25H was originally hypermethylated in HL-60 and MDS-L cells, but DAC treatment induced their hypomethylation together with increased CH25H mRNA expression, activation of CH25H-oxysterol pathway, 25-OHC production and apoptotic cell death. We further confirmed that normal CD34-positive cells revealed hypomethylated status of the promoter region of CH25H gene. CH25H-knockdown by transfection of shRNA lentiviral vector into the cell lines partially protected the cells from DAC-induced cell death. Exogenous addition of 25-OHC suppressed leukemic cell growth. The present study raises a possibility that DNMT inhibitors activate CH25H-oxysterol pathway by their hypomethylating mechanism and induce leukemic cell death. Further investigations of the promoter analysis of CH25H gene and therapeutic effects of DNMT inhibitors on MDS/leukemia will be warranted.

    DOI: 10.1038/srep16709

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  • Cyclin C interacts with steroid receptor coactivator 2 and upregulates cell cycle genes in MCF-7 cells. Reviewed International journal

    Olivera Bozickovic, Tuyen Hoang, Ingvild S Fenne, Thomas Helland, Linn Skartveit, Mamoru Ouchida, Gunnar Mellgren, Jørn V Sagen

    Biochimica et biophysica acta   1853 ( 10 Pt A )   2383 - 91   2015.10

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    DOI: 10.1016/j.bbamcr.2015.05.016

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  • Uncovering Direct Targets of MiR-19a Involved in Lung Cancer Progression. Reviewed International journal

    Kumiko Yamamoto, Sachio Ito, Hiroko Hanafusa, Kenji Shimizu, Mamoru Ouchida

    PloS one   10 ( 9 )   e0137887   2015.9

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    DOI: 10.1371/journal.pone.0137887

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  • MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors (vol 15, pg 1778, 2009) Reviewed

    T. Kubo, H. Yamamoto, W. W. Lockwood, Valencia, I, J. Soh, M. Peyton, M. Jida, H. Otani, T. Fujii, M. Ouchida, N. Takigawa, K. Kiura, K. Shimizu, H. Date, J. D. Minna, M. Varella-Garcia, W. L. Lam, A. F. Gazdar, S. Toyooka

    INTERNATIONAL JOURNAL OF CANCER   136 ( 2 )   E1 - E1   2015.1

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  • Methylphenidate improves learning impairments and hyperthermia-induced seizures caused by an Scn1a mutation. Reviewed International journal

    Iori Ohmori, Nozomi Kawakami, Sumei Liu, Haijiao Wang, Ikuko Miyazaki, Masato Asanuma, Hiroyuki Michiue, Hideki Matsui, Tomoji Mashimo, Mamoru Ouchida

    Epilepsia   55 ( 10 )   1558 - 67   2014.10

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    DOI: 10.1111/epi.12750

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  • PROTEOMIC ANALYSIS OF INVASION- AND ANGIOGENESIS-RELATED PROTEINS IN MALIGNANT GLIOMAS Reviewed

    Yu Takahashi, Tomotsugu Ichikawa, Tomoko Maruo, Kazuhiko Kurozumi, Manabu Onishi, Mamoru Ouchida, Kentaro Fuji, Yosuke Shimazu, Tetsuo Oka, E. Antonio Chiocca, Isao Date

    NEURO-ONCOLOGY   15   9 - 10   2013.11

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  • Truncated SSX protein suppresses synovial sarcoma cell proliferation by inhibiting the localization of SS18-SSX fusion protein. Reviewed International journal

    Yasushi Yoneda, Sachio Ito, Toshiyuki Kunisada, Yuki Morimoto, Hirotaka Kanzaki, Aki Yoshida, Kenji Shimizu, Toshifumi Ozaki, Mamoru Ouchida

    PloS one   8 ( 10 )   e77564   2013.10

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    DOI: 10.1371/journal.pone.0077564

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  • Inhalation of 10% carbon dioxide rapidly terminates Scn1a mutation-related hyperthermia-induced seizures Reviewed International journal

    Iori Ohmori, Keiichiro Hayashi, Haijiao Wang, Mamoru Ouchida, Naohiro Fujita, Takushi Inoue, Hiroyuki Michiue, Teiichi Nishiki, Hideki Matsui

    EPILEPSY RESEARCH   105 ( 1-2 )   220 - 224   2013.7

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    DOI: 10.1016/j.eplepsyres.2013.01.003

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  • CACNA1A VARIANTS AS A POTENTIAL GENETIC MODIFIER OF DRAVET SYNDROME Reviewed

    Ohmori, I, M. Ouchida, K. Kobayashi, Y. Ohtsuka, H. Matsui

    EPILEPSIA   54   195 - 196   2013.6

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  • Proteomics-based analysis of invasion-related proteins in malignant gliomas. Reviewed International journal

    Tomoko Maruo, Tomotsugu Ichikawa, Hirotaka Kanzaki, Satoshi Inoue, Kazuhiko Kurozumi, Manabu Onishi, Koichi Yoshida, Hirokazu Kambara, Mamoru Ouchida, Kenji Shimizu, Seiji Tamaru, E Antonio Chiocca, Isao Date

    Neuropathology : official journal of the Japanese Society of Neuropathology   33 ( 3 )   264 - 75   2013.6

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    DOI: 10.1111/j.1440-1789.2012.01361.x

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  • INHALATION OF CO2 SHOWS A POTENT AND FAST-ACTING ANTICONVULSANT EFFECT AGAINST SCN1A MUTATION-RELATED HYPERTHERMIA-INDUCED SEIZURES Reviewed

    Ohmori, I, K. Hayashi, H. Wang, M. Ouchida, H. Matsui

    EPILEPSIA   54   49 - 49   2013.6

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  • CACNA1A variants may modify the epileptic phenotype of Dravet syndrome Reviewed International journal

    Iori Ohmori, Mamoru Ouchida, Katsuhiro Kobayashi, Yoshimi Jitsumori, Akiko Mori, Hiroyuki Michiue, Teiichi Nishiki, Yoko Ohtsuka, Hideki Matsui

    NEUROBIOLOGY OF DISEASE   50   209 - 217   2013.2

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    DOI: 10.1016/j.nbd.2012.10.016

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  • High-frequency EEG oscillations in hyperthermia-induced seizures of Scn1a mutant rats. Reviewed International journal

    Katsuhiro Kobayashi, Iori Ohmori, Keiichiro Hayashi, Yuichiro Kitagawa, Mamoru Ouchida, Takushi Inoue, Yoko Ohtsuka

    Epilepsy research   103 ( 2-3 )   161 - 6   2013.2

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    DOI: 10.1016/j.eplepsyres.2012.07.020

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  • Spinal nerve injury causes upregulation of ErbB2 and ErbB3 receptors in rat dorsal root ganglia. Reviewed International journal

    Satoshi Mizobuchi, Hirotaka Kanzaki, Hiroki Omiya, Yoshikazu Matsuoka, Norihiko Obata, Ryuji Kaku, Hirochika Nakajima, Mamoru Ouchida, Kiyoshi Morita

    Journal of pain research   6   87 - 94   2013

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    It is generally known that peripheral nerve injury causes changes in expression of some growth factors in the dorsal root ganglion. Altered expression of ErbB receptors, a well-known growth factor in somatic cells, reportedly follows peripheral nerve injury in the spinal dorsal horn; however, it remains unknown whether the expression of these receptors is altered in the dorsal root ganglion after nerve injury. Therefore, this study examined the gene expression profiles of ErbB receptors in bilateral lumbar (L)4/L5 dorsal root ganglia, using L5-selective spinal nerve ligation in model rats as a peripheral nerve injury model. The expression of ErbB2 and ErbB3 was observed in the dorsal root ganglia of the mature rat, despite ErbB1 and ErbB4 showing only subtle expression. We also demonstrated that peripheral nerve injury induced significant increases in ErbB2 and ErbB3 in the ipsilateral dorsal root ganglion as compared with uninjured nerve. Expression changes in ErbB receptors appear to play important roles in nerve injury and subsequent nerve regeneration.

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  • MicroRNA-21 correlates with tumorigenesis in malignant peripheral nerve sheath tumor (MPNST) via programmed cell death protein 4 (PDCD4) Reviewed International journal

    Satoru Itani, Toshiyuki Kunisada, Yuki Morimoto, Aki Yoshida, Tsuyoshi Sasaki, Sachio Ito, Mamoru Ouchida, Shinsuke Sugihara, Kenji Shimizu, Toshifumi Ozaki

    JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY   138 ( 9 )   1501 - 1509   2012.9

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    DOI: 10.1007/s00432-012-1223-1

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  • Novel direct targets of miR-19a identified in breast cancer cells by a quantitative proteomic approach. Reviewed International journal

    Mamoru Ouchida, Hirotaka Kanzaki, Sachio Ito, Hiroko Hanafusa, Yoshimi Jitsumori, Seiji Tamaru, Kenji Shimizu

    PloS one   7 ( 8 )   e44095   2012.8

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  • Genetic risk of hepatocellular carcinoma in patients with hepatitis C virus: A case control study Reviewed International journal

    Takeshi Tomoda, Kazuhiro Nouso, Akiko Sakai, Mamoru Ouchida, Sayo Kobayashi, Koji Miyahara, Hideki Onishi, Shinichiro Nakamura, Kazuhide Yamamoto, Kenji Shimizu

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   27 ( 4 )   797 - 804   2012.4

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    DOI: 10.1111/j.1440-1746.2011.06948.x

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  • Different Responses to 5-fluoraouracil in Mutagenicity and Gene Expression between Two Human Lymphoblastoid Cell Lines with or without TP53 Mutation Reviewed

    Hiroaki Oka, Mamoru Ouchida, Takuya Kondo, Fumio Morita, Kenji Shimizu

    ACTA MEDICA OKAYAMA   66 ( 2 )   119 - 129   2012.4

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  • Expression changes of the neuregulin 1 isoforms in neuropathic pain model rats. Reviewed International journal

    Kanzaki H, Mizobuchi S, Obata N, Itano Y, Kaku R, Tomotsuka N, Nakajima H, Ouchida M, Nakatsuka H, Maeshima K, Morita K

    Neuroscience letters   508 ( 2 )   78 - 83   2012.2

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    The neuregulin1 (Nrg1) gene that is expressed in the dorsal root ganglion (DRG) contains an EGF-like domain, which is known to be a direct ligand for ErbB3 and ErbB4. Multiple splice variants of the Nrg1 gene are broadly classified into 3 groups by structural features (type I, type II and type III) and their functions differ in various tissues. The Nrg1 gene has emerged as a key mediator of axon-Schwann cell interactions and as a regulator of Schwann cell development. The Nrg1 gene is indicated as a promising growth factor for neuronal development. However, the function of the Nrg1 in pain has not been clarified. We therefore, examined the expression profiles of each type of the Nrg1 transcript in the bilateral L4/L5 DRGs using L5 spinal nerve ligation (SNL) model rats and complete Freund's adjuvant (CFA) model rats. Behavior tests have shown typical mechanical hyperalgesia in both the L5SNL model and the CFA model. In the L5SNL model, expression of the Nrg1 type I and type II were significantly increased in the L5 DRG. On the other hand, the expression of the Nrg1 type III was decreased in the L5 DRG. We demonstrated that the expression changes of the Nrg1 isoforms in the ipsilateral DRGs were preferentially related to the response to nerve injury. Our findings suggest that the aberrant expression may play an important role in nerve injury, regeneration and subsequent neuropathic pain on the L5SNL.

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  • Eradication of hepatitis C virus subgenomic replicon by interferon results in aberrant retinol-related protein expression. Reviewed

    Kazuko Koike, Akinobu Takaki, Nobuyuki Kato, Mamoru Ouchida, Hirotaka Kanzaki, Tetsuya Yasunaka, Hidenori Shiraha, Yasuhiro Miyake, Kazuhide Yamamoto

    Acta medica Okayama   66 ( 6 )   461 - 8   2012

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    Hepatitis C virus (HCV) infection induces several changes in hepatocytes, such as oxidative stress, steatosis, and hepatocarcinogenesis. Although considerable progress has been made during recent years, the mechanisms underlying these functions remain unclear. We employed proteomic techniques in HCV replicon-harboring cells to determine the effects of HCV replication on host-cell protein expression. We examined two-dimensional electrophoresis (2-DE) and mass spectrometry to compare and identify differentially expressed proteins between HCV subgenomic replicon-harboring cells and their "cured" cells. One of the identified proteins was confirmed using enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Full-length HCV genome RNA replicating and cured cells were also assessed using ELISA. Replicon-harboring cells showed higher expression of retinal dehydrogenase 1 (RALDH-1), which converts retinol to retinoic acid, and the cured cells showed higher expression of retinol-binding protein (RBP), which transports retinol from the liver to target tissues. The alteration in RBP expression was also confirmed by ELISA and Western blot analysis. We conclude that protein expression profiling demonstrated that HCV replicon eradication affected retinol-related protein expression.

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  • Antinociceptive effects of intrathecal landiolol injection in a rat formalin pain model. Reviewed

    Satoshi Mizobuchi, Yoshikazu Matsuoka, Norihiko Obata, Ryuji Kaku, Yoshitaro Itano, Naoto Tomotsuka, Arata Taniguchi, Hiroyuki Nishie, Hirotaka Kanzaki, Mamoru Ouchida, Kiyoshi Morita

    Acta medica Okayama   66 ( 3 )   285 - 9   2012

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    Perioperative beta-blocker administration has recently been recommended for patients undergoing cardiac or other surgery due to the beneficial cardiovascular effects of these agents. In addition, some studies have reported that perioperatively administered beta-blockers also have analgesic effects. In this study, to investigate the antinociceptive effects and the analgesic profile of landiolol, we examined the effects of intrathecal landiolol administration on nociceptive pain behavior and c-fos mRNA expression (a neural marker of pain) in the spinal cord using a rat formalin model. We found that pain-related behavior was inhibited by intrathecal landiolol administration. Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls. Thus, intrathecal administration of landiolol exhibited antinociceptive effects. Further investigation of the antinociceptive mechanism of landiolol is required.

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  • DNA repair/replication gene polymorphism and gastroenterological cancer risk Reviewed

    T. Sonoyama, H. Kato, A. Sakai, Y. Yasuda, M. Ouchida, K. Yamamoto, K. Shimizu

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   26   225 - 225   2011.10

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  • Dravet syndrome with an exceptionally good seizure outcome in two adolescents Reviewed International journal

    Katsuhiro Kobayashi, Iori Ohmori, Mamoru Ouchida, Yoko Ohtsuka

    EPILEPTIC DISORDERS   13 ( 3 )   340 - 344   2011.9

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    DOI: 10.1684/epd.2011.0453

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  • Identification of direct targets for the miR-17-92 cluster by proteomic analysis Reviewed International journal

    Hirotaka Kanzaki, Sachio Ito, Hiroko Hanafusa, Yoshimi Jitsumori, Seiji Tamaru, Kenji Shimizu, Mamoru Ouchida

    PROTEOMICS   11 ( 17 )   3531 - 3539   2011.9

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  • The Effect of SYT-SSX and Extracellular Signal-Regulated Kinase (ERK) on Cell Proliferation in Synovial Sarcoma International journal

    Wenjuan Cai, Yan Sun, Wei Wang, Chunrong Han, Mamoru Ouchida, Wenbin Xia, Xiulan Zhao, Baocun Sun

    PATHOLOGY & ONCOLOGY RESEARCH   17 ( 2 )   357 - 367   2011.6

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    DOI: 10.1007/s12253-010-9334-y

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  • TP53 codon 72 polymorphism is associated with pancreatic cancer risk in males, smokers and drinkers

    Takayuki Sonoyama, Akiko Sakai, Yuichiro Mita, Yukiko Yasuda, Hirofumi Kawamoto, Takahito Yagi, Masao Yoshioka, Tetsushige Mimura, Kei Nakachi, Mamoru Ouchida, Kazuhide Yamamoto, Kenji Shimizu

    MOLECULAR MEDICINE REPORTS   4 ( 3 )   489 - 495   2011.5

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    DOI: 10.3892/mmr.2011.449

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  • Therapy for hyperthermia-induced seizures in Scn1a mutant rats International journal

    Keiichiro Hayashi, Satoshi Ueshima, Mamoru Ouchida, Tomoji Mashimo, Teiichi Nishiki, Toshiaki Sendo, Tadao Serikawa, Hideki Matsui, Iori Ohmori

    EPILEPSIA   52 ( 5 )   1010 - 1017   2011.5

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    DOI: 10.1111/j.1528-1167.2011.03046.x

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  • Proteomic Analysis Reveals Aberrant Retinol Metabolism in Hepatitis C Virus Subgenomic Replicon-Harboring Cells

    Kazuko Koike, Akinobu Takaki, Nobuyuki Kato, Mamoru Ouchida, Tetsuya Yasunaka, Yasuhiro Miyake, Kazuhide Yamamoto

    GASTROENTEROLOGY   140 ( 5 )   S972 - S972   2011.5

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  • Decoy strategy targeting the brain-derived neurotrophic factor exon I to attenuate tactile allodynia in the neuropathic pain model of rats International journal

    Norihiko Obata, Satoshi Mizobuchi, Yoshitaro Itano, Yoshikazu Matsuoka, Ryuji Kaku, Naoto Tomotsuka, Kiyoshi Morita, Hirotaka Kanzaki, Mamoru Ouchida, Masataka Yokoyama

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   408 ( 1 )   139 - 144   2011.4

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    DOI: 10.1016/j.bbrc.2011.03.137

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  • Cumulative epigenetic abnormalities in host genes with viral and microbial infection during initiation and progression of malignant lymphoma/leukemia International journal

    Takashi Oka, Hiaki Sato, Mamoru Ouchida, Atae Utsunomiya, Tadashi Yoshino

    Cancers   3 ( 1 )   568 - 581   2011.3

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  • Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation

    Masamichi Tanaka, Kazufumi Nakamura, Kengo Fukushima Kusano, Hiroshi Morita, Keiko Ohta-Ogo, Daiji Miura, Aya Miura, Koji Nakagawa, Takeshi Tada, Masato Murakami, Nobuhiro Nishii, Satoshi Nagase, Yoshiki Hata, Kunihisa Kohno, Mamoru Ouchida, Kenji Shimizu, Chikao Yutani, Tohru Ohe, Hiroshi Ito

    Cardiovascular Pathology   20 ( 1 )   e37 - e42   2011.1

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  • Cumulative kinetics of epigenetic abnormalities during initiation and progression of Adult T-cell Leukemia/Lymphoma (ATLL).

    Oka T, Sato H, A Al-Kader L, Shinnou Y, Washio K, Takata K, Murakami I, Utsunomiya A, Ouchida M, Takahashi K, Yoshino T

    Retrovirology   8 ( Suppl 1 )   195 - 195   2011

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  • Electrophysiological properties of variant voltage-gated calcium channels in patients with epilepsy

    Iori Ohmori, Mamoru Ouchida, Haijiao Wang, Yuichiro Kitagawa, Hiroyuki Michiue, Teiichi Nishiki, Hideki Matsui

    NEUROSCIENCE RESEARCH   71   E294 - E294   2011

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  • Genetic seizure susceptibility underlying acute encephalopathies in childhood International journal

    Katsuhiro Kobayashi, Mamoru Ouchida, Akihisa Okumura, Yoshihiro Maegaki, Itsuko Nishiyama, Hideki Matsui, Yoko Ohtsuka, Iori Ohmori

    EPILEPSY RESEARCH   91 ( 2-3 )   143 - 152   2010.10

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  • A Missense Mutation of the Gene Encoding Voltage-Dependent Sodium Channel (Na(v)1.1) Confers Susceptibility to Febrile Seizures in Rats International journal

    Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Shizuka Ishihara, Takashi Yoshida, Akiko Takizawa, Megumi Kato, Masumi Hirabayashi, Masashi Sasa, Yasuo Mori, Tadao Serikawa

    JOURNAL OF NEUROSCIENCE   30 ( 16 )   5744 - 5753   2010.4

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    DOI: 10.1523/JNEUROSCI.3360-09.2010

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  • Identification of novel direct targets of miR-19a in MCF-7 breast cancer cells

    Hirotaka Kanzaki, Mamoru Ouchida, Sachio Ito, Seiji Tamaru, Hiroko Hanafusa, Yoshimi Jitsumori, Takashi Oka, Kenji Shimizu

    CANCER RESEARCH   70   2010.4

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  • Missense polymorphisms of PTPRJ and PTPN13 genes affect susceptibility to a variety of human cancers International journal

    Yuichiro Mita, Yukiko Yasuda, Akiko Sakai, Hiromasa Yamamoto, Shinichi Toyooka, Mehmet Gunduz, Shunsuke Tanabe, Yoshio Naomoto, Mamoru Ouchida, Kenji Shimizu

    JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY   136 ( 2 )   249 - 259   2010.2

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  • Frequent methylation of RASSF1A in synovial sarcoma and the anti-tumor effects of 5-aza-2'-deoxycytidine against synovial sarcoma cell lines International journal

    Kunihiko Numoto, Aki Yoshida, Shinsuke Sugihara, Toshiyuki Kunisada, Yuki Morimoto, Yasushi Yoneda, Yasuko Fujita, Keiichiro Nishida, Mamoru Ouchida, Toshifumi Ozaki

    JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY   136 ( 1 )   17 - 25   2010.1

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  • Multi-Step Aberrant CpG Island Hyper-Methylation Is Associated with the Progression of Adult T-Cell Leukemia/Lymphoma International journal

    Hiaki Sato, Takashi Oka, Yoko Shinnou, Takami Kondo, Kana Washio, Masayuki Takano, Katsuyoshi Takata, Toshiaki Morito, Xingang Huang, Maiko Tamura, Yuta Kitamura, Nobuya Ohara, Mamoru Ouchida, Koichi Ohshima, Kenji Shimizu, Mitsune Tanimoto, Kiyoshi Takahashi, Masao Matsuoka, Atae Utsunomiya, Tadashi Yoshino

    AMERICAN JOURNAL OF PATHOLOGY   176 ( 1 )   402 - 415   2010.1

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  • Multi-step accumulation of aberrant CpG island hypermethylation in specific genes promotes development and progression of lymphomas/leukemias

    Takashi Oka, Hiaki Sato, Takami Kondo, Yoko Shinnou, Kana Washio, Ichiro Murakami, A. B. D. Al-Kader Lamia, Xu Sun, Katsuyoshi Takata, Mamoru Ouchida, Koichi Ohshima, Mitsune Tanimoto, Atae Utsunomiya, Kiyoshi Takahashi, Tadashi Yoshino

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   26 ( Sup1 )   S44 - S44   2010

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  • A CACNB4 mutation shows altered Cav2.1 function in a patient with Dravet syndrome

    大守伊織, 大内田守, 御牧信義, 西木禎一, 富澤一仁, 松井秀樹

    岡山医学会雑誌   121 ( 3 )   149 - 156   2010

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  • Helicobacter pylori infection induce accumulation of aberrant CpG hypermethylation to promote development and progression of gastric MALT lymphoma

    Takashi Oka, Takami Kondo, Hiaki Sat, Yoko Shinnou, Kana Washio, Toshiaki Morit, Katsuyoshi Takat, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshin

    Proceedings of The 3rd International Symposium for Future Technology Creating Better Human Health and Society Comprehensive Approach to Cancer and Infectious Diseases   1 ( 1 )   105 - 105   2010

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  • REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells International journal

    Jie Chen, Masami Watanabe, Peng Huang, Masakiyo Sakaguchi, Kazuhiko Ochiai, Yasutomo Nasu, Mamoru Ouchida, Nam-Ho Huh, Kenji Shimizu, Yuji Kashiwakura, Haruki Kaku, Hiromi Kumon

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   24 ( 6 )   789 - 794   2009.12

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  • Dravet症候群患者に認められたカルシウムチャネル機能異常を引き起こすCACNB4遺伝子変異

    大守 伊織, 大内田 守, 御牧 信義, 西木 禎一, 富澤 一仁, 松井 秀樹

    岡山医学会雑誌   121 ( 3 )   149 - 156   2009.12

  • Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma International journal

    Takami Kondo, Takashi Oka, Hiaki Sato, Yoko Shinnou, Kana Washio, Masayuki Takano, Toshiaki Morito, Katsuyoshi Takata, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshino

    INTERNATIONAL JOURNAL OF ONCOLOGY   35 ( 3 )   547 - 557   2009.9

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  • Identification of novel target proteins for miR-17-92 cluster by proteomic analysis

    Hirotaka Kanzaki, Mamoru Ouchida, Sachio Ito, Seiji Tamaru, Hiroko Hanafusa, Kenji Shimizu

    CANCER RESEARCH   69   2009.5

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  • MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors International journal

    Takafumi Kubo, Hiromasa Yamamoto, William W. Lockwood, Ilse Valencia, Junichi Sob, Michael Peyton, Masaru Jida, Hiroki Otani, Tetsuva Fujii, Mamoru Ouchida, Nagio Takigawa, Katsuyuki Kiura, Kenji Shimizu, Hiroshi Date, John D. Minna, Marileila Varella-Garcia, Wan L. Lam, Adi F. Gazdar, Shinichi Toyooka

    INTERNATIONAL JOURNAL OF CANCER   124 ( 8 )   1778 - 1784   2009.4

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  • Hyperthermia-induced seizure-susceptible rats: a novel model of febrile seizures

    Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Yasuo Mori, Tadao Serikawa

    NEUROSCIENCE RESEARCH   65   S47 - S47   2009

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  • REIC/Dkk-3 in normal fibroblasts suppresses tumor growth via induction of interleukin-7.

    Chen J, Watanabe M, Huang P, Sakaguchi M, Ochiai K, Nasu Y, Ouchida M, Huh NH, Shimizu K, Kashiwakura Y, Kaku H, Kumon H

    Int J Mol Med   24 ( 6 )   789 - 794   2009

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  • Ca(v)2.1 DYSFUNCTION MAY BE A GENETIC MODIFIER OF SEVERE MYOCLONIC EPILEPSY IN INFANCY

    Iori Ohmori, Mamoru Ouchida, Takafumi Miki, Nobuyoshi Mimaki, Shigeki Kiyonaka, Teiichi Nishiki, Kazuhito Tomizawa, Yasuo Mori, Hideki Matsui

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   515 - 515   2009

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  • A CACNB4 mutation shows that altered Ca(v)2.1 function may be a genetic modifier of severe myoclonic epilepsy in infancy International journal

    Iori Ohmori, Mamoru Ouchida, Takafumi Miki, Nobuyoshi Mimaki, Shigeki Kiyonaka, Teiichi Nishiki, Kazuhito Tomizawa, Yasuo Mori, Hideki Matsui

    NEUROBIOLOGY OF DISEASE   32 ( 3 )   349 - 354   2008.12

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  • PROTEOMICS-BASED ANALYSIS OF INVASION-RELATED PROTEINS IN MALIGNANT GLIOMAS

    T. Maruo, T. Ichikawa, H. Kanzaki, M. Onishi, S. Inoue, K. Yoshida, H. Kambara, M. Ouchida, K. Shimizu, I. Date

    NEURO-ONCOLOGY   10 ( 6 )   1143 - 1143   2008.12

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  • EGFR変異とUracil-Tegafurによる肺腺癌術後補助療法の関連性についての検討

    末久 弘, 豊岡 伸一, 堀田 勝幸, 内田 亜希子, 宗 淳一, 藤原 義朗, 松尾 恵太郎, 大内田 守, 高田 穣, 木浦 勝行, 伊達 洋至

    岡山医学会雑誌   120 ( 3 )   265 - 269   2008.12

  • Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome

    Kazufumi Nakamura, Daiji Miura, Kaoru Kobayashi, Mamoru Ouchida, Kenji Shimizu, Iori Ohmori, Nobuhiro Nishii, Satoshi Nagase, Hiroshi Morita, Yoshiki Hata, Takefumi Oka, Kengo Kusano, Tohru Ohe

    CIRCULATION   118 ( 18 )   S981 - S981   2008.10

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  • Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome

    Kazufumi Nakamura, Daiji Miura, Kaoru Kobayashi, Mamoru Ouchida, Kenji Shimizu, Lori Ohmorl, Nobuhiro Nishii, Satoshi Nagase, Hiroshi Morita, Yoshiki Hata, Takefumi Oka, Kengo Kusano, Tohru Ohe

    CIRCULATION   118 ( 18 )   S1485 - S1485   2008.10

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  • The allelic distribution of a single nucleotide polymorphism in the PDCD5 gene locus of Japanese non-small cell lung cancer patients. Reviewed

    Nanba K, Toyooka S, Soh J, Tsukuda K, Yamamoto H, Sakai A, Ouchida M, Kobayashi N, Matsuo K, Koide N, Kusaka K, Shimizu K, Date H

    Molecular medicine reports   1   667 - 671   2008.9

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  • Single nucleotide polymorphism in reuced folate carrier-1 gene and methyleneterathydrofolate reductase gene in patients with osteosarcoma

    Y. Morimoto, A. Yoshida, M. Ouchida, T. Kunisada, K. Shimizu, T. Ozaki

    EJC SUPPLEMENTS   6 ( 9 )   117 - 118   2008.7

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 守都 敏晃, 大原 信哉, 大内田 守, 大島 孝一, 谷本 光音, 宇都宮 與, 高橋 聖之, 吉野 正

    日本リンパ網内系学会会誌   48   85 - 85   2008.5

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  • A screening test for the prediction of Dravet syndrome before one year of age International journal

    Junri Hattori, Mamoru Ouchida, Junko Ono, Susumu Miyake, Satoshi Maniwa, Nobuyoshi Mimaki, Yoko Ohtsuka, Iori Ohmori

    EPILEPSIA   49 ( 4 )   626 - 633   2008.4

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    DOI: 10.1111/j.1528-1167.2007.01475.x

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  • Rasmussen encephalitis associated with SCN1A mutation International journal

    Iori Ohmori, Mamoru Ouchida, Katsuhiro Kobayashi, Yoshimi Jitsumori, Takushi Inoue, Kenji Shimizu, Hideki Matsui, Yoko Ohtsuka, Yoshihiro Maegaki

    EPILEPSIA   49 ( 3 )   521 - 526   2008.3

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    DOI: 10.1111/j.1528-1167.2007.01411.x

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  • The association between RAD18 Arg302Gln polymorphism and the risk of human non-small-cell lung cancer International journal

    Hirotaka Kanzaki, Mamoru Ouchida, Hiroko Hanafusa, Hiromasa Yamamoto, Hiromitsu Suzuki, Masaaki Yano, Motoi Aoe, Kazue Imai, Hiroshi Date, Kei Nakachi, Kenji Shimizu

    JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY   134 ( 2 )   211 - 217   2008.2

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  • Decreased expression of the SIN3A gene, a candidate tumor suppressor located at the prevalent allelic loss region 15q23 in non-small cell lung cancer International journal

    Hiromitsu Suzuki, Mamoru Ouchida, Hiromasa Yamamoto, Masaaki Yano, Shinichi Toyooka, Motoi Aoe, Nobuyoshi Shimizu, Hiroshi Date, Kenji Shimizu

    LUNG CANCER   59 ( 1 )   24 - 31   2008.1

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  • Increased DOI-induced wet-dog shakes in adrenocorticotropic hormone-treated rats are not affected by chronic imipramine treatment: Possible involvement of enhanced 5-HT2A-receptor expression in the frontal cortex

    Yoshihisa Kitamura, Kazuhiko Shibata, Kozue Akiyama, Shizue Kirnoto, Yoshika Fujitani, Kouhei Kitagawa, Hirotaka Kanzaki, Mamoru Ouchida, Kenji Shimizu, Hiromu Kawasaki, Toshiaki Sendo, Yutaka Gomita

    JOURNAL OF PHARMACOLOGICAL SCIENCES   106 ( 1 )   100 - 106   2008.1

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    DOI: 10.1254/jphs.FP0071615

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  • Single nucleotide polymorphism in the RAD18 gene and risk of colorectal cancer in the Japanese population International journal

    Hirotaka Kanzaki, Mamoru Ouchida, Hiroko Hanafusa, Akiko Sakai, Hiromasa Yamamoto, Hiromitsu Suzuki, Masaaki Yano, Motoi Aoe, Kazue Imai, Hiroshi Date, Kei Nakachi, Kenji Shimizu

    ONCOLOGY REPORTS   18 ( 5 )   1171 - 1175   2007.11

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  • EGFR変異とUFTによる肺腺癌術後補助療法の関連性についての検討

    末久 弘, 豊岡 伸一, 堀田 勝幸, 内田 亜希子, 宗 淳一, 藤原 義朗, 松尾 恵太郎, 大内田 守, 高田 穣, 木浦 勝行, 伊達 洋至

    肺癌   47 ( 5 )   513 - 513   2007.10

  • Epidermal growth factor receptor mutation status and adjuvant chemotherapy with uracil-tegafur for adenocarcinoma of the lung International journal

    Hiroshi Suehisa, Shinichi Toyooka, Katsuyuki Hotta, Akiko Uchida, Junichi Soh, Yoshiro Fujiwara, Keitaro Matsuo, Mamoru Ouchida, Minoru Takata, Katsuyuki Kiura, Hiroshi Date

    JOURNAL OF CLINICAL ONCOLOGY   25 ( 25 )   3952 - 3957   2007.9

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    DOI: 10.1200/JCO.2007.11.8646

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  • Accumulating DNA methylation in background mucosa plays a role in esophageal squamous cell carcinogenesis

    Ishii Tatsuhiro, Murakami Jun, Notohara Kenji, Sasamoto Hiromi, Kambara Takeshi, Shirakawa Yasuhiro, Naomoto Yoshio, Ouchida Mamoru, Shimizu Kenji, JASS Jeremy R., Matsubara Nagahide, Tanaka Noriaki

    Okayama Igakkai Zasshi (Journal of Okayama Medical Association)   119 ( 2 )   113 - 117   2007.9

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    DOI: 10.4044/joma.119.113

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  • T75M-KCNJ2 mutation causing Andersen-Tawil syndrome enhances inward rectification by changing Mg2+ sensitivity International journal

    Yoshinori Tani, Daiji Miura, Junko Kurokawa, Kazufumi Nakamura, Mamoru Ouchida, Kenji Shimizu, Tohru Ohe, Tetsushi Furukawa

    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY   43 ( 2 )   187 - 196   2007.8

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    DOI: 10.1016/j.yjmcc.2007.05.005

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  • Epigenetically distinct malignant cell population forms lymphoma-involving lesions in acute type adult T cell Leukemia/Lymphoma (ATLL)

    Takashi Oka, Hiaki Sato, Yoko Nakatani, Takami Kondo, Kana Washio, Masayuki Takano, Ichiro Murakami, Nobuya Ohara, Mamoru Ouchida, Koichi Ohshima, Kenji Shimizu, Mitsune Tanimoto, Kiyoshi Takahashi, Atae Utsunomiya, Tadashi Yoshino

    AIDS RESEARCH AND HUMAN RETROVIRUSES   23 ( 4 )   627 - 628   2007.4

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  • The effect of gefitinib on B-RAF mutant non-small cell lung cancer and transfectants International journal

    Shinichi Toyooka, Akiko Uchida, Hisayuki Shigematsu, Junichi Soh, Atsuko Ogino, Minoru Takata, Katsuyuki Kiura, Mamoru Ouchida, Takayuki Kosaka, Motoi Aoe, Tetsuya Mitsudomi, Hiroshi Date

    JOURNAL OF THORACIC ONCOLOGY   2 ( 4 )   321 - 324   2007.4

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    DOI: 10.1097/01.JTO.0000263716.92191.be

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  • Oesophageal squamous cell carcinoma may develop within a background of accumulating DNA methylation in normal and dysplastic mucosa

    T. Ishii, J. Murakami, K. Notohara, H. M. Cullings, H. Sasamoto, T. Kambara, Y. Shirakawa, Y. Naomoto, M. Ouchida, K. Shimizu, N. Tanaka, J. R. Jass, N. Matsubara

    GUT   56 ( 1 )   13 - 19   2007.1

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    DOI: 10.1136/gut.2005.089813

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  • Anti-tumor effect of bisphosphonate (YM529) on non-small cell lung cancer cell lines International journal

    Ryuichiro Koshimune, Motoi Aoe, Shinichi Toyooka, Fumikata Hara, Mamoru Ouchida, Masaki Tokumo, Yoshifumi Sano, Hiroshi Date, Nobuyoshi Shimizu

    BMC CANCER   7 ( 8 )   1 - 8   2007.1

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    DOI: 10.1186/1471-2407-7-8

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  • Loss or down-regulation of HLA class I expression at the allelic level in freshly isolated leukemic blasts International journal

    Kozo Masuda, Akio Hiraki, Nobuharu Fujii, Toshiyuki Watanabe, Motoyuki Tanaka, Kosei Matsue, Yoichiro Ogama, Mamoru Ouchida, Kenji Shimizu, Kazuma Ikeda, Mitsune Tanimoto

    CANCER SCIENCE   98 ( 1 )   102 - 108   2007.1

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    DOI: 10.1111/j.1349-7006.2006.00356.x

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  • SCN1A missense mutation associated with infantile partial epilepsy

    Iori Ohmori, Mamoru Ouchida, Katsuhiro Kobayashi, Yoko Ohtsuka, Kenji Shimizu, Teiichi Nishiki, Kazuhito Tomizawa, Hideki Matsui

    NEUROSCIENCE RESEARCH   58   S187 - S187   2007

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  • HIGH FREQUENT GENE SILENCING OF HEMETOPOIETIC CELL SPECIFIC PROTEIN TYROSINEPHOSPHATASE SHP1 IN HEMETOPOIETIC CELL MALIGNANCIES.

    Oka T, Ouchida M, Tanimoto M, Shimizu K, Yoshino T

    International Journal of Medical and Biological Frontiers   11   11 - 42   2007

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  • The role of angiotensin type 2 receptor (AT2R) on nerve growth factor (NGF) induced-reinnervation of perivascular nerves

    Namika Yoshida, ayako Yokomizo, Mitsuhiro Goda, Mamoru Ouchida, Kenji Simizu, Fusako Takayama, Hiromu Kawasaki

    JOURNAL OF PHARMACOLOGICAL SCIENCES   103   219P - 219P   2007

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype(CIMP)の解析

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 高野正幸, 大原信哉, 大内田守, 大島孝一, 宇都宮與, 高橋聖之, 高橋聖之, 吉野正

    日本病理学会会誌   96 ( 1 )   2007

  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態・臨床症状との相関

    佐藤妃映, 佐藤妃映, 岡剛史, 近藤孝美, 高野正幸, 神農陽子, 鷲尾佳奈, 高田尚良, 守都敏晃, 大原信哉, 大内田守, 大島孝一, 谷本光音, 宇都宮與, 高橋聖之, 吉野正

    日本リンパ網内系学会会誌   47   2007

  • Highly frequent allelic loss of chromosome 6q16-23 in osteosarcoma: Involvement of cyclin C in osteosarcoma International journal

    Norihide Ohata, Sachio Ito, Aki Yoshida, Toshiyuki Kunisada, Kunihiko Numoto, Yoshimi Jitsumori, Hirotaka Kanzaki, Toshifumi Ozaki, Kenji Shimizu, Mamoru Ouchida

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   18 ( 6 )   1153 - 1158   2006.12

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  • Multiple splicing variants of Naf1/ABIN-1 transcripts and their alterations in hematopoietic tumors International journal

    Yasuhiro Shiote, Mamoru Ouchida, Yoshimi Jitsumori, Yoichiro Ogama, Yoshinobu Matsuo, Fumihiko Ishimaru, Mitsune Tanimoto, Kenji Shimizu

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   18 ( 5 )   917 - 923   2006.11

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  • Single nucleotide polymorphism of the AXIN2 gene is preferentially associated with human lung cancer risk in a Japanese population International journal

    Hirotaka Kanzaki, Mamoru Ouchida, Hiroko Hanafusa, Masaaki Yano, Hiromitsu Suzuki, Motoi Aoe, Kazue Imai, Nobuyoshi Shimizu, Kei Nakachi, Kenji Shimizu

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   18 ( 2 )   279 - 284   2006.8

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  • Presence of epidermal growth factor receptor gene T790M mutation as a minor clone in non-small cell lung cancer International journal

    Michio Inukai, Shinichi Toyooka, Sachio Ito, Hiroaki Asano, Shuji Ichihara, Junichi Soh, Hiroshi Suehisa, Mamoru Ouchida, Keisuke Aoe, Motoi Aoe, Katsuyuki Kiura, Nobuyoshi Shimizu, Hiroshi Date

    CANCER RESEARCH   66 ( 16 )   7854 - 7858   2006.8

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    DOI: 10.1158/0008-5472.CAN-06-1951

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  • カルバマゼピン投与ラットにおける血中と肝臓中の産生CYPmRNA量の相関性の検討

    林瑶子, 北村佳久, 大内田守, 清水憲二, 千堂年昭, 五味田裕

    TDM研究   23 ( 3 )   S165   2006.7

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  • Single nucleotide polymorphism at codon 133 of the RASSF1 gene is preferentially associated with human lung adenocarcinoma risk International journal

    Hirotaka Kanzaki, Hiroko Hanafusa, Hiromasa Yamamoto, Yukiko Yasuda, Kazue Imai, Masaaki Yano, Motoi Aoe, Nobuyoshi Shimizu, Kei Nakachi, Mamoru Ouchida, Kenji Shimizu

    CANCER LETTERS   238 ( 1 )   128 - 134   2006.7

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    DOI: 10.1016/j.canlet.2005.07.006

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  • Molecular pathological analysis of the protein tyrosine phosphatase: SHP1 gene in the pathogenesis of lymphoma and leukemias

    Takashi Oka, Yoko Nakatani, Takami Kondo, Hiaki Sato, Kana Washio, Masayuki Takano, Ichirou Murakami, Yuriko Nishikawa, Mamoru Ouchida, Nobuya Ohara, Kiyoshi Takahashi, Kazuhiko Hayashi, Mitsune Tanimoto, Kenji Shimizu, Tadashi Yoshino

    CANCER RESEARCH   66 ( 8 )   2006.4

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  • Abberant DNA methylation in the progression of adult T cell leukemia/lymphoma (ATLL)

    Hiaki Sato, Takashi Oka, Yoko Nakatani, Takami Kondo, Masayuki Takano, Nobuya Ohara, Mamoru Ouchida, Kouichi Oshima, Kenji Shimizu, Mitsune Tanimoto, Kiyoshi Tkahashi, Yoshino Tadashi

    CANCER RESEARCH   66 ( 8 )   2006.4

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  • Identification of a candidate tumor suppressor gene RHOBTB1 located at a novel allelic loss region 10q21 in head and neck cancer International journal

    LB Beder, M Gunduz, M Ouchida, E Gunduz, A Sakai, K Fukushima, H Nagatsuka, S Ito, N Honjo, K Nishizaki, K Shimizu

    JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY   132 ( 1 )   19 - 27   2006.1

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    DOI: 10.1007/s00432-005-0033-0

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  • Detection of EGFR gene mutation in lung cancer by mutant-enriched polymerase chain reaction assay International journal

    H Asano, S Toyooka, M Tokumo, K Ichimura, K Aoe, S Ito, K Tsukuda, M Ouchida, M Aoe, H Katayama, A Hiraki, K Sugi, K Kiura, H Date, N Shimizu

    CLINICAL CANCER RESEARCH   12 ( 1 )   43 - 48   2006.1

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    DOI: 10.1158/1078-0432.CCR-05-0934

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  • 異常メチル化によるSHP1 gene silencingと悪性リンパ腫・白血病発症機構

    岡剛史, 中谷陽子, 近藤孝美, 佐藤妃映, 佐藤妃映, 高野正幸, 鷲尾佳奈, 大内田守, 大原信哉, 清水憲二, 谷本光音, 高橋聖之, 吉野正

    日本癌学会学術総会記事   65th   2006

  • 成人T細胞白血病/リンパ腫(ATLL)における病期の進行とDNAメチル化の関連

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 高野正幸, 大原信哉, 大内田守, 宇都宮こう, 大島孝一, 高橋聖之, 吉野正

    日本病理学会会誌   95 ( 1 )   2006

  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype(CIMP)

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 大原信哉, 大内田守, 大島孝一, 谷本光音, 高橋聖之, 吉野正

    日本リンパ網内系学会会誌   46   2006

  • SHP1遺伝子発現抑制と悪性リンパ腫・白血病発症機構の解析

    岡剛史, 大内田守, 中谷陽子, 近藤孝美, 佐藤妃映, 佐藤妃映, 鷲尾佳奈, 高野正幸, 村上一郎, 大原信哉, 高橋聖之, 吉野正

    日本病理学会会誌   95 ( 1 )   2006

  • Heparanase is involved in angiogenesis in esophageal cancer through induction of cyclooxygenase-2 International journal

    T Okawa, Y Naomoto, T Nobuhisa, M Takaoka, T Motoki, Y Shirakawa, T Yamatsuji, H Inoue, M Ouchida, M Gunduz, M Nakajima, N Tanaka

    CLINICAL CANCER RESEARCH   11 ( 22 )   7995 - 8005   2005.11

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    DOI: 10.1158/1078-0432.CCR-05-1103

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  • Deletional Mapping of 2q21-37 Region in Oral Cancer(International Symposium of Maxillofacial and Oral Regenerative Biology in Okayama 2005)

    Cengiz Beyhan, Gunduz Mehmet, Gunduz Esra, Ouchida Mamoru, Shimizu Kenji, Inoue Tomio, Nagai Noriyuki

    Journal of hard tissue biology   14 ( 2 )   227 - 228   2005.10

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    Tumor suppressor genes are defined as genetic elements whose loss or mutational inactivation allows cells to display one or more phenotypes of neoplastic growth. Frequent deletion in a chromosomal region suggests existence of a candidate tumor suppressor gene. We analyzed Ch2q21-37.3 region by using 17 polymorphic microsatellite markers in 39 matched oral normal and cancer tissues. Loss of heterozygosity (LOH) was detected at least one location in 36 of 39 (92%) tumor tissues. High deletions were detected at microsatellite marker locations, D2S2304 (35%), D2S111 (40%), D2S155 (35%), D2S164 (29%), D2S125 (71%) and D2S140 (39%). Three frequently deleted regions at 2q22, 2q35-36 and 2q37.3 were observed. Chromosomal 2q22-37.3 region is highly populated with genes. Several candidate tumor suppressor genes in this region including such as ING5, CASP8, CASP10, PPP1R7 and BOK are located. We are currently analyzing inactivation mutations and mRNA expressions in oral squaomus cell carcinomas.

    DOI: 10.2485/jhtb.14.227

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  • Frequent deletion and down-regulation of ING4, a candidate tumor suppressor gene at 12p13, in head and neck squamous cell carcinomas International journal

    M Gunduz, H Nagatsuka, K Demircan, E Gunduz, B Cengiz, M Ouchida, H Tsujigiwa, E Yamachika, K Fukushima, L Beder, S Hirohata, Y Ninomiya, K Nishizaki, K Shimizu, N Nagai

    GENE   356   109 - 117   2005.8

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    DOI: 10.1016/j.gene.2005.02.014

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  • Mutation screen of GABRA1, GABRB2 and GABRG2 genes in Japanese patients with absence seizures International journal

    M Ito, Ohmori, I, T Nakahori, M Ouchida, Y Ohtsuka

    NEUROSCIENCE LETTERS   383 ( 3 )   220 - 224   2005.8

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    DOI: 10.1016/j.neulet.2005.04.017

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  • Fine deletional mapping of chromosome 4q22-35 region in oral cancer International journal

    Y Shinno, E Gunduz, M Gunduz, H Nagatsuka, H Tsujigiwa, B Cengiz, YJ Lee, R Tamamura, M Ouchida, K Fukushima, K Shimizu, N Nagai

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   16 ( 1 )   93 - 98   2005.7

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  • Significant growth suppression of synovial sarcomas by the histone deacetylase inhibitor FK228 in vitro and in vivo International journal

    T Ito, M Ouchida, Y Morimoto, A Yoshida, Y Jitsumori, T Ozaki, H Sonobe, H Inoue, K Shimizu

    CANCER LETTERS   224 ( 2 )   311 - 319   2005.6

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    DOI: 10.1016/j.canlet.2004.10.030

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  • Single nucleotide polymorphisms in the EXO1 gene and risk of colorectal cancer in a Japanese population International journal

    H Yamamoto, H Hanafusa, M Ouchida, M Yano, H Suzuki, M Murakami, M Aoe, N Shimizu, K Nakachi, K Shimizu

    CARCINOGENESIS   26 ( 2 )   411 - 416   2005.2

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    DOI: 10.1093/carcin/bgh335

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  • Aberrant promoter methylation of human DAB2 interactive protein (hDAB2IP) gene in lung cancers International journal

    M Yano, S Toyooka, K Tsukuda, H Dote, M Ouchida, T Hanabata, M Aoe, H Date, AF Gazdar, N Shimizu

    INTERNATIONAL JOURNAL OF CANCER   113 ( 1 )   59 - 66   2005.1

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    DOI: 10.1002/ijc.20531

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  • Genetic and epigenetic alterations of BRG1 promote oral cancer development International journal

    E Gunduz, M Gunduz, M Ouchida, H Nagatsuka, L Beder, H Tsujigiwa, K Fukushima, K Nishizaki, K Shimizu, N Nagai

    INTERNATIONAL JOURNAL OF ONCOLOGY   26 ( 1 )   201 - 210   2005.1

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  • 膜肉腫細胞株に対するHDAC抑制剤FK228のin vivo,in vitroにおける抗腫瘍効果の検討.

    伊藤達男, 尾崎敏文, 大内田守

    医学のあゆみ   213,12,1041-1046   2005

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  • Frequent Deletion and Down-Regulation of ING3 in Head and Neck Cancer

    Beyhan Cengiz, Mehmet Gunduz, Esra Gunduz, Mamoru Ohuchida, Kenji Shimizu, Noriyuki Nagai, Deng Chunfu, Goichi Kinoshita

    Journal of Hard Tissue Biology   14 ( 2 )   298 - 299   2005

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    DOI: 10.2485/jhtb.14.298

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  • Aberrant methylation of p57KIP2 gene in lung and breast cancers and malignant mesotheliomas International journal

    T Kobatake, M Yano, S Toyooka, K Tsukuda, H Dote, T Kikuchi, M Toyota, M Ouchida, M Aoe, H Date, HI Pass, H Doihara, N Shimizu

    ONCOLOGY REPORTS   12 ( 5 )   1087 - 1092   2004.11

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  • SYT, a partner of SYT-SSX oncoprotein in synovial sarcomas, interacts with mSin3A, a component of histone deacetylase complex International journal

    T Ito, M Ouchida, S Ito, Y Jitsumori, Y Morimoto, T Ozaki, A Kawai, H Inoue, K Shimizu

    LABORATORY INVESTIGATION   84 ( 11 )   1484 - 1490   2004.11

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    DOI: 10.1038/labinvest.3700174

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  • 高齢にて発症したQT延長症候群の1例 同一家系内で異なる発症様式を示したLQT1の1家系

    三浦 大志, 中村 一文, 久松 研一, 森田 宏, 森田 志保, 永瀬 聡, 齋藤 博則, 草野 研吾, 江森 哲郎, 大江 透, 大内田 守, 清水 憲二, 西内 崇将, 幡 芳樹, 水尾 浩三, 大杉 保

    Therapeutic Research   25 ( 11 )   2137 - 2141   2004.11

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  • Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer International journal

    M Yano, M Ouchida, H Shigematsu, N Tanaka, K Ichimura, K Kobayashi, Y Inaki, S Toyooka, K Tsukuda, N Shimizu, K Shimizu

    INTERNATIONAL JOURNAL OF CANCER   112 ( 1 )   8 - 13   2004.10

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  • Severity dependent up-regulations of LOX-1 and MCP-1 in early sclerotic changes of common carotid arteries in spontaneously hypertensive rats

    Y Hamakawa, N Omori, M Ouchida, M Nagase, K Sato, Nagano, I, M Shoji, T Fujita, K Abe

    NEUROLOGICAL RESEARCH   26 ( 7 )   767 - 773   2004.10

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  • Loss of heterozygosity on chromosome 10q associated with malignancy and prognosis in astrocytic tumors, and discovery of novel loss regions International journal

    S Daido, S Takao, T Tamiya, Y Ono, K Terada, S Ito, M Ouchida, Date, I, T Ohmoto, K Shimizu

    ONCOLOGY REPORTS   12 ( 4 )   789 - 795   2004.10

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  • Prevalent hyper-methylation of the CDH13 gene promoter in malignant B cell lymphomas International journal

    Y Ogama, M Ouchida, T Yoshino, S Ito, H Takimoto, Y Shiote, F Ishimaru, M Harada, M Tanimoto, K Shimizu

    INTERNATIONAL JOURNAL OF ONCOLOGY   25 ( 3 )   685 - 691   2004.9

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  • Positive correlation between allelic loss at chromosome 14q24-31 and poor prognosis of patients with renal cell carcinoma International journal

    H Kaku, S Ito, S Ebara, M Ouchida, Y Nasu, T Tsushima, H Kumon, K Shimizu

    UROLOGY   64 ( 1 )   176 - 181   2004.7

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    DOI: 10.1016/j.urology.2004.03.015

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  • Aberrant promoter methylation in human DAB2 interactive protein (hDAB2IP) gene in breast cancer International journal

    H Dote, S Toyooka, K Tsukuda, M Yano, M Ouchida, H Doihara, M Suzuki, H Chen, JT Hsieh, AF Gazdar, N Shimizu

    CLINICAL CANCER RESEARCH   10 ( 6 )   2082 - 2089   2004.3

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    DOI: 10.1158/1078-0432.CCR-03-0236

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  • Establishment and characterization of a biphasic synovial sarcoma cell line, SYO-1 International journal

    A Kawai, N Naito, A Yoshida, Y Morimoto, M Ouchida, K Shimizu, Y Beppu

    CANCER LETTERS   204 ( 1 )   105 - 113   2004.2

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  • 高齢にて発症したQT延長症候群の一例

    三浦大志, 中村一文, 久松研一, 森田宏, 森田志保, 永瀬聡, 齋藤博則, 草野研吾, 江森哲朗, 大江透, 大内田 守, 清水憲二, 西内崇将, 幡芳樹, 水尾浩三, 大杉保

    Therapeutic Research   68 ( Suppl.III )   946 - 946   2004

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  • Activated proliferation of B-cell lymphomas/leukemias with the SHP1 gene silencing by aberrant CpG methylation International journal

    M Koyama, T Oka, M Ouchida, Y Nakatani, R Nishiuchi, T Yoshino, K Hayashi, T Akagi, Y Seino

    LABORATORY INVESTIGATION   83 ( 12 )   1849 - 1858   2003.12

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    DOI: 10.1097/01.LAB.0000106503.65258.2B

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  • Frequent deletion and increased mRNA expression of a candidate tumor suppressor gene at 19p13 region, BRG1, in oral cancers(2nd ASIAN SCIENCE SEMINAR IN OKAYAMA 2003)

    Gunduz Esra, Gunduz Mehmet, Nagatsuka Hitoshi, Tsujigiwa Hidetsugu, Ouchida Mamoru, Shinnou Yasuo, Cengiz Beyhan, Shimizu Kenji, Nagai Noriyuki

    Journal of hard tissue biology   12 ( 2 )   73 - 73   2003.12

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  • Single nucleotide polymorphism in fibroblast growth factor receptor 4 at codon 388 is associated with prognosis in high-grade soft tissue sarcoma International journal

    Y Morimoto, T Ozaki, M Ouchida, N Umehara, N Ohata, A Yoshida, K Shimizu, H Inoue

    CANCER   98 ( 10 )   2245 - 2250   2003.11

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  • 現代医学の焦点(254)広範な悪性リンパ腫・白血病発症に関連するSHP1遺伝子に関する最新知見

    岡 剛史, 大内田 守

    日本臨床   61 ( 11 )   2025 - 2032   2003.11

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  • [Recent progress in the protein-tyrosine phosphatase SHP1 gene: the significant correlation of the SHP1 gene silencing with the onset of lymphomas/leukemias].

    Takashi Oka, Mamoru Ouchida

    Nihon rinsho. Japanese journal of clinical medicine   61 ( 11 )   2025 - 32   2003.11

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    Using cDNA expression array and tissue microarray, we comprehensively and systematically analyzed the expression profile to investigate the lymphomagenesis. We detected the significant decrease of hematopoietic cell specific protein-tyrosine phosphatase SHP1 gene expression in various malignant lymphomas and leukemias. High-frequent silencing of the SHP1 gene by promoter methylation was detected in various kinds of leukemias and lymphomas as well as in many hematopoietic cell lines. The promoter methylation of the SHP1 gene was significantly correlated with the clinical stage. Loss of heterozygosity with microsatellite markers around the SHP1 gene was detected in 79% of informative ALL cases. These results suggest that loss of functional SHP1 is closely associated with the pathogenesis of leukemias/lymphomas.

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  • Is phenotype difference in severe myoclonic epilepsy in infancy related to SCN1A mutations? International journal

    Ohmori, I, Y Ohtsukaa, M Ouchida, T Ogino, S Maniwa, K Shimizu, E Oka

    BRAIN & DEVELOPMENT   25 ( 7 )   488 - 493   2003.10

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    DOI: 10.1016/S0387-7604(03)00038-X

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  • Paroxysmal movement disorders in severe myoclonic epilepsy in infancy International journal

    Y Ohtsuka, Ohmori, I, T Ogino, M Ouchida, K Shimizu, E Oka

    BRAIN & DEVELOPMENT   25 ( 6 )   401 - 405   2003.9

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    DOI: 10.1016/S0387-7604(03)00025-1

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  • Detection of codon 61 point mutations of the K-ras gene in lung and colorectal cancers by enriched PCR

    S Toyooka, K Tsukuda, M Ouchida, M Tanino, Y Inaki, K Kobayashi, M Yano, J Soh, T Kobatake, N Shimizu, K Shimizu

    ONCOLOGY REPORTS   10 ( 5 )   1455 - 1459   2003.9

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  • Splicing isoform of SYT-SSX fusion protein accelerates transcriptional activity and cell proliferation International journal

    Y Morimoto, M Ouchida, T Ozaki, A Kawai, T Ito, A Yoshida, H Inoue, K Shimizu

    CANCER LETTERS   199 ( 1 )   35 - 43   2003.9

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    DOI: 10.1016/S0304-3835(03)00314-8

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  • Genome-wide analyses on loss of heterozygosity in head and neck squamous cell carcinomas International journal

    LB Beder, M Gunduz, M Ouchida, K Fukushima, E Gunduz, S Ito, A Sakai, N Nagai, K Nishizaki, K Shimizu

    LABORATORY INVESTIGATION   83 ( 1 )   99 - 105   2003.1

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  • 難治性リンパ腫発症関連遺伝子SHP1に関する最新知見

    岡 剛史, 大内田守

    日本臨床   61(11): 2025-2032   2003

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  • Significant correlation of the SCN1A mutations and severe myoclonic epilepsy in infancy.

    Iori Ohmori, Mamoru Ouchida, Yoko Ohtsuka, Eiji Oka, Kenji Shimizu

    Review Series Neurology,   2, 14-17   2003

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  • Gene silencing of the tyrosine phosphatase SHP1 gene by aberrant methylation in leukemias/lymphomas. International journal

    Takashi Oka, Mamoru Ouchida, Maho Koyama, Yoichiro Ogama, Shinichi Takada, Yoko Nakatani, Takehiro Tanaka, Tadashi Yoshino, Kazuhiko Hayashi, Nobuya Ohara, Eisaku Kondo, Kiyoshi Takahashi, Junjiro Tsuchiyama, Mitsune Tanimoto, Kenji Shimizu, Tadaatsu Akagi

    Cancer research   62 ( 22 )   6390 - 4   2002.11

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    High-frequent silencing of hematopoietic cell-specific protein-tyrosine phosphatase SHP1 gene by promoter methylation was detected in various kinds of leukemias and lymphomas, as well as in many hematopoietic cell lines, which is supported by our previous observation of strong decrease of SHP1 mRNA and protein. The promoter methylation of the SHP1 gene was clearly correlated with the clinical stage. Loss of heterozygosity with microsatellite markers near the SHP1 gene was shown in 79% of informative acute lymphoblastic leukemia cases. These results suggest that functional loss of SHP1 is associated with the pathogenesis of leukemias/lymphomas.

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  • Prognostic value of loss of heterozygosity around three candidate tumor suppressor genes on chromosome 10q in astrocytomas International journal

    K Terada, T Tamiya, S Daido, H Kambara, H Tanaka, Y Ono, K Matsumoto, S Ito, M Ouchida, T Ohmoto, K Shimizu

    JOURNAL OF NEURO-ONCOLOGY   58 ( 2 )   107 - 114   2002.6

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  • Allelic loss and reduced expression of the ING3, a candidate tumor suppressor gene at 7q31, in human head and neck cancers International journal

    M Gunduz, M Ouchida, K Fukushima, S Ito, Y Jitsumori, T Nakashima, N Nagai, K Nishizaki, K Shimizu

    ONCOGENE   21 ( 28 )   4462 - 4470   2002.6

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  • Astrocytomaにおける10番染色体長腕遺伝子異常と悪性度との関連

    大同 茂, 田宮 隆, 小野 恭裕, 大塚 真司, 松下 博和, 黒住 和彦, 大本 尭史, 伊藤 佐智夫, 大内田 守, 清水 憲二

    Brain Tumor Pathology   19 ( Suppl. )   96 - 96   2002.5

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  • Reduced expression of the REIC/Dkk-3 gene by promoter-hypermethylation in human tumor cells International journal

    K Kobayashi, M Ouchida, T Tsuji, H Hanafusa, M Miyazaki, M Namba, N Shimizu, K Shimizu

    GENE   282 ( 1-2 )   151 - 158   2002.1

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    DOI: 10.1016/S0378-1119(01)00838-1

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  • Effect of naturally occurring E2F-4 alterations on transcriptional activation and proliferation in transfected cells

    H Takashima, Y Matsumoto, N Matsubara, Y Shirakawa, R Kawashima, M Tanino, S Ito, H Isozaki, M Ouchida, SJ Meltzer, K Shimizu, N Tanaka

    LABORATORY INVESTIGATION   81 ( 11 )   1565 - 1573   2001.11

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  • A novel WD40 repeat protein, WDC146, highly expressed during spermatogenesis in a stage-specific manner

    S Ito, A Sakai, T Nomura, Y Miki, M Ouchida, J Sasaki, K Shimizu

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   280 ( 3 )   656 - 663   2001.1

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    DOI: 10.1006/bbrc.2000.4163

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  • HD-PTP: A novel protein tyrosine phosphatase gene on human chromosome 3p21.3

    S Toyooka, M Ouchida, Y Jitsumori, K Tsukuda, A Sakai, A Nakamura, N Shimizu, K Shimizu

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   278 ( 3 )   671 - 678   2000.11

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    DOI: 10.1006/bbrc.2000.3870

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  • A reverse transcriptase-polymerase chain reaction assay in the diagnosis of soft tissue sarcomas

    N Naito, A Kawai, M Ouchida, T Dan'ura, Y Morimoto, T Ozaki, K Shimizu, H Inoue

    CANCER   89 ( 9 )   1992 - 1998   2000.11

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    DOI: 10.1002/1097-0142(20001101)89:9<1992::AID-CNCR16>3.0.CO;2-R

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  • グリオーマの悪性度と10番染色体遺伝子異常との関連性に関する検討

    大同 茂, 寺田 欣矢, 神原 啓和, 小野 恭裕, 田宮 隆, 松本 健五, 大本 尭史, 伊藤 佐智夫, 大内田 守, 清水 憲二

    日本脳神経外科学会総会抄録集   59回   221 - 221   2000.10

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  • Genomic structure of the human ING1 gene and tumor-specific mutations detected in head and neck squamous cell carcinomas

    M Gunduz, M Ouchida, K Fukushima, H Hanafusa, T Etani, S Nishioka, K Nishizaki, K Shimizu

    CANCER RESEARCH   60 ( 12 )   3143 - 3146   2000.6

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  • Functional mutation of DNA polymerase β found in human gastric cancer - Inability of the base excision repair in vitro

    Akinari Iwanaga, Mamoru Ouchida, Kohji Miyazaki, Katsuji Hori, Tsunehiro Mukai

    Mutation Research - DNA Repair   435 ( 2 )   121 - 128   1999.10

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  • Osteoclast-derived zinc finger (OCZF) protein with POZ domain, a possible transcriptional repressor, is involved in osteoclastogenesis Reviewed

    A Kukita, T Kukita, M Ouchida, H Maeda, H Yatsuki, O Kohashi

    BLOOD   94 ( 6 )   1987 - 1997   1999.9

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  • Osteoclast-derived zinc finger (OCZF) protein with POZ domain, a possible transcriptional regulator, is involved in osteoclastogenesis.

    Kukita A, Kukita T, Maeda H, Ouchida M, Yatsuki H, Kohashi O

    Blood   1999

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  • Transforming activity of the RL-akt gene, a c-akt gene activated by long terminal repeat insertion in murine leukemia RL♂1 cells

    Motohiko Tanino, Mitsutoshi Matsuo, Akiko Uenaka, Kazunori Tsukuda, Mamoru Ouchida, Eiichi Nakayama, Kenji Shimizu

    Molecular Carcinogenesis   26 ( 4 )   286 - 297   1999

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    DOI: 10.1002/(SICI)1098-2744(199912)26:4<286::AID-MC7>3.0.CO;2-U

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  • Cloning of the Xenopus laevis aldolase C gene and analysis of its promoter function in developing Xenopus embryos and A6 cells

    Hitomi Yatsuki, Mamoru Outida, Yasuo Atsuchi, Tunehiro Mukai, Koichiro Shiokawa, Katsuji Hori

    Biochimica et Biophysica Acta - Gene Structure and Expression   1442 ( 2-3 )   199 - 217   1998.11

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    DOI: 10.1016/S0167-4781(98)00165-1

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  • Inhibition of apoptosis by normal and aberrant Fli-1 and erg proteins involved in human solid tumors and leukemias. International journal

    H Yi, Y Fujimura, M Ouchida, D D Prasad, V N Rao, E S Reddy

    Oncogene   14 ( 11 )   1259 - 68   1997.3

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    Two ets family members, namely erg and Fli-1 are fused with two EWS family members namely EWS and TLS/FUS as a result of chromosome translocation in human solid tumors and leukemias. EWS-erg and EWS-Fli-1, which are involved in greater than 95% of Ewing family of tumors, were shown to function as transcriptional activators. TLS/FUS-erg, which is involved in human myeloid leukemias also functions as a transcriptional activator. Expression of these fusion proteins (EWS-erg and EWS-Fli-1) are shown to be essential for maintaining the oncogenic and tumorigenic properties of tumor cells. Cancer is thought to be caused not only by uncontrolled cell proliferation but also by deregulation of programmed cell death. Therefore, we have studied the role of normal (Fli-1 and erg) and aberrant fusion proteins (EWS-erg, EWS-Fli-1 and TLS/FUS-erg) in apoptosis. We have found that expression of normal (Fli-1 and erg) and aberrant fusion proteins inhibit the apoptosis of NIH3T3 cells induced by either serum deprivation or by treatment with calcium ionophore. We have also observed similar suppression of apoptosis in Ewing's sarcoma cells expressing EWS-Fli-1 and EWS-erg proteins suggesting that these fusion proteins may be responsible for the decreased ability of these tumor cells to undergo apoptosis. Inhibition of the expression of these aberrant fusion proteins by antisense RNA technique resulted in increased susceptibility to apoptosis leading to the death of tumor cells. Therefore, our results suggest that one can use therapeutic agents which can down regulate the expression of fusion proteins in combination with chemotherapeutic agents as an effective treatment for these human solid tumors and leukemias.

    DOI: 10.1038/sj.onc.1201099

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  • Telomerase activity in gynecologic tumors

    Peng-Sheng Zheng, Tsuyoshi Iwasaka, Fumio Yamasaki, Mamoru Ouchida, Masatoshi Yokoyama, Yoshifumi Nakao, Koichi Fukuda, Toshitake Matsuyama, Hajime Sugimori

    Gynecologic Oncology   64 ( 1 )   171 - 175   1997

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    DOI: 10.1006/gyno.1996.4523

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  • Growth suppression of a cervical cancer cell line (TMCC-1) by the human wild-type p53 gene

    Peng-Sheng Zheng, Tsuyoshi Iwasaka, Mamoru Ouchida, Koichi Fukuda, Masatoshi Yokoyama, Hajime Sugimori

    Gynecologic Oncology   60 ( 2 )   245 - 250   1996

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    DOI: 10.1006/gyno.1996.0033

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  • Cytologic changes in two cervical carcinoma cell lenes after transfection of the wild-type p53 genes. Reviewed

    Iwasaka T, Zheng PS, Ouchida M, Yamasaki H, Yokoyama M, Sugimori H

    Acta Obset. Gynecol. Scand.   75 ( 9 )   797 - 803   1996

  • Cytologic changes in two cervical carcinoma cell lines after transfection of the wild-type p53 gene

    Tsuyoshi Iwasaka, Peng-Sheng Zheng, Mamoru Ouchida, Humio Yamasaki, Masatoshi Yokoyama, Hajime Sugimori

    Acta Obstetricia et Gynecologica Scandinavica   75 ( 9 )   797 - 803   1996

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    DOI: 10.3109/00016349609054706

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  • Loss of tumorigenicity of Ewing's sarcoma cells expressing antisense RNA to EWS-fusion transcripts. International journal

    M Ouchida, T Ohno, Y Fujimura, V N Rao, E S Reddy

    Oncogene   11 ( 6 )   1049 - 54   1995.9

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    Cytogenetic analysis of Ewing's sarcoma, primitive neuroectodermal tumors and Askin tumors revealed characteristic translocations t(11;22) or t(21;22). Molecular analysis of these translocations revealed 5'-region of EWS gene (from band 22q12) is fused to the 3'-region of either Fli-1 gene (from band 11q24) or erg gene (from band 21q22). Functional characterization of the EWS-Fli-1 and EWS-erg chimeric proteins suggested that they function as transcriptional activators. In order to develop therapeutic agents, it is essential to know whether expression of the EWS-fusion gene products is coupled to tumorigenicity of Ewing's sarcoma cells and if targeting the EWS-fusion products results in loss of tumorigenicity of Ewing's sarcoma cells. For this reason, we have made stable Ewing's sarcomas expressing antisense EWS-Fli-1 or EWS-erg expression plasmids. Expression of antisense EWS fusion transcripts resulted in a significant loss of endogenous EWS-Fli-1 and EWS-erg proteins in Ewing's sarcoma cells. These cells expressing antisense EWS fusion transcripts showed loss of anchorage independent growth and tumorigenicity in nude mice unlike the parental Ewing's sarcoma cells. These results demonstrate the necessity of a certain threshold level of expression of EWS-fusion products in the clonogenicity and tumorigenicity of Ewing's sarcoma cells and therefore emphasizes the importance of targeting the EWS-fusion products as a therapy for Ewing family of tumors.

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  • TLS/FUS fusion domain of TLS/FUS-erg chimeric protein resulting from the t(16;21) chromosomal translocation in human myeloid leukemia functions as a transcriptional activation domain. International journal

    D D Prasad, M Ouchida, L Lee, V N Rao, E S Reddy

    Oncogene   9 ( 12 )   3717 - 29   1994.12

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    EWS and TLS/FUS genes, which code for RNA binding proteins are involved in a wide variety of human solid tumors. The TLS/FUS gene is involved both in human myxoid liposarcomas which carry a characteristic chromosomal translocation, t(12;16)(q13;p11) and in human myeloid leukemias with recurrent chromosomal translocation, t(16;21)(p11:q22). The TLS/FUS gene is fused to a transcriptional repressor, CHOP (in human myxoid liposarcomas) or transcriptional activator, erg (in human myeloid leukemias). To understand better the functional role of TLS/FUS-erg in human myeloid leukemias, we have cloned the TLS/FUS and TLS/FUS-erg cDNAs and studied the functional properties of their gene products. TLS/FUS protein binds to RNA in vitro and shows preferential binding to poly G. Both the amino- and the carboxy- terminal regions of TLS/FUS containing the conserved RNA binding motifs are needed for poly G specific RNA binding activity. The TLS/FUS fusion domain (TFD) appears to regulate the DNA binding activity of TLS/FUS-erg chimeric protein which shows weaker transcriptional activation properties compared to normal erg proteins. Mutational analysis of the TLS/FUS-erg chimeric protein reveals TFD to function as a transcriptional activation domain thus replacing the amino terminal transcriptional activation domain of the erg protein. Therefore alterations in both DNA binding and transcriptional activation properties of aberrant erg proteins may be responsible for the genesis of t(16;21) chromosomal translocation-bearing human myeloid leukemias.

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  • THE EWS GENE, INVOLVED IN EWING FAMILY OF TUMORS, MALIGNANT-MELANOMA OF SOFT PARTS AND DESMOPLASTIC SMALL ROUND-CELL TUMORS, CODES FOR AN RNA-BINDING PROTEIN WITH NOVEL REGULATORY DOMAINS

    T OHNO, M OUCHIDA, L LEE, Z GATALICA, VN RAO, ESP REDDY

    ONCOGENE   9 ( 10 )   3087 - 3097   1994.10

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  • PCR法によるABO式血液型(糖転移酵素の遺伝子型判定).

    袖崎賢一郎, 的場梁次, 大内田守

    法医学の実際と研究   36   33 - 37   1993

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  • Correlation between HPV Positivity and state of the p53 gene in cervical Carcinoma cell lines

    Iwasaka T, Oh-uchida M, Matsuo N, Yokoyama M, Fukuda K, Hara K, Fukuyama K, Hori K, Sugimori H

    48, 104-109   1993

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  • Detection of human papillomavirus genome and analysis of expression of c-myc and Ha-ras oncogenes in invasive cervical carcinomas

    Tsuyoshi Iwasaka, Masatoshi Yokoyama, Mamoru Oh-uchida, Norito Matsuo, Kouichi Hara, Kouzou Fukuyama, Toru Hachisuga, Kouichi Fukuda, Hajime Sugimori

    Gynecologic Oncology   46 ( 3 )   298 - 303   1992

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    DOI: 10.1016/0090-8258(92)90220-D

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  • Altered Structure and Expression of the p 53 Gene in Human Neuroepithelial Tumors

    Tabuchi Kazuo, Fukuyama Kouzou, Mineta Toshihiro, Mamoru Oh-Uchida, Hori Katsuji

    neurologia medico-chirurgica   32 ( 10 )   725 - 732   1992

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    DOI: 10.2176/nmc.32.725

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  • Suppression of anchorage-independent growth of human glioblastoma cell by major histocompativility complex class I gene-Transfection.

    Momozaki N, Oh-uchida M, Tabuchi K, Ikezaki K, Hori K

    J. Neurosurg.   76   845 - 849   1992

  • ヒト神経膠腫における癌抑制遺伝子の単離と遺伝子および遺伝子産物の分子生物学的解析

    大内田 守

    佐川がん研究助成振興財団研究報告集   2   13   1991

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  • Transformation‐specific Decrease of Phosphorylation of 80K Protein, a Substrate of Protein Kinase C, in NIH3T3 Cells

    Mamoru Oh‐uchida, Kazumi Yano, Shoko Kawamoto, Kenji Shimizu

    Japanese Journal of Cancer Research   81 ( 8 )   799 - 806   1990

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    DOI: 10.1111/j.1349-7006.1990.tb02648.x

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  • グリオーマにおける癌抑制遺伝子の単離及びその解析

    大内田 守

    日本脳神経財団報告書   6   73   1990

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  • Changes in the patterns of RNA synthesis in early embryogenesis of Xenopus laevis. Reviewed

    Shiokawa K, Misumi Y, Tashiro K, Nakakura N, Yamana K, Oh-uchida M

    Cell Differ Dev.   28 ( 1 )   17 - 25   1989

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  • Activated c-raf-1 gene from human stomach cancer

    K. Shimizu, Y. Nakatsu, M. Oh-uchida, S. Nomoto, M. Sekiguchi

    Japanese Journal of Cancer and Chemotherapy   14 ( 6 )   2140 - 2146   1987.6

  • Structure of the Activated C-raf-1 gene from Human Stomach Cancer

    Nakatsu Y, Nomoto S, Oh-uchida M, Shimizu K, Sekiguchi M

    Cold Spring Harbor Symposia on Quantitative Biology   51   1986

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  • S III-2. Detection of human transforming genes using DNA-transfection

    K. Shimizu, Y. Nakatsu, M. Ohuchida, M. Sekiguchi

    Japanese Journal of Human Genetics   30 ( 2 )   93 - 94   1985

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Books

  • てんかん治療研究振興財団研究年報 第30集

    大内田 守, 真下 知二, 大守 伊織( Role: Joint author)

    てんかん治療研究振興財団  2019 

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  • T cell leukemia

    Oka T, Sato H, Ouchida M, Utsunomiya A, Ennishi D, Tanimoto M, Yoshino T(Accumulation of Specific Epigenetic Abnormalities During Development and Progression of T cell Leukemia/Lymphoma.)

    2011 

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  • てんかん治療研究振興財団研究年報 第21集

    芹川忠夫, 大守伊織, 大内田守, 大野行弘, 鶴見東志子, 三木崇史, 若森実, 石原靜, 吉田卓史, 滝沢明子, 加藤めぐみ, 平林真澄, 笹征史, 森泰生, 真下知士(ナトリウムチャネル遺伝子Scn1a変異ラットの開発解析研究)

    てんかん治療研究振興財団  2010 

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  • てんかん治療研究振興財団研究年報 第18集

    大内田 守, 大守伊織(研究褒賞受賞記念報告;乳児重症ミオクロニーてんかんとその辺縁てんかん症候群におけるSCN1A遺伝子異常)

    てんかん治療研究振興財団  2007 

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  • Gene Silencing

    Nova Science Publishers,New York  2006 

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  • てんかん治療研究振興財団研究年報 第17集

    大内田 守, 大守伊織, 大塚頌子(乳児重症ミオクロニーてんかんにおける変異遺伝子の検索と、変異型イオンチャネルの機能解析)

    てんかん治療研究振興財団  2006 

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  • Atlas of Genetics and Cytogenetics in Oncology and Haematology.(ISSN 1768-3262)

    Poitiers University Hospital, France  2006 

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  • 小児科診療

    診断と治療社  2003 

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  • 小児内科第35巻増刊号:小児疾患診療のための病態生理2.

    東京医学社  2003 

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  • 日本臨床

    岡 剛史, 大内田 守(広範な悪性リンパ腫・白血病発症に関連するSHP1遺伝子に関する最新知見)

    2003 

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  • PROCEEDING OF ASIAN SCIENCE SEMINAR IN OKAYAMA 2000.

    2000 

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  • Biological Aspects of Brain Tumors 1

    Springer- Verlag Tokyo, Inc.  1991 

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  • Biological Aspects of Brain Tumors 2

    Springer- Verlag Tokyo, Inc.  1991 

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  • Isozymes

    Wiley-Liss Inc., New York,  1990 

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MISC

  • てんかん発作と関連するラットチオレドキシン変異体の結晶構造

    馬場匠望, 馬場匠望, 大内田守, 大守伊織, 上野剛, 山本雅貴, 山本雅貴, 竹下浩平

    日本蛋白質科学会年会プログラム・要旨集   23rd (CD-ROM)   2023

  • Cacnala遺伝子変異/Scnla遺伝子変異ラットにおける欠神発作のビデオ脳波解析(Video-EEG analysis of absence seizures in Cacnala/Scnla double mutant rats)

    大守 伊織, 小林 聖佳, 大内田 守

    てんかん研究   40 ( 2 )   421 - 421   2022.8

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  • Video-EEG analysis of absence seizures in Cacnala/Scnla double mutant rats

    大守 伊織, 小林 聖佳, 大内田 守

    てんかん研究   40 ( 2 )   421 - 421   2022.8

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  • Video-EEG analysis of absence seizures in Cacna1a/Scn1a double mutant rats

    大守伊織, 小林聖佳, 大内田守

    てんかん研究   40 ( 2 )   2022

  • Cacna1a遺伝子変異はScna遺伝子変異ラットの表現型を変化させる

    大守伊織, 大内田守, 小林聖佳, 大守伊織

    日本人類遺伝学会大会プログラム・抄録集   65th (CD-ROM)   2020

  • Txn1遺伝子変異ラットのてんかんの表現型

    大守 伊織, 真下 知士, 大内田 守, 豊國 伸哉

    てんかん研究   37 ( 2 )   647 - 647   2019.9

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  • Txn1遺伝子ミスセンス変異をもつ新規CKDモデルラット

    大守 伊織, 真下 知士, 大内田 守, 豊國 伸哉

    日本腎臓学会誌   61 ( 3 )   399 - 399   2019.5

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  • ミオクローヌス・ジストニア(DYT11ジストニア)の1例

    濱田 朋弥, 細川 卓利, 齊藤 志穂, 石原 正行, 古谷 博和, 大内田 守, 大守 伊織, 阿部 エリカ, 豊島 至, 熊田 聡子, 浜田 文彦, 藤枝 幹也

    脳と発達   51 ( Suppl. )   S259 - S259   2019.5

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  • アトピー性皮膚炎患者におけるSPINK5遺伝子変異解析

    森実 真, 大内田 守, 砂川 滉, 杉本 佐江子, 小橋 美那, 杉原 悟, 野村 隼人, 三宅 智子, 岩月 啓氏

    日本皮膚科学会雑誌   127 ( 5 )   1176 - 1176   2017.5

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  • 成人T細胞白血病/リンパ腫(ATL)を発症したHTLV-1キャリアにおける異常DNAメチル化の解析

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌   57   88 - 88   2017.5

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態の変動との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 村上 一郎, 大内田 守, 宇都宮 與, 吉野 正

    日本病理学会会誌   106 ( 1 )   355 - 355   2017.3

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  • PRRT2遺伝子変異を認めたepisodic ataxiaの女児

    柴田 敬, 岡 牧郎, 小林 勝弘, 大内田 守, 大守 伊織

    脳と発達   48 ( 6 )   446 - 446   2016.11

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  • 肺癌に関わるmiR-19aの標的遺伝子解析

    大内田 守, 山本 久美子, 伊藤 佐智夫

    日本癌学会総会記事   75回   P - 3076   2016.10

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  • 日本におけるPRRT2関連てんかんの臨床的様相(A clinical picture of PRRT2-related epilepsy in Japan)

    Kurahashi Hirokazu, 奥村 彰久, 五十嵐 鮎子, 安部 信平, 高須 倫彦, 小林 勝弘, 大守 伊織, 大内田 まもる, 石井 敦士, 廣瀬 伸一, 高橋 悟, 粟屋 智就, 山本 俊至

    てんかん研究   34 ( 2 )   395 - 395   2016.9

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  • 肺癌におけるmiR-19a新規標的遺伝子の機能解析

    山本 久美子, 伊藤 佐智夫, 清水 憲二, 大内田 守

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   88回・38回   [1P1051] - [1P1051]   2015.12

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌   55   117 - 117   2015.6

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  • 成人T細胞白血病/リンパ腫(ATL)における特異的DNAメチル化と病態との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本病理学会会誌   104 ( 1 )   494 - 494   2015.3

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  • 成人T細胞白血病リンパ腫に於ける 細胞DNAメチル化の変動解析

    岡 剛史, 大内田 守, 岡田 康志, 上田 潤, 山縣 一夫, 吉野 正

    日本病理学会会誌   104 ( 1 )   494 - 494   2015.3

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株における特異的DNAメチル化の解析

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 宇都宮 與, 高橋 聖之, 吉野 正

    日本リンパ網内系学会会誌   54   108 - 108   2014.6

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株における特異的DNAメチル化の解析

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   103 ( 1 )   294 - 294   2014.3

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  • 乳児期早期に皮質性ミオクローヌスを認めたDravet症候群の一例

    小林 由典, 秋山 倫之, 中尻 智史, 柴田 敬, 井上 拓志, 小林 勝弘, 大守 伊織, 大内田 守, 吉永 治美

    臨床神経生理学   41 ( 5 )   490 - 490   2013.10

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  • ICCA症候群および乳児期発症良性痙攣性疾患におけるPRRT2遺伝子解析

    大内田 守, 小林 勝弘, 榎 日出夫, 横田 卓也, 伊予田 邦昭, 吉永 治美, 大守 伊織

    脳と発達   45 ( Suppl. )   S375 - S375   2013.5

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  • 症候の異なる発作性ジスキネジアにおけるPRRT2遺伝子変異の有無

    榎 日出夫, 横田 卓也, 大守 伊織, 大内田 守, 小林 勝弘

    脳と発達   45 ( Suppl. )   S374 - S374   2013.5

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  • ドラベ症候群で検出されるCACNA1A遺伝子変異の電気生理学的特性

    大守 伊織, 大内田 守

    脳と発達   45 ( Suppl. )   S349 - S349   2013.5

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  • CACNA1A遺伝子変異/多型がドラベ症候群の臨床症状に及ぼす影響

    大守 伊織, 小林 勝弘, 大内田 守, 大塚 頌子

    脳と発達   45 ( Suppl. )   S320 - S320   2013.5

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  • ICCA症候群に片麻痺性片頭痛を合併した1家系

    大守 伊織, 大内田 守, 小林 勝弘, 吉永 治美

    脳と発達   45 ( Suppl. )   S378 - S378   2013.5

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と予後との相関

    佐藤 妃映, 岡 剛史, Lamia Abd Alkader, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   102 ( 1 )   482 - 482   2013.4

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  • SCN9A遺伝子変異/多型がドラベ症候群の臨床型に及ぼす影響

    大守 伊織, Wang Haijiao, 大内田 守, 小林 勝弘, 松井 秀樹

    てんかん研究   30 ( 2 )   358 - 358   2012.9

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  • Scn1a遺伝子変異ラットにおける発達障害

    大守 伊織, 大内田 守

    脳と発達   44 ( Suppl. )   S205 - S205   2012.5

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  • ポドシンの輸送システムの探索

    宮原 宏幸, 綾 邦彦, 宮井 貴之, 大内田 守, 森島 恒雄

    日本小児腎臓病学会雑誌   25 ( 1Suppl. )   184 - 184   2012.5

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  • P/Q型電位依存性カルシウムチャネル変異に伴う発達障害

    大内田 守, 大守 伊織

    脳と発達   44 ( Suppl. )   S302 - S302   2012.5

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  • 熱性けいれん既往患者におけるSCN9A遺伝子解析

    大守 伊織, 小林 勝弘, 大内田 守

    脳と発達   44 ( Suppl. )   S232 - S232   2012.5

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常の動態解析

    岡 剛史, Abd Al-Kader Lamia, 佐藤 妃映, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本病理学会会誌   101 ( 1 )   291 - 291   2012.3

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  • 代謝性および呼吸性アシドーシスはCacna1a変異ラットの欠神発作を抑制する

    大内田 守, 改田 祐子, 大守 伊織, 上原 孝, 松井 秀樹

    てんかん研究   29 ( 2 )   382 - 382   2011.9

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  • Scn1a変異ラットの高体温誘発発作における高周波振動

    小林 勝弘, 大守 伊織, 林 桂一郎, 大内田 守, 井上 拓志, 大塚 頌子

    てんかん研究   29 ( 2 )   251 - 252   2011.9

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  • Scn1a遺伝子変異による熱性けいれんの二酸化炭素吸入療法

    大守 伊織, 大内田 守, 王 海こう, 林 桂一郎, 松井 秀樹

    てんかん研究   29 ( 2 )   251 - 251   2011.9

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネティックス異常

    岡 剛史, 佐藤 妃映, Lamia Abd. Al-Kader, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 田村 麻衣子, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌   51   118 - 118   2011.6

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  • 急性脳症における遺伝性けいれん素因とSCN1A遺伝子変異

    大守 伊織, 小林 勝弘, 大内田 守, 奥村 彰久, 前垣 義弘, 西山 逸子, 大塚 頌子

    脳と発達   43 ( Suppl. )   S352 - S352   2011.5

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常の解析

    岡 剛史, 佐藤 妃映, Abd. Al-Kader Lamia, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 田村 麻衣子, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   100 ( 1 )   323 - 323   2011.3

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるDNAメチル化と病態との関連

    平岩 千尋, 岡 剛史, 佐藤 妃映, Abd. Al-Kader Lamia, 神農 陽子, 鷲尾 佳奈, 佐藤 康晴, 高田 尚良, 田村 麻衣子, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本病理学会会誌   100 ( 1 )   496 - 496   2011.3

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  • HTLV-1キャリアにおけるDNAメチル化の解析

    佐藤 妃映, 岡 剛史, Abd.Al-Kader Lamia, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 田村 麻衣子, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   100 ( 1 )   416 - 416   2011.3

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  • 遺伝子検査が診断に有用であった非典型的Rett症候群の1例

    松岡 剛司, 葛原 誠人, 大塚 頌子, 清水 憲二, 大内田 守, 大守 伊織

    日本小児科学会雑誌   114 ( 11 )   1756 - 1756   2010.11

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  • 末梢神経系腫瘍microRNA発現プロファイリングの検討

    井谷 智, 森本 裕樹, 伊藤 佐智夫, 大内田 守, 吉田 晶, 上甲 良二, 米田 泰史, 佐々木 剛, 国定 俊之, 尾崎 敏文

    日本整形外科学会雑誌   83 ( 8 )   S1151 - S1151   2009.8

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  • 2種類のチャネル機能異常をもつ乳児重症ミオクロニーてんかん

    大守 伊織, 御牧 信義, 大内田 守

    脳と発達   41 ( Suppl. )   S241 - S241   2009.5

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との相関

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 高田 尚良, 守都 敏晃, 田村 麻衣子, 黄 新剛, 北村 雄太, 村上 一郎, 大内田 守, 大原 信哉, 大島 孝一, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   98 ( 1 )   275 - 275   2009.3

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  • プロテオミクス解析を用いた悪性グリオーマの浸潤に関わるタンパクの同定

    丸尾 智子, 市川 智継, 神崎 浩孝, 田丸 聖治, 大西 学, 井上 智, 吉田 光一, 小坂 洋志, 道上 宏之, 黒住 和彦, 神原 啓和, 大内田 守, 清水 憲二, 伊達 勲

    日本脳神経外科学会総会CD-ROM抄録集   67回   2J - 05   2008.10

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  • ゲフィチニブ未使用肺癌におけるMET遺伝子増幅について

    久保 孝文, 山本 寛斉, 宗 淳一, 藤井 徹也, 大内田 守, 瀧川 奈義夫, 木浦 勝行, 清水 憲二, 伊達 洋至, 豊岡 伸一

    肺癌   48 ( 5 )   508 - 508   2008.10

  • 1歳未満の乳幼児を対象としたDravet症候群を予測するためのスクリーニング(A screening test for the prediction of Dravet syndrome before one year of age)

    服部 旬里, 大内田 守, 大野 順子, 三宅 進, 真庭 聡, 御牧 信義, 大塚 頌子, 大守 伊織

    てんかん研究   26 ( 2 )   260 - 260   2008.9

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  • 滑膜肉腫関連蛋白の細胞内局在に影響を与える薬剤および蛋白に関する検討

    米田 泰史, 大内田 守, 神崎 浩孝, 吉田 晶, 佐々木 剛, 森本 裕樹, 国定 俊之, 清水 憲二, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 8 )   S1023 - S1023   2008.8

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  • 骨肉腫患者における葉酸代謝関連遺伝子の一塩基多型の検討

    森本 裕樹, 吉田 晶, 大内田 守, 米田 泰史, 国定 俊之, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 8 )   S926 - S926   2008.8

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  • ヒストン脱アセチル化酵素阻害剤とDNA脱メチル化剤の併用による滑膜肉腫細胞株に対する抗腫瘍効果の検討

    佐藤 千明, 吉田 晶, 森本 裕樹, 米田 泰史, 佐々木 剛, 国定 俊之, 大内田 守, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 8 )   S1228 - S1228   2008.8

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  • 橋本病を合併したMazabraud syndromeの1例

    大畑 範英, 森本 裕樹, 吉田 晶, 佐々木 剛, 米田 泰史, 国定 俊之, 大内田 守, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 6 )   S853 - S853   2008.6

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  • MECP2遺伝子エキソン1およびプロモーター領域に変異をもつレット症候群

    大内田 守, 吉永 治美, 大守 伊織, 大塚 頌子, 岡 えい次

    脳と発達   40 ( Suppl. )   S288 - S288   2008.5

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  • 乳児重症ミオクロニーてんかんの早期スクリーニング法

    大守 伊織, 服部 旬里, 大内田 守, 真庭 聡, 御牧 信義, 三宅 進, 大塚 頌子

    脳と発達   40 ( Suppl. )   S374 - S374   2008.5

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  • SCN1A変異を認めたRasmussen脳炎の1例

    小林 勝弘, 大守 伊織, 大内田 守, 井上 拓志, 前垣 義弘, 大塚 頌子

    脳と発達   40 ( Suppl. )   S353 - S353   2008.5

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と予後との相関について

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 高野 正幸, 高田 尚良, 守都 敏晃, 大原 信哉, 大内田 守, 大島 孝一, 宇都宮 與, 高橋 聖之, 吉野 正

    日本病理学会会誌   97 ( 1 )   358 - 358   2008.3

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  • 悪性グリオーマの浸潤に関わるタンパクのプロテオミクス解析による同定

    丸尾 智子, 市川 智継, 神崎 浩孝, 田丸 聖治, 井上 智, 小坂 洋志, 吉田 光一, 神原 啓和, 大内田 守, 清水 憲二, 伊達 勲

    日本脳神経外科学会総会CD-ROM抄録集   66回   2K - 17   2007.10

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  • 日本人乳癌患者におけるHER2のSNP解析

    伊藤 充矢, 清水 憲二, 松岡 順治, 大内田 守, 堺 明子, 神崎 浩孝, 山本 泰久, 中地 敬, 田中 紀章

    日本癌治療学会誌   42 ( 2 )   774 - 774   2007.9

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  • 滑膜肉腫特異的転座型融合蛋白SS18-SSXおよびSS18、SSX蛋白の細胞内局在の解析

    米田 泰史, 大内田 守, 神崎 浩孝, 国定 俊之, 清水 憲二, 尾崎 敏文

    日本整形外科学会雑誌   81 ( 8 )   S1119 - S1119   2007.8

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  • SCN1A遺伝子変異I1616Tの臨床型

    服部 旬里, 御牧 信義, 大守 伊織, 大野 順子, 大内田 守, 大塚 頌子

    脳と発達   39 ( Suppl. )   S154 - S154   2007.6

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  • 熱性痙攣のSCN1A遺伝子異常

    大内田 守, 大野 順子, 大守 伊織, 服部 旬里, 眞庭 聡, 御牧 信義, 三宅 進, 大塚 頌子

    脳と発達   39 ( Suppl. )   S154 - S154   2007.6

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Presentations

  • RNA-seq analysis of neurodegeneration caused by hypofunction of thioredoxin

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    Event date: 2024.7.24 - 2024.7.27

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  • てんかん発作と関連するラットチオレドキシン変異体の結晶構造

    馬場匠望, 馬場匠望, 大内田守, 大守伊織, 上野剛, 山本雅貴, 山本雅貴, 竹下浩平

    日本蛋白質科学会年会プログラム・要旨集  2023 

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    Event date: 2023

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  • Cacnala遺伝子変異/Scnla遺伝子変異ラットにおける欠神発作のビデオ脳波解析(Video-EEG analysis of absence seizures in Cacnala/Scnla double mutant rats)

    大守 伊織, 小林 聖佳, 大内田 守

    てんかん研究  2022.8  (一社)日本てんかん学会

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    Event date: 2022.8

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  • A Txn1 missense mutation links to epilepsy with vacuolar degeneration

    Ohmori I, Ouchida M, Toyokuni S, Ishida S, Mashimo T

    39th Congress of the International Union of Physiological Sciences (IUPS) 

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    Event date: 2022.5.7 - 2022.5.11

    Language:English   Presentation type:Poster presentation  

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  • Cacna1a遺伝子変異はScna遺伝子変異ラットの表現型を変化させる

    大守伊織, 大内田守, 小林聖佳, 大守伊織

    日本人類遺伝学会大会プログラム・抄録集  2020 

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    Event date: 2020

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  • Txn1遺伝子変異ラットのてんかんの表現型

    大守伊織, 真下知士, 大内田守, 内藤有香, 今井宏彦, 豊國伸哉

    日本てんかん学会  2019.10.31  日本てんかん学会

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    Event date: 2019.10.31 - 2019.11.2

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  • The expression of p19 and EBI3 in epidermal keratinocytes under the stimulation with inflammatory cytokines

    K. Tachibana, M. Kobashi, S. Sugimoto, H. Nomura, M. Ouchida, S. Morizane

    JOURNAL OF INVESTIGATIVE DERMATOLOGY  2019.9  ELSEVIER SCIENCE INC

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    Event date: 2019.9

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  • Txn1遺伝子ミスセンス変異をもつ新規CKDモデルラット

    大守 伊織, 真下 知士, 大内田 守, 豊國 伸哉

    日本腎臓学会  2019.6.21  日本腎臓学会

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    Event date: 2019.5

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  • ミオクローヌス・ジストニア(DYT11ジストニア)の1例

    濱田 朋弥, 細川 卓利, 齊藤 志穂, 石原 正行, 古谷 博和, 大内田 守, 大守 伊織, 阿部 エリカ, 豊島 至, 熊田 聡子, 浜田 文彦, 藤枝 幹也

    脳と発達  2019.5  (一社)日本小児神経学会

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    Event date: 2019.5

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  • Txn1遺伝子ミスセンス変異をもつ新規CKDモデルラット

    大守 伊織, 真下 知士, 大内田 守, 豊國 伸哉

    日本腎臓学会誌  2019.5  (一社)日本腎臓学会

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    Event date: 2019.5

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  • CDH17のハプロタイプSNPは、日本人の膵がん発症リスクに関与する

    堺 明子, 保田 雪子, 園山 隆之, 伊藤 佐智夫, 笹井 香織, 大内田 守, 清水 憲二, 片山 博志

    生命科学系学会合同年次大会  2017.12  生命科学系学会合同年次大会運営事務局

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    Event date: 2017.12

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  • ある輸送蛋白の生体内機能

    綾邦彦, 大内田守

    平成29年度文部科学省新学術領域研究 先端モデル動物支援プラットフォーム 若手支援技術講習会  2017.9.7 

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    Event date: 2017.9.7 - 2017.9.9

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  • HTLV-1キャリアにおける異常DNAメチル化と成人T細胞白血病/リンパ腫(ATL)発症との関連について

    佐藤妃映, 岡 剛史, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 吉野 正

    第4回日本HTLV-1学会学術集会  2017.8.18 

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    Event date: 2017.8.18 - 2017.8.20

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  • 成人T細胞白血病/リンパ腫(ATL)を発症したHTLV-1キャリアにおける異常DNAメチル化の解析

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌  2017.6.29  日本リンパ網内系学会

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    Event date: 2017.6.29 - 2017.7.1

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  • アトピー性皮膚炎患者におけるSPINK5遺伝子変異解析

    森実 真, 大内田 守, 砂川 滉, 杉本 佐江子, 小橋 美那, 杉原 悟, 野村 隼人, 三宅 智子, 岩月 啓氏

    日本皮膚科学会雑誌  2017.5  (公社)日本皮膚科学会

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    Event date: 2017.5

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  • 成人T細胞白血病/リンパ腫(ATL)を発症したHTLV-1キャリアにおける異常DNAメチル化の解析

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌  2017.5  (一社)日本リンパ網内系学会

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    Event date: 2017.5

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態の変動との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 村上 一郎, 大内田 守, 宇都宮 與, 吉野 正

    日本病理学会会誌  2017.3  (一社)日本病理学会

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    Event date: 2017.3

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態との関連

    佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 吉野正

    日本HTLV-1学会学術集会  2017 

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  • PRRT2遺伝子変異を認めたepisodic ataxiaの女児

    柴田 敬, 岡 牧郎, 小林 勝弘, 大内田 守, 大守 伊織

    脳と発達  2016.11  (一社)日本小児神経学会

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    Event date: 2016.11

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  • 肺癌に関わるmiR-19aの標的遺伝子解析

    大内田 守, 山本 久美子, 伊藤 佐智夫

    日本癌学会総会記事  2016.10  日本癌学会

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    Event date: 2016.10

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  • 肺癌に関わるmiR-19aの標的遺伝子解析

    大内田 守, 山本 久美子, 伊藤 佐智夫

    日本癌学会総会記事  2016.10  (一社)日本癌学会

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  • 日本におけるPRRT2関連てんかんの臨床的様相(A clinical picture of PRRT2-related epilepsy in Japan)

    Kurahashi Hirokazu, 奥村 彰久, 五十嵐 鮎子, 安部 信平, 高須 倫彦, 小林 勝弘, 大守 伊織, 大内田 まもる, 石井 敦士, 廣瀬 伸一, 高橋 悟, 粟屋 智就, 山本 俊至

    てんかん研究  2016.9  (一社)日本てんかん学会

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  • アズレンスルホン酸ナトリウム含嗽希釈液の希釈法に関する検討

    八木 健太, 神崎 浩孝, 田中 雄太, 大内田 守, 丸尾 陽成, 真鍋 洋平, 小沼 利光, 定金 典明, 北村 佳久, 千堂 年昭

    日本薬学会年会要旨集  2016.3  (公社)日本薬学会

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  • 肺癌におけるmiR-19a新規標的遺伝子の機能解析

    山本 久美子, 伊藤 佐智夫, 清水 憲二, 大内田 守

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集  2015.12  (公社)日本生化学会

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  • 成人T細胞白血病リンパ腫に於けるHTLV-1Tax遺伝子発現によるDNAメチル化の一細胞変動

    岡 剛史, 大内田 守, 岡田 康志, 山縣 一夫, 吉野 正

    日本癌学会総会記事  2015.10  (一社)日本癌学会

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態との関連

    佐藤 妃映, 岡 剛史, 神農 陽子, 鷲尾 佳奈, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本リンパ網内系学会会誌  2015.6  (一社)日本リンパ網内系学会

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  • 成人T細胞白血病リンパ腫に於ける 細胞DNAメチル化の変動解析

    岡 剛史, 大内田 守, 岡田 康志, 上田 潤, 山縣 一夫, 吉野 正

    日本病理学会会誌  2015.3  (一社)日本病理学会

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  • miR-19a標的遺伝子の同定と肺癌細胞に及ぼす影響の解析

    山本 久美子, 伊藤 佐智夫, 大内田 守

    日本生化学会大会プログラム・講演要旨集  2014.10  (公社)日本生化学会

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株における特異的DNAメチル化の解析

    佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 高橋聖之, 吉野正

    日本病理学会会誌  2014 

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株におけるDNA異常メチル化の解析

    佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 高橋聖之, 吉野正

    日本HTLV-1学会学術集会  2014 

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株における特異的DNAメチル化の解析

    佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 高橋聖之, 吉野正

    日本リンパ網内系学会会誌  2014 

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  • 乳児期早期に皮質性ミオクローヌスを認めたDravet症候群の一例

    小林 由典, 秋山 倫之, 中尻 智史, 柴田 敬, 井上 拓志, 小林 勝弘, 大守 伊織, 大内田 守, 吉永 治美

    臨床神経生理学  2013.10  (一社)日本臨床神経生理学会

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  • 食道癌細胞株におけるmicroRNA-29aの標的遺伝子の同定(Identification of direct targets of MicroRNA-29a in Esophageal cancer cell lines)

    伊藤 佐智夫, 山本 久美子, 大内田 守, 片山 博志

    日本癌学会総会記事  2013.10  日本癌学会

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  • プロテオミクス解析によるmiR-19aの標的蛋白質の同定(Identification of novel target proteins for miR-19a in breast cancer cells by proteomic analysis)

    大内田 守, 神崎 浩孝, 山本 久美子, 伊藤 佐智夫, 片山 博志

    日本癌学会総会記事  2013.10  日本癌学会

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  • miR-19aの標的遺伝子の同定と解析

    山本 久美子, 大内田 守, 伊藤 佐智夫, 花房 裕子, 片山 博志

    日本生化学会大会プログラム・講演要旨集  2013.9  (公社)日本生化学会

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  • CACNA1A遺伝子変異/多型がドラベ症候群の臨床症状に及ぼす影響

    大守 伊織, 小林 勝弘, 大内田 守, 大塚 頌子

    脳と発達  2013.5  (一社)日本小児神経学会

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  • 症候の異なる発作性ジスキネジアにおけるPRRT2遺伝子変異の有無

    榎 日出夫, 横田 卓也, 大守 伊織, 大内田 守, 小林 勝弘

    脳と発達  2013.5  (一社)日本小児神経学会

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  • ドラベ症候群で検出されるCACNA1A遺伝子変異の電気生理学的特性

    大守 伊織, 大内田 守

    脳と発達  2013.5  (一社)日本小児神経学会

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  • ICCA症候群に片麻痺性片頭痛を合併した1家系

    大守 伊織, 大内田 守, 小林 勝弘, 吉永 治美

    脳と発達  2013.5  (一社)日本小児神経学会

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  • ICCA症候群および乳児期発症良性痙攣性疾患におけるPRRT2遺伝子解析

    大内田 守, 小林 勝弘, 榎 日出夫, 横田 卓也, 伊予田 邦昭, 吉永 治美, 大守 伊織

    脳と発達  2013.5  (一社)日本小児神経学会

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と予後との相関

    佐藤妃映, 岡剛史, LAMIA Abd Alkader, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 大島孝一, 宇都宮與, 高橋聖之, 吉野正

    日本病理学会会誌  2013 

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  • 成人T細胞白血病/リンパ腫(ATL)における特異的DNAメチル化と予後との相関

    佐藤妃映, 岡剛史, AL-KADER Lamia Abd, 神農陽子, 鷲尾佳奈, 村上一郎, 大内田守, 宇都宮與, 高橋聖之, 吉野正

    ATLシンポジウム/HTLV-1国際シンポジウム/HTLV-1研究会プログラム・抄録集  2013 

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  • SCN9A遺伝子変異/多型がドラベ症候群の臨床型に及ぼす影響

    大守 伊織, Wang Haijiao, 大内田 守, 小林 勝弘, 松井 秀樹

    てんかん研究  2012.9  (一社)日本てんかん学会

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  • 熱性けいれん既往患者におけるSCN9A遺伝子解析

    大守 伊織, 小林 勝弘, 大内田 守

    脳と発達  2012.5  (一社)日本小児神経学会

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  • Scn1a遺伝子変異ラットにおける発達障害

    大守 伊織, 大内田 守

    脳と発達  2012.5  (一社)日本小児神経学会

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  • ポドシンの輸送システムの探索

    宮原 宏幸, 綾 邦彦, 宮井 貴之, 大内田 守, 森島 恒雄

    日本小児腎臓病学会雑誌  2012.5  (一社)日本小児腎臓病学会

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  • P/Q型電位依存性カルシウムチャネル変異に伴う発達障害

    大内田 守, 大守 伊織

    脳と発達  2012.5  (一社)日本小児神経学会

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常の動態解析

    岡剛史, ABD AL Kader Lamia, 佐藤妃映, 神農陽子, 鷲尾佳奈, 高田尚良, 村上一郎, 村上一郎, 大内田守, 大島孝一, 宇都宮與, 吉野正

    日本病理学会会誌  2012 

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  • 成人T細胞白血病・リンパ腫(ATL)の発症・進展におけるエピジェネテイックス異常のダイナミックス

    岡剛史, ABD AL-Kader Lamia, 佐藤妃映, 神農陽子, 鷲尾佳奈, 村上一郎, 村上一郎, 大内田守, 宇都宮與, 吉野正

    ATLシンポジウム/HTLV-1国際シンポジウム/HTLV-1研究会プログラム・抄録集  2012 

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  • 代謝性および呼吸性アシドーシスはCacna1a変異ラットの欠神発作を抑制する

    大内田 守, 改田 祐子, 大守 伊織, 上原 孝, 松井 秀樹

    てんかん研究  2011.9  (一社)日本てんかん学会

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  • 急性脳症における遺伝性けいれん素因とSCN1A遺伝子変異

    大守 伊織, 小林 勝弘, 大内田 守, 奥村 彰久, 前垣 義弘, 西山 逸子, 大塚 頌子

    脳と発達  2011.5  (一社)日本小児神経学会

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるDNAメチル化と病態との関連

    平岩 千尋, 岡 剛史, 佐藤 妃映, Abd. Al-Kader Lamia, 神農 陽子, 鷲尾 佳奈, 佐藤 康晴, 高田 尚良, 田村 麻衣子, 村上 一郎, 大内田 守, 大島 孝一, 宇都宮 與, 吉野 正

    日本病理学会会誌  2011.3  (一社)日本病理学会

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常の解析

    岡剛史, 佐藤妃映, LAMIA ABD AL-Kader, 神農陽子, 鷲尾佳奈, 高田尚良, 田村麻衣子, 村上一郎, 大内田守, 大島孝一, 宇都宮與, 高橋聖之, 吉野正

    日本病理学会会誌  2011 

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常

    岡剛史, 佐藤妃映, ABD AL-KADER Lamia, 神農陽子, 鷲尾佳奈, 高田尚良, 田村麻衣子, 村上一郎, 大内田守, 大島孝一, 宇都宮與, 吉野正

    日本リンパ網内系学会会誌  2011 

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  • Helicobacter pylori infection induce accumulation of aberrant CpG hypermethylation to promote development and progression of gastric MALT lymphoma

    Takashi Oka, Takami Kondo, Hiaki Sat, Yoko Shinnou, Kana Washio, Toshiaki Morit, Katsuyoshi Takat, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshin

    Proceedings of The 3rd International Symposium for Future Technology Creating Better Human Health and Society Comprehensive Approach to Cancer and Infectious Diseases  2010 

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  • A CACNB4 mutation shows altered Cav2.1 function in a patient with Dravet syndrome

    大守伊織, 大内田守, 御牧信義, 西木禎一, 富澤一仁, 松井秀樹

    岡山医学会雑誌  2010 

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  • Dravet症候群患者に認められたカルシウムチャネル機能異常を引き起こすCACNB4遺伝子変異

    大守 伊織, 大内田 守, 御牧 信義, 西木 禎一, 富澤 一仁, 松井 秀樹

    岡山医学会雑誌  2009.12  岡山医学会

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    Dravet症候群患者に認められたカルシウムチャネル機能異常を引き起こすCACNB4遺伝子変異について検討した。SCN1A遺伝子解析で変異を認めたDravet症候群患者38例を対象とした。健常者200例を対照とした。Dravet症候群患者で、SCN1B遺伝子とGABRG2遺伝子に変異を持つ症例はなかったが、CACNB4遺伝子変異を持つ症例を1例見出した。全細胞記録では、R568X変異からは背景電流異常のナトリウム電流は認めなかった。変異チャネルが野生型に比し有意にBa2+電流が増大した。ピーク電圧、細胞キャパシタンス、電流密度も変異型が野生型よりも有意に高値であった。

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    Other Link: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2009&ichushi_jid=J00175&link_issn=&doc_id=20091215200002&doc_link_id=10.4044%2Fjoma.121.149&url=https%3A%2F%2Fdoi.org%2F10.4044%2Fjoma.121.149&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

  • 末梢神経系腫瘍microRNA発現プロファイリングの検討

    井谷 智, 森本 裕樹, 伊藤 佐智夫, 大内田 守, 吉田 晶, 上甲 良二, 米田 泰史, 佐々木 剛, 国定 俊之, 尾崎 敏文

    日本整形外科学会雑誌  2009.8  (公社)日本整形外科学会

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との相関

    佐藤妃映, 佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 高田尚良, 守都敏晃, 田村麻衣子, 黄新剛, 北村雄太, 村上一郎, 村上一郎, 大内田守, 大原信哉, 大島孝一, 宇都宮與, 高橋聖之, 吉野正

    日本病理学会会誌  2009 

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  • EGFR変異とUracil-Tegafurによる肺腺癌術後補助療法の関連性についての検討

    末久 弘, 豊岡 伸一, 堀田 勝幸, 内田 亜希子, 宗 淳一, 藤原 義朗, 松尾 恵太郎, 大内田 守, 高田 穣, 木浦 勝行, 伊達 洋至

    岡山医学会雑誌  2008.12  岡山医学会

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    完全切除された肺腺癌患者に補助療法としてUracil-Tegafur(UFT)を投与した場合における、EGFR変異の予後判定因子としての可能性を検討した。また、in vitro系のEGFR遺伝子導入細胞株における5-FUの効果も検討した。UFT投与群68例、手術のみの経過観察群119例であった。EGFR変異は187例中79例に認め、49例がエクソン19欠失変異、30例がエクソン21点突然変異であった。女性、非喫煙者に有意に変異が多かった。単変量解析では、UFT投与群が経過観察群よりも、EGFR変異群が野生群よりも予後がよい傾向であった。多変量解析では、術後補助療法が独立して有意に予後を延長していた。EGFR変異群では術後補助療法による予後延長の効果は認めなかった。EGFR変異型細胞株は5-FU低感受性を有することが示唆された。

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    Other Link: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2008&ichushi_jid=J00175&link_issn=&doc_id=20081205250002&doc_link_id=10.4044%2Fjoma.120.265&url=https%3A%2F%2Fdoi.org%2F10.4044%2Fjoma.120.265&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

  • J-1 A screening test for the prediction of Dravet syndrome before one year of age(The 42^<nd> Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society  2008.9.30  Japan Epilepsy Society

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との関連

    佐藤妃映, 佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 高田尚良, 守都敏晃, 大原信哉, 大内田守, 大島孝一, 谷本光音, 宇都宮與, 高橋聖之, 吉野正

    日本リンパ網内系学会会誌  2008 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と予後との相関について

    佐藤妃映, 佐藤妃映, 岡剛史, 神農陽子, 鷲尾佳奈, 高野正幸, 高田尚良, 守都敏晃, 大原信哉, 大内田守, 大島孝一, 宇都宮與, 高橋聖之, 高橋聖之, 吉野正

    日本病理学会会誌  2008 

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    Event date: 2008

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  • Accumulating DNA methylation in background mucosa plays a role in esophageal squamous cell carcinogenesis

    Ishii Tatsuhiro, Murakami Jun, Notohara Kenji, Sasamoto Hiromi, Kambara Takeshi, Shirakawa Yasuhiro, Naomoto Yoshio, Ouchida Mamoru, Shimizu Kenji, JASS Jeremy R., Matsubara Nagahide, Tanaka Noriaki

    Okayama Igakkai Zasshi (Journal of Okayama Medical Association)  2007  Okayama Medical Association

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    Language:Japanese  

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    Other Link: http://eprints.lib.okayama-u.ac.jp/13191

  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype(CIMP)の解析

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 高野正幸, 大原信哉, 大内田守, 大島孝一, 宇都宮與, 高橋聖之, 高橋聖之, 吉野正

    日本病理学会会誌  2007 

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  • HIGH FREQUENT GENE SILENCING OF HEMETOPOIETIC CELL SPECIFIC PROTEIN TYROSINEPHOSPHATASE SHP1 IN HEMETOPOIETIC CELL MALIGNANCIES.

    Oka T, Ouchida M, Tanimoto M, Shimizu K, Yoshino T

    International Journal of Medical and Biological Frontiers  2007 

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  • カルバマゼピン投与ラットにおける血中と肝臓中の産生CYPmRNA量の相関性の検討

    林瑶子, 北村佳久, 大内田守, 清水憲二, 千堂年昭, 五味田裕

    TDM研究  2006.7.1 

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    Event date: 2006.7.1

    Language:Japanese  

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  • SHP1遺伝子発現抑制と悪性リンパ腫・白血病発症機構の解析

    岡剛史, 大内田守, 中谷陽子, 近藤孝美, 佐藤妃映, 佐藤妃映, 鷲尾佳奈, 高野正幸, 村上一郎, 大原信哉, 高橋聖之, 吉野正

    日本病理学会会誌  2006 

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  • 異常メチル化によるSHP1 gene silencingと悪性リンパ腫・白血病発症機構

    岡剛史, 中谷陽子, 近藤孝美, 佐藤妃映, 佐藤妃映, 高野正幸, 鷲尾佳奈, 大内田守, 大原信哉, 清水憲二, 谷本光音, 高橋聖之, 吉野正

    日本癌学会学術総会記事  2006 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype(CIMP)

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 大原信哉, 大内田守, 大島孝一, 谷本光音, 高橋聖之, 吉野正

    日本リンパ網内系学会会誌  2006 

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  • 成人T細胞白血病/リンパ腫(ATLL)における病期の進行とDNAメチル化の関連

    佐藤妃映, 佐藤妃映, 岡剛史, 中谷陽子, 近藤孝美, 鷲尾佳奈, 高野正幸, 大原信哉, 大内田守, 宇都宮こう, 大島孝一, 高橋聖之, 吉野正

    日本病理学会会誌  2006 

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  • 膜肉腫細胞株に対するHDAC抑制剤FK228のin vivo,in vitroにおける抗腫瘍効果の検討.

    伊藤達男, 尾崎敏文, 大内田守

    医学のあゆみ  2005 

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  • Frequent deletion and increased mRNA expression of a candidate tumor suppressor gene at 19p13 region, BRG1, in oral cancers(2nd ASIAN SCIENCE SEMINAR IN OKAYAMA 2003)

    Gunduz Esra, Gunduz Mehmet, Nagatsuka Hitoshi, Tsujigiwa Hidetsugu, Ouchida Mamoru, Shinnou Yasuo, Cengiz Beyhan, Shimizu Kenji, Nagai Noriyuki

    Journal of hard tissue biology  2003.12  The Society of Hard Tissue Biology

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    Language:English  

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  • ある種の分子標的薬はSYT-SSX発現細胞株に特異的な抗腫瘍効果を発揮する

    沼本 邦彦, 伊藤 達男, 尾崎 敏文, 大内田 守, 国定 俊之, 伊藤 佐智夫, 森本 裕樹, 大畑 範英, 中川 寧子, 清水 憲二, 井上 一

    日本整形外科学会雑誌  2003.8  (公社)日本整形外科学会

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    Language:Japanese  

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  • 滑膜肉腫に認められる転座遺伝子SYT-SSXのtwo hybrid assayを用いた機能解析

    伊藤 達男, 尾崎 敏文, 大内田 守, 国定 俊之, 森本 裕樹, 大畑 範英, 中川 寧子, 武田 健, 沼本 邦彦, 吉田 晶, 伊藤 佐智夫, 清水 憲二, 井上 一

    日本整形外科学会雑誌  2003.6  (公社)日本整形外科学会

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    Language:Japanese  

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  • 染色体7q31に位置する癌抑制遺伝子候補ING3の頭頸部癌におけるヘテロ接合性の消失と発現の解析(Allelic loss and reduced expression of the ING3, a candidate TSG at 7q31, in human head and neck cancers)

    Gunduz Mehmet, 大内田 守, 伊藤 佐智夫, 永井 教之, 清水 憲二

    日本癌学会総会記事  2001.9  日本癌学会

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    Event date: 2001.9

    Language:Japanese  

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  • 軟部肉腫の診断における分子生物学的手法の有用性 : SYT-SSX融合遺伝子を中心に

    内藤 訓子, 川井 章, 檀浦 智幸, 大内田 守, 清水 憲二, 田口 孝爾, 井上 一

    日本整形外科學會雜誌 = The Journal of the Japanese Orthopaedic Association  1999.6.25 

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    Event date: 1999.6.25

    Language:Japanese  

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  • Osteoclast-derived zin finger gene (OCZF), a novel member of the Kruppel family, is involved in osteoclastogenesis

    KUKITA Akiko, KUKITA Toshio, OUCHIDA Mamoru, YATSUKI Hitomi, KOHASHI Osamu

    1998.12.1 

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    Event date: 1998.12.1

    Language:Japanese  

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  • 酸化ストレス障害に伴うてんかんの基礎病態

    大守伊織, 大内田守, 石田紗恵子, 真下知士

    第18回日本てんかん学会中国・四国地方会  2023.12.17 

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  • Txn1遺伝子変異ラットにおける慢性腎臓病は、ミトコンドリア異常と複数の細胞死パスウェイが関与する

    大守伊織、大内田 守、秦 昌紫子、内田 治仁、豊國 伸哉、真下 知士

    第34回腎とフリーラジカル研究会  2023.11.11 

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  • チオレドキシンの機能低下は神経細胞とオリゴデンドロサイトの細胞死を惹起する

    大守伊織, 大内田守, 今井宏彦, 豊國伸哉, 真下知士

    第44回 日本分子生物学会年会 (MBSJ2021)  2021.12.3 

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  • 慢性腎臓病を伴う早発老化モデル動物の発見

    大内田 守, 真下 知士, 豊國 伸哉, 大守 伊織

    第44回 日本分子生物学会年会 (MBSJ2021)  2021.12.3 

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  • チオレドキシン機能低下は年齢依存的かつ臓器特異的細胞障害を惹起する

    大守伊織, 大内田守, 豊國伸哉, 真下知士

    文部科学省 新学術領域研究 先端モデル動物支援プラットフォーム成果発表会  2020.2.4 

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  • A novel model rat of chronic kidney disease generated by NEU mutagenesis

    Iori Ohmori, Mamoru Ouchida, Tomoji Mashimo, Shinya Toyokuni

    The 9th Federation of the Asian and Oceanian Physiological Societies Congress  2019.3.28 

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  • 年齢依存性てんかん性脳症の分子病態解析

    大内田 守, 真下 知二, 大守 伊織

    公益財団法人 てんかん治療研究振興財団第30回研究報告会  2019.3.1 

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  • 年齢依存性てんかん脳症を示すTxn1遺伝子変異ラットの病態解析

    大守伊織, 真下知士, 大内田守, 加藤(内藤)有香, 豊國伸哉

    文部科学省 新学術領域研究 先端モデル動物支援プラットフォーム成果発表会  2019.1.30 

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  • Txn1における新規ミスセンス変異がひきおこす多臓器障害の解析

    加藤(内藤)有香, 真下知士, 大内田守, 豊國 伸哉, 大守伊織

    先端モデル動物プラットフォーム平成30年度若手支援技術講習会  2018.9.6 

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  • A Txn1 missense mutation damages multiple organs

    Iori OHMORI, Tomoji MASHIMO, Mamoru OUCHIDA, Kyoko YAMASHITA, Shinya TOYOKUNI

    2018.5.31 

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  • 新規Txn1遺伝子ミスセンス変異による多臓器障害

    大守 伊織, 真下知士, 大内田守, 山下享子, 豊國伸哉

    第71回日本酸化ストレス学会 第18回日本NO学会 合同学術集会  2018.5.17 

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  • Txn1遺伝子変異ラットの表現型解析

    大守伊織, 真下知士, 大内田守, 山下享子, 豊國伸哉

    平成29年度文部科学省 新学術領域研究 先端モデル動物支援プラットフォーム成果発表会  2018.1.24 

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  • 人工細胞膜を用いた慢性疼痛治療薬の開発研究

    大内田 守

    平成28年度特別電源所在県科学技術振興事業研究成果発表会  2017.3.10 

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  • Aberrant DNA methylation is associated with the clinical course in the same patients with ATL

    Hiaki Sato, Takashi Oka, Yoko Shinnou-Nakatani, Kana Washio, Ichiro Murakami, Mamoru Ouchida, Atae Utsunomiya, Tadashi Yoshino

    2017.3.7 

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  • 発作性運動誘発性舞踏アテトーゼの一家系例

    板村真司, 瀧川遼, 長岡義晴, 桑原健太郎, 越智英明, 小川和則, 安井耕三, 大内田守, 大守伊織

    第68回中国四国小児科学会  2016.10.29 

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  • A clinical picture of PRRT2-related epilepsy in Japan

    2016.10.7  (一社)日本てんかん学会

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  • PRRT2遺伝子変異を認めたepisodic ataxiaの女児

    柴田 敬, 岡 牧郎, 小林 勝弘, 大内田 守, 大守 伊織

    第27回 日本小児神経学会  2016.7.16  日本小児神経学会

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  • ゲノム編集の基礎知識と状況報告

    大内田 守

    岡山臨床カンファレンス  2016.6.24 

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  • 人工細胞膜を用いた慢性疼痛治療薬の開発研究

    大内田 守

    岡山リサーチパーク研究・展示発表会  2016.3.18 

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  • Direct targets of miR-19a related to lung cancer

    第75回日本癌学会  2016 

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と予後との関連について

    第3回日本HTLV-1学会学術集会  2016 

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  • Metabolic and respiratory acidosis suppresses absence seizures in Cacna 1 a mutant rats

    第45回日本てんかん学会  2011 

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  • Cumulative aberrant methylation in specific genes during progression of Adult T-cell Leukemia/Lymphoma (ATLL).

    The 4th International Symposium for Future Technology Creating Better Human Health and Society  2011 

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  • Scn1a 遺伝子変異に伴う熱性けいれんの新規治療薬の開発.

    第41回中国・四国点頭てんかん研究会  2011 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるDNAメチル化と病態との関連.

    第100回日本病理学会総会  2011 

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常の解析.

    第100回日本病理学会総会  2011 

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  • HTLV-1キャリアにおけるDNA メチル化の解析.

    第100回日本病理学会総会  2011 

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  • Electrophysiological properties of variants of voltage-gated calcium channels in patients with epilepsy

    第34回日本神経科学大会  2011 

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  • Metabolic and respiratory acidosis suppresses absence seizures in Cacna1a mutant rats

    第34回日本神経科学大会  2011 

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  • 食道癌におけるEXO1及びIRF3遺伝子多型と発癌リスクの解析

    第34回日本がん疫学・分子疫学研究会、第18回日本がん予防学会  2011 

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  • Clonal Epigenetic Changes in Specific Genes during Progression of Adult T-cell Leukemia/Lymphoma (ATLL).

    XV International Congress of Virology  2011 

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  • Aberrant expression of PcG proteins in Non-Hodgkin B- and T-Cell Lymphoma: A relation to aggressive sub-types.

    The XXV Symposium of the International Association for Comparative Research on Leukemia and Related Diseases  2011 

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  • Dynamic changes of epigenetic status in specific genes during progression of Adult-T cell Leukemia/Lymphoma (ATLL).

    70th Annual meeting of the Japanese Cancer Associartion  2011 

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  • Cumulative kinetics of epigenetic abnormalities during initiation and progression of Adult T-cell Leukemia/Lymphoma (ATLL).

    15th International Conference on Human Retrovirology  2011 

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  • 肺腺癌のEGFR mutationに関与する遺伝子多型

    第34回日本がん疫学・分子疫学研究会、第18回日本がん予防学会  2011 

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  • Proteomic analysis reveals aberrant retinol metabolism in hepatitis C virus subgenomic replicon-harboring cells

    Digestive Disease Week 2011  2011 

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  • Genetic seizure susceptibility and a SCN1A mutation in patients with acute encephalopathy.

    第53回日本小児神経学総会  2011 

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  • Proteomic analysis of target genes of miR-92-1 in lung cancer.

    The 34th Annual Meeting of the Molecular Biology Society of Japan.  2011 

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  • Identification of direct targets of microRNA-29a in Esophageal squamous cell carcinoma.

    The 34th Annual Meeting of the Molecular Biology Society of Japan.  2011 

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  • 超微量検体による悪性リンパ腫・白血病の早期発見・診断・高感度病態モニタリング技術の開発

    BioJapan2011  2011 

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  • Scn1a変異ラットの高体温誘発発作における高周波振動

    第45回日本てんかん学会  2011 

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  • Identification and functional analysis of miR-19a target genes in lung cancers.

    The 34th Annual Meeting of the Molecular Biology Society of Japan.  2011 

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  • Scn1a遺伝子変異による熱性けいれんの二酸化炭素吸入療法

    第45回日本てんかん学会  2011 

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  • Identification of novel direct target of miR-19a in MCF-7 breast cancer cell

    The AACR 101st Annual Meeting 2010  2010 

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  • Proteomic analysis of target proteins of miR-17-92 cluster in cancer cells

    第69回日本癌学会学術総会  2010 

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  • Identification of true targets of microRNA-183 using labeled miRNA in lung cancer cells.

    第69回日本癌学会学術総会  2010 

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  • 特異的遺伝子群の異常DNAメチル化の集積とMALTリンパ腫の発症・進展

    第69回日本癌学会学術総会  2010 

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  • Identification of target genes of miR-17-92 cluster by proteomic analysis.

    第83回日本分子生物学会  2010 

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  • Identification of true targets of miRNA-183 in lung cancers using labeled ds-miRNA in vitro pull-down assay.

    第83回分子生物学会  2010 

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  • DNA修復、複製遺伝子多型と膵臓発癌リスク

    第69回日本癌学会学術総会  2010 

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  • Multi-step accumulation of aberrant CpG island hypermethylation in specific genes promotes development and progression of lymphomas/leukemias

    15th World Congress on Advances in Oncology and 13th International Symposium on Molecular Medicine.  2010 

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  • Identification of novel target of miR17-92 cluster by proteomic analysis.

    日本分子生物学会年会  2009 

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  • MicroRNA expression profiling in human tumors.

    日本分子生物学会年会  2009 

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  • TP53 遺伝子多型と膵臓癌発症リスク

    第68回日本癌学会学術総会  2009 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるSHP1遺伝子の特異的メチル化と病態との関連

    第2回HTLV-1研究会・合同班会議  2009 

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  • Hyperthermia-induced seizure-susceptible rats as a novel model of febrile seizures

    第32回日本神経科学会  2009 

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  • Proteomic analysis of lung cancer cell lines aimed to identify novel target proteins for miR-17-92 cluster

    日本ヒトプロテオーム機構 第7回大会  2009 

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  • A CACNB4 mutation shows altered Cav2.1 function may be a genetic modifier of severe myoclonic epilepsy in infancy.

    第36回国際生理学会世界大会  2009 

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  • Identification of novel target protein for miR-17-92 cluster by proteomic analysis

    第100回米国癌学会  2009 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNA メチル化と病態との相関

    日本病理学会  2009 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるDNAメチル化の解析

    第28回岡山免疫懇話会  2009 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との関連

    第49回日本リンパ網内系学会総会  2009 

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  • Severe myoclonic epilepsy in infancy with dual channel dysfunction

    第51回日本小児神経学会総会  2009 

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  • 進む癌遺伝子検査について

    福山市民公開講座  2009 

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  • Association of aberrant DNA methylation with the clinicopahthologic characteristics in Adult T cell leukemia/lymphoma

    第68回日本癌学会学術総会  2009 

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  • 難治性小児てんかんの罹患リスク判定技術の開発

    岡山大学知恵の見本市  2009 

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  • Gene therapeutic agent for intractable chronic pain.

    日本分子生物学会年会  2009 

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  • 日本人におけるMMP9遺伝子多型と大腸癌発症リスクとの関係

    第68回日本癌学会学術総会  2009 

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  • 難治性慢性疼痛の新規治療技術の開発

    岡山大学知恵の見本市  2009 

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  • Proteomic analysis of lung cancer cell lines aimed to identify novel target proteins for miR-17-92

    国際ヒトプロテオーム機構会議  2009 

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  • Identification of novel target proteins for miR-17-92 cluster in breast cancer

    第68回日本癌学会学術総会  2009 

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  • 難治性の慢性疼痛に対する新規遺伝子治療薬

    イノベーション・ジャパン2009  2009 

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  • 超微量検体による悪性リンパ腫・白血病の早期発見診断・予後推定法の開発

    イノベーション・ジャパン2009  2009 

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  • Proteomic analysis of miR-17-92 cluster-overexpressing lung cancer cell line aimed to identify novel immediate target protein

    第68回日本癌学会学術総会  2009 

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  • MMP family遺伝子のSNPsと日本人における非小細胞癌発症リスクとの関連

    第31回日本分子生物学会年会 第81回日本生化学会大会  2008 

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  • A patient with Rasmussen encephalitis and SCN1A mutation

    The 11t Annual Meeting of Infantile Seizure Society  2008 

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  • Novel SCN5A Mutations Associated with Japanese Brugada Syndrome Patients

    第72回日本循環器学会総会  2008 

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  • A screening test for the prediction of Dravet syndrome before one year of age

    The 11t Annual Meeting of Infantile Seizure Society  2008 

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  • LC/MS を用いたmicroRNAの標的蛋白の解析

    岡山大学学内COE 平成19年度報告会  2008 

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  • 発がんに関わるmicroRNAの標的蛋白のプロテオミクス解析

    岡山大学重点プロジェクト公開シンポジウム  2008 

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  • ヒト疾患に関連する機能性RNAの同定とその機能解析

    国家プロジェクト「機能性RNA」 研究進捗報告会  2008 

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  • A screening test for the prediction of Dravet syndrome before one year of age

    第42回日本てんかん学会  2008 

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  • 滑膜肉腫関連蛋白の細胞内局在に影響を与える薬剤、及び蛋白に関する検討

    第23回日本整形外科学会基礎学術集会  2008 

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  • プロテオミクス解析を用いた悪性グリオーマの浸潤に関わるタンパクの同定

    第67回日本脳神経外科学会  2008 

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  • IRAK1遺伝子のSNPと食道癌発癌リスクとの関係

    第31回日本がん疫学研究会  2008 

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  • 乳児重症ミオクロニーてんかんの早期診断スクリーニングテスト

    第50回日本小児神経学会総会  2008 

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  • MET amplification in untreated lung cancer patients with EGFR activating mutation, but without T790M mutation, contributes to resistance to gefitinib

    American Association for Cancer Research  2008 

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  • Proteomics based analysis of invasion-related proteins in malignant gliomas

    American Association for Cancer Research  2008 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNA メチル化と病態・予後との相関

    第1回HTLV1研究会  2008 

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  • Proteomics-based analysis of invasion-related proteins in malignant gliomas.

    The 8th Meeting of the Europian Association of Neurooncology  2008 

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  • MECP2遺伝子エキソン1およびプロモーター領域に変異をもつレット症候群

    第50回日本小児神経学会総会  2008 

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  • SCN1A変異を認めたRasmussen脳炎の1例

    第50回日本小児神経学会総会  2008 

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  • Rasmussen encephalitis associated with SCN1A mutation

    BMB2008 (BIOCHEMISTRY AND MOLECULAR BIOLOGY) 2008  2008 

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  • プロテオミクス解析によるmiRNA cluster の新規標的タンパク質の探索

    第31回日本分子生物学会年会 第81回日本生化学会大会  2008 

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  • MicroRNA expression profiling in human esophageal cancer

    BMB2008 (BIOCHEMISTRY AND MOLECULAR BIOLOGY) 2008  2008 

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  • MET gene amplification in lung cancers untreated with Gefitinib.

    67th Annual Meetiong of the Japanese Cancer Association.  2008 

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  • 日本人におけるPTPN13遺伝子多型と各種癌の発症リスクとの関係

    第67回 日本癌学会学術総会  2008 

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  • ヒストン脱アセチル化酵素阻害剤valproic acidと脱メチル化剤zebularineの併用による滑膜肉腫細胞株に対する抗腫瘍効果の検討

    第23回日本整形外科学会基礎学術集会  2008 

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  • 骨肉腫患者における葉酸代謝関連遺伝子の一塩基多型の検討

    第67回 日本癌学会学術総会  2008 

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  • ゲフィニチブ未使用肺癌におけるMET遺伝子増幅について

    第49回日本肺癌学会総会  2008 

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  • 日本における主要な8種のがんの易罹患性に関与する48ミズセンスSNPの総合的解析

    第67回 日本癌学会学術総会  2008 

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  • Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome

    American Heart Association  2008 

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  • High frequent allelic loss of chromosome 6q16-23 in osteosarcoma

    BMB2007(Biochemistry and Molecular Biology 2007)  2007 

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  • 胃原発悪性リンパ腫におけるmethylator phenotypeとH.pylori感染に関する検討

    第96回日本病理学会総会  2007 

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  • Nerve growth factor (NGF) の血管周囲神経再分布作用におけるアンジオテンシン タイプ2受容体 (AT2R)の役割

    第80回日本薬理学会年会  2007 

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  • Significant correlation of the SCN1A mutations and severe myoclonic epilepsy in infancy.

    財団法人てんかん治療研究振興財団第18回研究報告会;研究褒賞受賞特別講演  2007 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype (CIMP)の解析

    第96回日本病理学会総会  2007 

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  • LC/MS解析を目的とした2次元電気泳動における分離能の改善と評価

    岡山大学重点プロジェクト(学内COE)「医歯薬融合による統合的疾患プロテオミクスの構築とその応用研究」公開シンポジウム  2007 

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  • LC/MS を用いたmicroRNAの標的蛋白の解析

    岡山大学重点プロジェクト(学内COE)「医歯薬融合による統合的疾患プロテオミクスの構築とその応用研究」公開シンポジウム  2007 

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  • 網羅的プロテオーム解析による癌および疾病原因遺伝子産物の標的蛋白群の同定と発症機構の解明

    岡山大学学内COE「医歯薬融合による統合的疾患プロテオミクスの構築とその応用研究」研究経過報告会  2007 

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  • ヒト疾患に関連する機能性RNAの同定とその機能解析

    機能性RNAプロジェクト 研究進捗報告会  2007 

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  • ヒト疾患に関連する機能性RNAの同定とその機能解析

    機能性RNAプロジェクト 研究成果報告ヒアリング  2007 

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  • CPG ISLAND METHYLATOR PHENOTYPE (CIMP) PROMOTES THE PROGRESSION OF ADULT TミCELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference of Human Retrovirology HTLV and Related Viruses.  2007 

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  • 胃原発悪性リンパ腫の発症・進展と特異的遺伝子のepigeneticな変化に関する検討

    第47回日本リンパ網内系学会総会  2007 

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  • EPIGENETICALLY DISTINST MALIGNANT CELL POLULATION FORMS LYMPHOMA-INVOLVING LESION IN ACUTE TYPE ADULT TミCELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference of Human Retrovirology HTLV and Related Viruses.  2007 

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  • ABERRANT DNA METHYLATION IS ASSOCIATED WITH THE CLINICOPATHOLOGIC CHARACTERISTICS IN PATIENTS WITH ADULT TミCELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference of Human Retrovirology HTLV and Related Viruses.  2007 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態・臨床症状との相関

    第47回日本リンパ網内系学会総会  2007 

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  • NONFUNCTIONAL SCN1A IS COMMON IN SEVERE MYOCLONIC EPILEPSY IN INFANCY

    International Symposium on Biology of Seizure Susceptibility  2007 

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  • Association of the RAD18 gene Arg302Gln polymorphism with human non-small-cell lung cancer risk

    98th Annual Meeting of American Association for Cancer Research, AACR Annual Meeting  2007 

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  • EGFR mutation status and adjuvant chemotherapy with uracil-tegafur for adenocarcinoma of the lung

    98th Annual Meeting of American Association for Cancer Research, AACR Annual Meeting  2007 

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  • EPIGENETIC ABNORMALITIES ASSOCIATED WITH GENE SILENCING INDUCE ONSET AND PROGRESSION OF LYMPHOMAS/LEUKEMIAS

    98th Annual Meeting of American Association for Cancer Research, AACR Annual Meeting  2007 

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  • CPG ISLAND METHYLATOR PHENOTYPE (CIMP) PROMOTES THE PROGRESSION OF ADULT T–CELL LEUKEMIA/LYMPHOMA (ATLL).

    98th Annual Meeting of American Association for Cancer Research, AACR Annual Meeting  2007 

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  • Trafficking defective SCN1A mutations associated with epilepsy

    IBRO(International Brain Research Organization) WORLD CONGRESS OF NEUROSCIENCE  2007 

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  • Association of the RAD18 gene Arg302Gln polymorphism with human non-small-cell lung cancer risk

    科学研究費補助金「特定領域」・がん研究に係わる特定領域研究・若手研究者ワークショップ  2007 

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  • RASSF6遺伝子のSNPと各種癌の発癌リスクとの関係

    がん予防大会in TOKYO 2007. 第14回日本がん予防学会、第8回日本がん分子疫学研究会、第30回日本がん疫学研究会。  2007 

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  • IPG Strip Gelを用いた2次元電気泳動のspot matching rate向上の検討

    JHUPO 2007(日本ヒトプロテオーム機構 第5回大会)  2007 

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  • Molecular mechanism of loss-of-function for mutant Nav1.1 channels associated with epilepsy

    第49回日本小児神経学会総会  2007 

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  • SCN1A mutation analysis of febrile seizures

    第49回日本小児神経学会総会  2007 

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  • RAD18遺伝子多型と肺癌発症リスクの関連

    がん予防大会in TOKYO 2007. (第14回日本がん予防学会、第8回日本がん分子疫学研究会、第30回日本がん疫学研究会)  2007 

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  • PTPRJ遺伝子のSNPと各種癌の発癌リスクとの関係

    がん予防大会in TOKYO 2007. 第14回日本がん予防学会、第8回日本がん分子疫学研究会、第30回日本がん疫学研究会。  2007 

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  • Clinical characteristics of epilepsy with I1616T mutation of the SCN1A gene

    第49回日本小児神経学会総会  2007 

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  • ミスセンスSNP34種の多重解析によるヒトがん発症危険度の総合的予測

    がん予防大会 in TOKYO 2007(第14回日本がん予防学会、第8回日本がん分子疫学研究会、第30回日本がん疫学研究会)  2007 

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  • Prevalence and Characteristics of SCN5A Gene Abnormalities in Japanese Patients with Brugada Syndrome.

    American Heart Association.  2007 

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  • 滑膜肉腫特異的転座型融合蛋白SS18-SSX及びSS18、SSX蛋白の細胞内局在の解析

    第22回日本整形外科学会基礎学術集会  2007 

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  • 血管周囲神経の再生・分布におけるアンジオテンシンII受容体の発現

    第45回日本薬学・日本病院薬剤師会中国四国支部学術大会2007  2007 

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  • SCN1A missense mutation associated with infantile partial epilepsy.

    Neuro2007(The 30th annual Meeting of the Japan Neuroscience Society, 50th Annual Meeting of the Japanese Society for Neurochemistry, 17th Annual Meeting of the Japanese Neural Network Society)  2007 

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  • High frequent allelic loss of chromosome 6q16-23 in osteosarcoma: Involvement of cyclin C in osteosarcoma

    66th Annual Meeting of the Japanese Cancer Association  2007 

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  • グリオーマ浸潤規定タンパクのプロテオミクス解析

    第8回分子脳神経外科学会  2007 

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  • Proteomics based analysis of invasion-related proteins in malignant gliomas

    第66回日本脳神経外科学会総会  2007 

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  • Proteome analysis of invasion-related proteins in malignant gliomas

    The Human Proteome Organazation (HUPO) 6th Annual World Congress  2007 

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  • Increased risk of lung cancer and colorectal cancer is associated with the the RAD18 polymorphism in Japanese population.

    66th Annual Meeting of the Japanese Cancer Association  2007 

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  • Association of aberrant DNA methylation with clinicopahthologic characteristics in Adult T cell leukemia/lymphoma (ATLL).

    66th Annual Meeting of the Japanese Cancer Association  2007 

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  • プロテオミクス解析を用いた悪性グリオーマの浸潤に関わるタンパクの同定

    第25回日本脳腫瘍学会  2007 

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  • Proteome analysis of invasion-related proteins in malignant gliomas

    BMB2007(Biochemistry and Molecular Biology 2007)  2007 

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  • EFGR変異とUFTによる肺腺癌術後補助療法の関連性についての検討

    第48回日本肺癌学会総会  2007 

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  • Prevalence and Characteristics of SCN5A Gene Abnormalities in Japanese Patients with Brugada Syndrome.

    World Congress on Cardiac Pacing & Electrophysiology Society(ICPES)(WCCPE)  2007 

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  • HIGH SENSITIVE AND HIGH FIDELITY EPIGENETIC DETECTION OF HEMATOPOIETIC MALIGNANCIES

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • Helicobacter pylori infection induces the aberrant CpG island methylation in gastric MALT lymphoma

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • Single nucleotide polymorphism of the RASSF1 gene is associated with human lung adenocarcinoma risk in Janapnese population.

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • Aberrant DNA methylation during the progression of adult T cell leukemia/lymphoma (ATLL).

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • 乳児重症ミオクロニーてんかんにおける変異遺伝子の検索と、変異型イオンチャネルの機能解析

    財団法人てんかん治療研究振興財団第17回研究報告会  2006 

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  • MOLECULAR PATHOLOGICAL ANALYSIS OF THE PROTEIN TYROSINE PHOSPHATASE: SHP1 GENE IN THE PATHOGENESIS OF LYMPHOMAS AND LEUKEMIAS

    97th Annual Meeting of American Association for Cancer Research  2006 

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  • 網羅的プロテオーム解析による癌および疾病原因遺伝子産物の標的蛋白群の同定と発症機構の解明

    岡山大学学内COE「医歯薬融合による統合的疾患プロテオミクスの構築とその応用研究」研究経過報告会  2006 

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  • Abberant DNA metylation in the progression of adult T cell leukemia/lymphoma (ATLL).

    97th Annual Meeting of American Association for Cancer Research  2006 

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  • SHP1 遺伝子発現抑制 と悪性リンパ腫・白血病発症機構の解析

    第95回日本病理学会総会  2006 

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  • 滑膜肉腫細胞株におけるFK-228による細胞増殖抑制機構のプロテオーム解析。

    骨軟部腫瘍セミナー  2006 

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  • CpG ISLAND METHYLATOR PHENOTYPE (CIMP) PROMOTES THE PROGRESSION OF ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL).

    The 10th Japanese-Korean Lymphoreticular Workshop  2006 

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  • EXO1遺伝子のms-SNPと肺癌発症リスクの関連

    第65回 日本癌学会学術総会  2006 

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  • 胃原発悪性リンパ腫におけるHelicobacter pylori感染とmethylator phenotype

    第65回 日本癌学会学術総会  2006 

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  • GENE SILENCING ASSOCIATED WITH EPIGENETIC ABNORMALITIES INDUCES ONSET AND PROGRESSION OF LYMPHOMAS/LEUKEMIAS

    The 10th Japanese-Korean Lymphoreticular Workshop  2006 

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  • THE ABERRANT DNA HYPERMETHYLATION INDUCED BY HELICOBACTER PYLORI INFECTION HELICOBACTER PYLORI INFECTION DEVELOPS THE PROGRESSION OF GASTRIC MALT LYMPHOMA

    The 10th Japanese-Korean Lymphoreticular Workshop  2006 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype (CIMP)

    第46回日本リンパ網内系学会総会  2006 

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  • 胃原発悪性リンパ腫におけるHelicobacter pylori感染とmethylator phenotype

    第46回日本リンパ網内系学会総会  2006 

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  • OSZF, a novel human oncoprotein, recruits mSin3A corepressor to mediate transcriptional repression.

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • Functional analysis of SYT-SSX fusion protein in synovial sarcoma

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB congress.  2006 

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  • カルバマゼピン投与ラットにおける血中と肝臓中の生産CYPmRNA量の相関性の検討。

    第23回日本TDM(Therapeutic Drug Monitoring)学会学術大会  2006 

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  • 血管周囲神経の再生・分布におけるアンジオテンシンⅡ受容体の発現

    第45回日本薬学会日本病院薬剤師会中国四国支部学術大会  2006 

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  • 乳児重症ミオクロニーてんかんとその辺縁てんかん症候群におけるSCN1A遺伝子異常

    日本分子生物学2006フォーラム  2006 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype (CIMP)の解析

    第65回 日本癌学会学術総会  2006 

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  • 異常メチル化によるSHP1 gene silencing と悪性リンパ腫・白血病発症機構

    第65回 日本癌学会学術総会  2006 

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  • 食道癌におけるアルコール代謝関連及びがん関連遺伝子のSNPs解析

    第7回日本がん分子疫学研究会・第29回日本がん疫学研究会合同学術集会  2006 

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  • 肺癌におけるDNA修復遺伝子EXO1のSNP解析

    日本分子生物学2006フォーラム  2006 

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  • 滑膜肉腫における転座遺伝子SYT-SSX蛋白とヒストン脱アセチル化酵素複合体因子の相互作用

    第28回日本分子生物学会年会  2005 

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  • AXIN2遺伝子のミスセンス一塩基多型(Pro50Ser)と肺癌発症リスクの関連

    第64回日本癌学会学術総会  2005 

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  • Ewing’s sarcoma family of tumor融合遺伝子の検索

    第20回日本整形外科学会基礎学術集会  2005 

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  • Clinical and genetic variables in predicting the occurance of ventricular fibrillation in Janpanese patients with Brugarda type ECG.

    American Heart Association  2005 

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  • 成人T細胞性白血病(ATL)におけDNA異常メチル化の解析

    第64回日本癌学会学術総会  2005 

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  • Deletion Mapping of 2q21-37 Region in Oral Cancer.

    Proceedings of International Symposium of Maxillofacial and Oral Regenerative Biology  2005 

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  • Detection of epidermal growth factor receptor (EGFR) gene mutations in lung cancer patients by enriched PCR assay.

    96th Annual Meeting of American Association for Cancer Research  2005 

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  • 滑膜肉腫における転座遺伝子SYT-SSXの機能解析

    熊本大学理学部生物学科生物学科特別セミナー  2005 

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  • 造血器腫瘍の高感度・高精度検出技術の開発

    第94回日本病理学会  2005 

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  • 悪性リンパ腫/白血病の発症機構におけるSHP-1 gene silencingの果たす役割についての解析

    第94回日本病理学会総会  2005 

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  • T細胞性悪性リンパ腫における、SHP1 gene silencingの解析

    第64回日本癌学会学術総会  2005 

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  • 悪性リンパ腫・白血病におけ異常メチル化によるSHP1 gene silencingの解析

    第64回日本癌学会学術総会  2005 

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  • 滑膜肉腫における転座遺伝子SYT-SSX蛋白とヒストン脱アセチル化酵素複合体因子mSin3Aの相互作用

    第27回日本分子生物学会年会  2004 

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  • がん抑制遺伝子群のミスセンス1塩基多型と肺がん、頭頸部がんのリスク

    第5回日本がん分子疫学研究会学術集会  2004 

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  • 滑膜肉腫における転座遺伝子SYT-SSXの機能解析

    骨軟部腫瘍研究会、特別講演  2004 

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  • 造血器腫瘍とepigenetics関連疾患の早期発見・診断技術

    国際バイオEXPO (BIO EXPO JAPAN) 、  2004 

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  • Inactivation of p57Kip2 by promoter hypermethylation in non-small cell lung cancers.

    95th Annual Meeting of American Association for Cancer Research,  2004 

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  • 高齢にて発症したQT延長症候群の一例

    第12回臨床心臓病研究会、シンポジウム  2004 

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  • HEMATOPOIETIC CELL SPECIFIC TYROSINE PHOSPHATASE: SHP1 AS A NOVEL BIOMARKER OF HEMATOPOIETIC MALIGNANCIES

    The 7th International Symposium on Predictive Oncology and Intervention Strategies.  2004 

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  • B細胞性悪性リンパ腫におけるH-cadherin遺伝子領域のLOH解析とDNAメチル化の検討

    第63回日本癌学会学術総会  2004 

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  • SHP1遺伝子CpGisland メチル化によるB細胞リンパ腫の異常増殖

    第63回日本癌学会学術総会  2004 

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  • 非小細胞癌におけるSNF2family遺伝子、SMARCA6の発現異常

    第63回日本癌学会学術総会  2004 

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  • CGH法、マイクロサテライト解析を用いた骨肉腫における染色体不安定性の検討

    日本整形外科学会 骨・軟部腫瘍学術集会  2004 

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  • 新規高感度・高精度悪性リンパ腫・白血病biomarker:チロシンフォスファターゼSHP1

    第1回日本病理学会カンファレンス、日本病理学会カンファレンス2004広島  2004 

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  • がん関連遺伝子のミスセンス1塩基多型と肺がん、頭頸部がんのリスク

    第5回日本がん分子疫学研究会学術集会  2004 

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  • 高齢にて発症したQT延長症候群の一例

    日本循環器学会中国地方会  2004 

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  • 腎癌患者における14q24ー31の染色体欠質と予後不良の相関性

    第63回日本癌学会学術総会  2004 

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  • 日本人におけるEXO1遺伝子のSNPと大腸癌リスクの関連についての解析

    第63回日本癌学会学術総会  2004 

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  • 超微量検体を用いた造血器腫瘍関連疾患の早期発見・診断技術の開発

    Inovation Japan  2004 

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  • 滑膜肉腫におけるSYT-SSX蛋白結合因子の解析

    第63回日本癌学会学術総会  2004 

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  • Posotive correlation between allelic loss at chromosome 14q24-31 and poor prognosis of patients with renal cell carcinoma.

    第27回日本分子生物学会年会  2004 

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  • 肺癌、大腸癌におけるIKKB,HER2遺伝子のミスセンス1塩基多型

    第27回日本分子生物学会年会  2004 

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  • B細胞性悪性リンパ腫におけるCDH13遺伝子プロモーター領域の高頻度メチル化

    第27回日本分子生物学会年会  2004 

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  • 食道癌におけるWWOX・ATR遺伝子のSNPs及びLOH解析

    第63回日本癌学会学術総会  2004 

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  • 骨肉腫における染色体欠失と癌抑制遺伝子候補の検討

    第19回日本整形外科学会基礎学術集会  2004 

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  • POZ-Znフィンガー蛋白質OCZFの新しい転写制御機構

    第63回日本癌学会学術総会  2004 

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  • RASSF1遺伝子におけるms-SNP(Ala133Ser)と肺癌リスクの検討

    第63回日本癌学会学術総会  2004 

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  • EXO1遺伝子のSNP

    第27回日本分子生物学会年会  2004 

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  • DUSP6遺伝子のミスセンス1塩基多型(Val114Leu)と肺癌の関連

    第27回日本分子生物学会年会  2004 

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  • Molecular Pathological Analyses of the Gene Related to the Pathogenesis of Lymphomas/leukemias with Complementary DNA and Tissue Microarray. Chromatin, Chromosomes and Cancer Epigenetics.

    An AACR Special Conference in Cancer Research.  2004 

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  • Frequent deletion and increased mRNA expression of a candidate tumor suppressor gene at 19p13 region, BRG1, in oral cancers.

    International Symposium of Molecular Biology on Tooth Induction, Odontogenic Tumor and Oral Cancer.  2003 

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  • Aberrant Promoter Methylation in human DAB2 interactive protein (hDAB2IP) Gene in Breast Cancer.

    94rd Annual Meeting of the American Association for Cancer Research.  2003 

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  • Frequent deletion and reduced expression of a candidate tumor suppression gene at 9p24 region, hBRM, in head and neck cancers.

    94rd Annual Meeting of the American Association for Cancer Research.  2003 

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  • 悪性リンパ腫・白血病におけるSHP1遺伝子の発現抑制機構の解析

    日本病理学会2003年4月23-25日  2003 

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  • 滑膜肉腫に認められる転座遺伝子SYT-SSXのTwo Hybrid Assayを用いた機能解析

    第36回日本整形外科学会骨・軟部腫瘍学術集会  2003 

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  • Gene silencing of the SHP1 Tyrosine Phosphatase gene by aberrant methylation in leukemias/lymphomas

    United States and Canadian Academy of Pathology  2003 

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  • B細胞系悪性リンパ腫におけるSHP1遺伝子の発現抑制とCpG islandのメチル化の解析

    日本病理学会  2003 

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  • MOLECULAR PATHOLOGICAL ANALYSIS OF THE GENES RELATED TO THE PATHOGENESIS OF LYMPHOMAS/LEUKEMIAS WITH cDNA AND TISSUE MICROARRAYS.

    8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine  2003 

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  • SYT-SSXアイソフォーム蛋白による転写活性能と細胞増殖能の昂進

    第62回日本癌学会総会  2003 

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  • 滑膜肉腫関連蛋白SYT、SSXの機能解析と治療への応用:

    第18回日本整形外科学会基礎学術集会  2003 

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  • 新規ヒト遺伝子OSZFはmSin3Aを介して転写制御する

    第62回日本癌学会総会  2003 

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  • 悪性リンパ腫・白血病におけるチロシンフォスファターゼSHP1遺伝子発現抑制機構

    第62回日本癌学会総会  2003 

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  • SYT蛋白とSSX蛋白のyeast two hybrid assayを用いた機能解析

    第62回日本癌学会総会  2003 

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  • 骨肉腫におけるRFC1(Reduced Folate Carrier1)の一塩基多型の検討

    第62回日本癌学会総会  2003 

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  • Fibroblast growth factor receptor 4 (FGFR4)のSNPと骨軟部肉腫の予後の検討

    第62回日本癌学会総会  2003 

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  • 白血病細胞におけるHLA class Iの発現低下および再発との関連性

    第62回日本癌学会総会  2003 

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  • astrocytic tumor における19番染色体長腕の遺伝子異常と悪性度との関係

    第62回日本癌学会総会  2003 

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  • 滑膜肉腫における新しいSYT-SSXアイソフォーム蛋白の機能解析

    日本分子生物学会  2003 

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  • 分子標的を用いたSYT-SSX発現細胞に株特異的な抗腫瘍効果の検討

    日本分子生物学会  2003 

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  • REDUCED EXPRESSION OF THE SHP1 GENE IN B-CELL MALIGNANCIES BY THE ABERRANT METHYLATION.

    8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine  2003 

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  • Quantitative and Qualitative Analyses of Free DNA in Blood from Cancer Patients

    The 13th International Symposium of the Hiroshima Cancer Seminar.  2003 

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  • 乳児重症ミオクロニーてんかん患者にて検出されたナトリウムチャンネル遺伝子SCN1Aの高頻度突然変異

    第25回日本分子生物学会年会  2002 

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  • Mutation analysis of Nav1.1 and GABRG2 in patients with severe myoclonic epilepsy in infancy and its borderland.

    The 9th International Child Neurology Congress  2002 

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  • ヒト腫瘍細胞における、プロモーター領域高メチル化によるREIC/Dkk-3遺伝子の発現制御

    第61回日本癌学会総会  2002 

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  • 乳児重症ミオクロニーてんかんおよび辺縁群21症例のNav1.1遺伝子解析と臨床症状との関連性

    第44回日本小児神経学会総会  2002 

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  • mRNA expression analysis oh ING1 splicing variants and methylation status in head and nech cancers

    11th Biennial Meeting of International Association of Oral Pathlogy  2002 

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  • Astrocytic tumorにおける10番染色体長腕遺伝子異常と悪性度との関連

    第61回日本癌学会総会  2002 

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  • Allelic loss and reduced expression of the ING3, a candidate tumor supressor gene at 7q31, in human head and neck cancers.

    93rd Annual Meeting of the American Association for Cancer Research.  2002 

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  • 末梢血遊離DNAによる担癌患者の高感度早期発見分子診断法

    第3回日本がん分子疫学研究会  2002 

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  • Molecular Genetical Analysis of ING Family Genes in Head and Neck Cancers.

    The 48th Annual Congress of Lapa Section International College of Surgeons.  2002 

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  • 14q24-31 IS A NEW SUPPRESSOR GENE LUCUS OF RENAL CELL CARCINOMA -INTER-ALU LONG PCR GENOMIC SCAN AND MICROSATELLITE ANALYSIS-

    97th Annual Meeting of the American Urology Association  2002 

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  • Astrocytomaにおける10番染色体長腕遺伝子異常と悪性度との関連

    第20回日本脳腫瘍病理学会  2002 

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  • 新規癌抑制遺伝子hBRMの頭頚部癌における発現と遺伝子解析

    第61回日本癌学会総会  2002 

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  • 二相性滑膜肉腫より樹立した培養細胞株(SYO-1)の性状

    第61回日本癌学会総会  2002 

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  • 新規ヒト遺伝子OSZFはmSin3Aを介して転写制御する。

    第25回日本分子生物学会年会  2002 

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  • ヒト癌組織特異的ING1変異型遺伝子の機能解析

    第24回日本分子生物学会年会  2001 

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  • ヒト癌組織特異的ING1変異型遺伝子の解析

    第60回日本癌学会総会  2001 

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  • BTB/POZ domainとZinc-Fingerをもつ新規ヒト遺伝子OSZFの解析

    第60回日本癌学会総会  2001 

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  • Cloning and chracterization of a novel human gene, OSZF, encoding a Zinc-finger protein with the BTB/POZ domain

    文部科学省がん研究に係わる特定領域研究C第2回若手研究者ワークショップ  2001 

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  • 末梢血遊離DNAによる癌の高感度遺伝子診断に関する基礎的研究

    第60回日本癌学会総会  2001 

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  • 食道扁平上皮癌おける17qのヘテロ接合性欠失の意義

    第60回日本癌学会総会  2001 

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  • 染色体7q31に位置する癌抑制遺伝子候補ING3の頭頚部癌におけるヘテロ接合性の消失と発現の解析

    第60回日本癌学会総会  2001 

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  • Non-small cell lung carcinomaにおけるAlix/AIP1のSNP解析

    第60回日本癌学会総会  2001 

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  • 腎細胞癌における染色体14qでの微小欠失の検討

    第10回泌尿器科細胞解析研究会  2001 

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  • 破骨細胞で発現するPOZ-Zn フィンガー型転写制御因子OCZFの機能

    第24回日本分子生物学会年会  2001 

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  • 滑膜肉腫培養細胞に対するBcl-2アンチセンスオリゴヌクレオチドの効果

    第60回日本癌学会総会  2001 

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  • BTB/POZ domain とZinc-Fingerをもつ新規ヒト遺伝子、OSZFの解析

    第23回日本分子生物学会年会  2000 

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  • Poperties of the mutant E2F-4 detected in gastrointestinal cancers on growth control and transactivation.

    91st Annual Meeting of the American Association for Cancer Research.  2000 

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  • PCR-SSCP and DNA sequencing analyses

    Asian science seminar in Okayama 2000  2000 

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  • グリオーマの悪性度と10番染色体遺伝子異常との関連性に関する検討

    第59回日本脳神経外科学会  2000 

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  • POZドメインZnフィンガー型転写制御因子osteoclast zinc finger protein (OCZF)の破骨細胞の分化における役割。

    第18回日本骨代謝学会年会。  2000 

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  • DNA cloning into plasmid vector and DNA analysis by restriction enzymes.

    Asian science seminar in Okayama 2000.  2000 

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  • BTB/POZ-Zn フィンガー型蛋白質OCZFの転写抑制及び促進作用

    第23回日本分子生物学会年会  2000 

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  • ヒトING1遺伝子のゲノム構造解析と頭頸部癌における癌部特異的遺伝子変異の解析

    第23回日本分子生物学会年会  2000 

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  • WDC-146の遺伝子構造と転写調節機構の解析

    第22回日本分子生物学会年会  1999 

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  • 軟部肉腫の診断における分子生物学的手法の有用性、-SYT-SSX融合遺伝子を中心に-。

    第32回 日本整形外科学会  1999 

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  • E2F4による発癌機構。

    第10回日本消化器癌発生学会総会、  1999 

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  • 破骨細胞で発現するPOZ-Zn型蛋白質OCZFの転写活性の解析

    第22回日本分子生物学会年会  1999 

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  • HD-PTP:3p21.3に位置する新たなヒトチロシンホスファターゼ癌抑制遺伝子候補。

    第58回 日本癌学会総会、  1999 

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  • ヒト染色体3p21.3に位置するチロシンフォスファターゼHD-PTP遺伝子の解析

    第22回日本分子生物学会年会  1999 

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  • 消化器癌で発見された変異E2F4による発癌機構。

    第58回日本癌学会総会  1999 

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  • 腎癌における染色体14qでの微小欠失の検討。

    第58回日本癌学会総会  1999 

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Industrial property rights

  • 遺伝子改変非ヒトモデル動物

    大守 伊織, 大内田 守, 真下 知士

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    Applicant:大守 伊織

    Application no:特願2019-514326  Date applied:2018.12.6

    Publication no:WO2019-117022  Date published:2019620

    Patent/Registration no:特許6650649  Date registered:2020.1.23 

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  • 抗てんかん薬

    大守 伊織, 大内田 守

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    Applicant:大守 伊織

    Application no:特願2018-188510  Date applied:2018.10.3

    Announcement no:特開2018-203782  Date announced:2018.12.27

    Patent/Registration no:特許6587299  Date registered:2019.9.20 

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  • TrkBアンタゴニストを含む医薬組成物

    大内田 守, 中塚 秀輝, 板野 義太郎, 羽間 恵太, 池田 佳恵, 三棹 聡美

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    Applicant:国立大学法人 岡山大学

    Application no:特願2018-150847  Date applied:2018.8.9

    Announcement no:特開2020-026397  Date announced:2020.2.20

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  • てんかん波を伴う疾患治療剤

    大内田 守, 大守 伊織, 改田 祐子

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    Applicant:国立大学法人 岡山大学

    Application no:特願2015-154053  Date applied:2015.8.4

    Announcement no:特開2015-227365  Date announced:2015.12.17

    Patent/Registration no:特許5791604  Date registered:2017.6.16 

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  • ATLLの診断のためのデータ取得方法、ATLL診断用キットおよびATLL診断システム

    岡 剛史, 大内田 守, 吉野 正

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    Applicant:国立大学法人 岡山大学

    Application no:特願2013-026614  Date applied:2013.2.14

    Announcement no:特開2013-188208  Date announced:2013.9.26

    Patent/Registration no:特許第6156621号  Date registered:2017.6.16 

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  • microRNAを有効成分とするIMPDH阻害剤

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    Application no:特願2013-545886  Date applied:2012.11.14

    Patent/Registration no:特許5632101  Date registered:2014.10.17 

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  • 腎障害の新規マーカー

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    Application no:特願2011-210489  Date applied:2011.9.27

    Announcement no:特開2012-093351  Date announced:2012.5.17

    Patent/Registration no:特許5830329  Date registered:2015.10.30 

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  • 疼痛の治療剤

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    Application no:特願2011-172529  Date applied:2011.8.8

    Announcement no:特開2012-067081  Date announced:2012.4.5

    Patent/Registration no:特許6105838  Date registered:2017.3.10 

    特開2012-067081

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  • microRNA標的遺伝子検出用キット及びmicroRNA標的遺伝子の検出方法

    大内田 守, 伊藤 佐智夫

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    Applicant:国立大学法人 岡山大学

    Application no:特願2012-520465  Date applied:2011.6.15

    Patent/Registration no:特許第5841941号  Date registered:2015.11.20 

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  • Dravet症候群の発症可能性の判定方法およびその利用

    大守 伊織, 大内田 守

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    Applicant:国立大学法人 岡山大学

    Application no:特願2011-551907  Date applied:2011.1.27

    Patent/Registration no:特許5846372  Date registered:2015.12.4 

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  • 疼痛の治療剤およびその利用

    板野 義太郎, 松岡 義和, 大内田 守

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    Applicant:国立大学法人 岡山大学

    Application no:特願2010-514435  Date applied:2009.5.14

    Patent/Registration no:特許5545211  Date registered:2014.5.23 

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  • 成人T細胞白血病・リンパ腫の予後推定法およびキット

    岡 剛史, 佐藤 妃映, 大内田 守, 吉野 正

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    Applicant:国立大学法人 岡山大学

    Application no:特願2009-068048  Date applied:2009.3.19

    Announcement no:特開2009-254357  Date announced:2009.11.5

    Patent/Registration no:特許5522348  Date registered:2014.4.18 

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  • 小児てんかん患者における急性脳炎または急性脳症の罹患リスク判定データの取得方法およびその利用

    大守 伊織, 大内田 守

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    Applicant:国立大学法人 岡山大学

    Application no:特願2008-274887  Date applied:2008.10.24

    Announcement no:特開2009-131247  Date announced:2009.6.18

    Patent/Registration no:特許5540343  Date registered:2014.5.16 

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  • MALTリンパ腫の検査方法及びキット

    岡 剛史, 近藤 孝美, 吉野 正, 大内田 守

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    Applicant:国立大学法人 岡山大学

    Application no:特願2008-521274  Date applied:2007.6.15

    Patent/Registration no:特許EP 2034029  Date registered:2012.6.8 

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  • 造血器腫瘍の検査方法およびキット

    岡 剛史, 佐藤 妃映, 大内田 守, 吉野 正

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    Applicant:国立大学法人 岡山大学

    Application no:特願2007-033603  Date applied:2007.2.14

    Announcement no:特開2007-244377  Date announced:2007.9.27

    Patent/Registration no:特許第4088694号  Date registered:2008.3.7 

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  • Dravet症候群の早期診断を可能にするためのデータを取得する方法及びその利用

    大守 伊織, 大内田 守, 大塚 頌子

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    Applicant:国立大学法人 岡山大学

    Application no:特願2007-007449  Date applied:2007.1.16

    Announcement no:特開2008-173193  Date announced:2008.7.31

    Patent/Registration no:特許4461263  Date registered:2010.2.26 

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  • 軟部肉腫治療剤

    伊藤 達男, 尾崎 敏文, 大内田 守

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    Applicant:アステラス製薬株式会社

    Application no:特願2006-516853  Date applied:2004.6.25

    Patent/Registration no:特許4661782  Date registered:2011.1.14 

    特許第4661782号

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  • メチル化DNA検出方法

    岡 剛史, 大内田 守

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    Applicant:独立行政法人科学技術振興機構

    Application no:特願2004-136550  Date applied:2004.4.30

    Announcement no:特開2005-058217  Date announced:2005.3.10

    Patent/Registration no:特許第4166725号  Date registered:2008.8.8 

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  • 遺伝子改変非ヒトモデル動物

    大守伊織, 真下知士, 大内田 守

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    Application no:特願CN 201880080055.4 

    Patent/Registration no:特許ZL201880080055.4  Date registered:2024.2.9 

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  • 遺伝子改変非ヒトモデル動物

    大守伊織, 真下知士, 大内田 守

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    Application no:特願EP18887944.9 

    Patent/Registration no:特許EP3725879  Date registered:2024.7.3 

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Works

  • 第8回 DSANJ Digital Bio Conference 2021

    大内田 守

    2021.8.25

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  • BioJapan 2011

    岡 剛史, 大内田 守

    2011.10.5

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  • 創薬シーズ・基盤技術アライアンスネットワーク 疾患別・基盤技術別商談会

    大内田守

    2010.11.30

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  • 中国地域さんさんコンソ 新技術説明会

    大内田守

    2010.8.20

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  • 国際バイオEXPO

    大内田守

    2010.6.30

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  • 第9回 国際バイオEXPO バイオアカデミックフォーラム

    大内田守

    2010.6.30

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  • 岡山大学知恵の見本市(2)

    大内田 守, 大守伊織

    2009.11.6

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  • 岡山大学知恵の見本市(1)

    大内田 守

    2009.11.6

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  • Inovation Japan

    大内田守, 板野義太郎

    2009.9.16

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  • イノベーションジャパン

    岡剛史, 佐藤妃映, 吉野正, 大内田守

    2009.9.16

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  • Inovation Japan

    大内田 守

    2004

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  • 国際バイオEXPO

    大内田 守

    2004

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Awards

  • 財団法人てんかん治療研究振興財団研究褒賞

    2007  

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    Country:Japan

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Research Projects

  • 機能的インターラクトーム解析による滑膜肉腫抗腫瘍作用のメカニズムの解明

    Grant number:23K08652  2023.04 - 2026.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    大内田 守

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

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  • 酸化ストレスによる神経細胞死とてんかん発症機序に関する多層オミックス解析

    Grant number:22K07914  2022.04 - 2025.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    大守 伊織, 大内田 守

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

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  • MCLMR症候群における輸送蛋白の役割

    Grant number:21K07845  2021.04 - 2025.03

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    綾 邦彦, 大内田 守

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

    MCLMR症候群(Microcephaly with or without chorioretinopathy,lymphedema,or mental retardation)は、ある輸送蛋白の異常が原因と考えられている。症状は多彩で、小頭症、網脈絡膜症を含む眼症状、下肢の先天性リンパ浮腫、軽度から中度の知的障害以外に、筋力低下、静脈瘤、肺血管異常、口蓋裂、糖尿病、線維肉腫、糸球体症、蛋白尿、反復性皮膚感染症、反復性尿路感染症、重複腎、脊髄くも膜嚢胞、尿細管間質性腎炎、翼状頸、蜂窩織炎、ファロー四徴症心室中隔欠損など様々な症状が報告されている(syndromefinder.ncchd.go.jp/UR-DBMS/)。また 本輸送蛋白は、中枢神経、呼吸器、膵臓を含む消化器、腎尿路、精巣を含む男性生殖器、卵巣を含む女性生殖器、心筋を含む筋組織、皮膚、リンパ組織、骨髄、内分泌器官など広範囲に発現しており、多彩な症状を発症することとよく相関する。本輸送蛋白の通常のノックアウトマウスが胎生致死であるため、本輸送蛋白のコンディショナルノックアウトマウスは、現時点では最適な本疾患のモデルマウスになりうると考えられる。これを解析することでMCLMR症候群における本輸送蛋白の役割を明らかにすることができると推測される。また、表現系を詳細に解析することで、各症状自体の発症メカニズムの解明にもつながることが期待される。今年度は、マウスの系統維持を行いながら、妊娠マウスを使って、胎齢の異なる胎児マウスに時期特異的に本輸送蛋白をノックアウトする実験を行い、ノックアウトする時期とその表現系の確認を行った。

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  • 肺がんにおける癌関連遺伝子MYNNとp53の相互制御機構の解明

    Grant number:21K08668  2021.04 - 2024.03

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    伊藤 佐智夫, 堺 明子, 大内田 守

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

    これまでに申請者は、マウス尾静脈接種実験を行い、MYNN過剰発現細胞では肺への癌細胞の浸潤および定着が亢進すること、MYNN発現抑制細胞では浸潤および定着が抑制されることを発見した。またMYNNとp53が直接結合していること、DNA損傷刺激によるp53の活性化でMYNNタンパク質量が減少すること、MYNN過剰発現でp53およびp21が減少すること、MYNN抗体を用いたクロマチン免疫沈降 (ChIP)でMYNNがいくつかのp53標的遺伝子の調節領域に結合することを発見した。
    まずp53によるMYNNの発現調節機構を転写制御および転写後抑制から検証した。p53の過剰発現に伴いMYNN mRNAは僅かながら減少がみられたため、MYNNの調節領域・遺伝子領域に存在するp53レスポンスエレメント (p53RE)を同定し、それらp53REをルシフェラーゼレポータープラスミドにクローニングする。p53-wtをもつA549・H460ヒト肺腺癌細胞に構築したルシフェラーゼレポータープラスミドを導入し、エトポシド等のDNA切断型抗がん剤でp53を活性化させた後、ルシフェラーゼ活性を計測した。その結果では有意差は確認されなかったが引き続き検証を行う。また、p53活性化に伴い発現誘導されるmicroRNA (miRNA)が報告されており、申請者は、これらmiRNAの標的配列をMYNN mRNA-3’UTR上で確認している。p53活性化後、miRNAの発現亢進をTaqMan miRNAアッセイで、MYNNタンパク質発現低下をウェスタンブロット法で検証した。miRNA発現ベクターとMYNN-3’UTRの標的配列(wt/mut)をもつルシフェラーゼレポータープラスミドをそれぞれ構築してルシフェラーゼ活性を計測した。その結果、1つのmiRNAによる転写後抑制が確認された。

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  • Development of irregular X-chromosome inactivation-specific targeted therapy

    Grant number:20K07687  2020.04 - 2023.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    伊藤 達男, 中田 英二, 大槻 剛巳, 大内田 守

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

    研究目的:国内での第1相試験開始に向けた非臨床POC獲得のための試験データの回収
    研究内容:BET抑制剤Plx2に対して、抗腫瘍効果が期待できるバイオマーカーとして融合遺伝子SS18-SSX以外の項目を探索するため、性差での薬剤感受性評価検証試験を行う。
    結果:BET抑制剤である化合物Plx2が抗腫瘍効果を発揮する条件として、融合タンパク質SS18-SSXの存在と性差が重要因子であるとの結果を得た。更に、性差での効果の差は明確には確認できなかった。IC50が低値を示した滑膜肉腫細胞株2株はいずれも女性由来であった。追加で検証した項目では、BET遺伝子の発現を抑制した女性由来の滑膜肉腫細胞株ではX染色体上にある遺伝子群で優位に発現量の変化をきたしていた。

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  • 染色体転座型癌遺伝子産物に対する新規阻害剤の探索

    2017.12 - 2019.11

    日本医療研究開発機構  創薬支援推進事業 

    大内田 守

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  • Practical Application of Cancer Suppressor BAP1 Activity as a Biomarker for Malignant Mesothelioma

    Grant number:17K09157  2017.04 - 2020.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Ito Tatsuo

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

    BRCA1-associated protein 1 (BAP1) is one of the major tumor suppressor genes in malignant pleural mesothelioma. In this study, we clarified the role of BAP1 in nonhomologous end-joining (NHEJ).
    RESULTS: We found that inactivation of BAP1 was associated with increased DNA damage in both human mesothelial cells and human malignant mesothelioma cell lines. Furthermore, proteomic analysis identified DNA protein kinases (DNA-PKcs), which function in the NHEJ pathway of DNA repair, as interaction partners of the BAP1 protein complex in MPM and 293T cells.

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  • Single cell analysis of dynamic change of epigenetic abnormalities in adult T cell leukemia/lymphoma (ATL)

    Grant number:16K08667  2016.04 - 2021.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Oka Takashi

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    Grant amount:\4810000 ( Direct expense: \3700000 、 Indirect expense:\1110000 )

    Adult T-cell leukemia/lymphoma (ATL), an aggressive type of T-cell malignancy, is induced by human T-cell leukemia virus type I (HTLV-1) infection. The outcomes, following therapeutic interventions for ATL, have not been satisfactory. In the present investigation, we established live-cell imaging method of DNA methylation using methylated DNA binding protein (MBD) fused with enhanced green fluorescent protein (EGFP); MBD-EGFP to detect dynamic changes of DNA methylation induced by endogenous and/or exogenous environmental perturbations in human leukemia cells. Comprehensive global DNA methylation and gene expression analyses revealed dynamic changes of target gene methylation and gene expression followed by HTLV1tax gene expression. In vitro live cell imaging of DNA methylation with HTLV-1tax-oncogene ON/OFF system is useful system to investigate epigenetic mechanism of ATL leukemogenesis/lymphomagenesis.

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  • Study of the pathogenesis of west syndrome using a new model rat

    Grant number:16H05354  2016.04 - 2020.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    Ouchida Mamoru

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    Grant amount:\17030000 ( Direct expense: \13100000 、 Indirect expense:\3930000 )

    On the study of mutant rats established by ENU mutagenesis, we found a lineage of diseased rats with developmental and epileptic encephalopathy-like epilepsy. Epileptic seizures occurred during a limited period of 4 to 6 weeks of age. The brain lesions were recovered spontaneously. The causative gene found in the rats is a missense mutation of a gene that regulates oxidative stress by redox reaction. Our results suggested that there may be a critical period when the oxidative stress becomes particularly high in the local region of the brain during the developmental process of the brain. Mutant rats may have reduced ability to properly suppress the oxidative stress due to its low function of antioxidant activity, resulting in damage of the brain.

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  • clarification of the mechanism of proteinuria related with tranport protein

    Grant number:26461611  2014.04 - 2018.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    AYA KUNIHIKO

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    Grant amount:\4940000 ( Direct expense: \3800000 、 Indirect expense:\1140000 )

    Though we induced proteinuria the podocyte-specific conditional knockout mice of this transport protein with LPS, we could not find strong tendency of the degree of albuminuria in knockout mice compared with control. We created the tamoxifen-inducible knockout mice of this transport protein. After tamoxifen administration, poor weight gain and atypical glands in intestine was found in these knockout mice.

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  • Development of a animal model of acute encephalopathy and an antibody therapy

    Grant number:26670500  2014.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research  Grant-in-Aid for Challenging Exploratory Research

    Ohmori Iori

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    Grant amount:\3250000 ( Direct expense: \2500000 、 Indirect expense:\750000 )

    We tried to establish an animal model of acute encephalopathy with convulsive status epilepticus. We used Scn1a mutant rats because SCN1A mutations have been linked to hyperthermia-induced seizure susceptibility and acute encephalopathy with a prolonged seizure in human. We induced seizures with various conditions or by using drugs with a proinflammatory effect. Seizures are evoked in Scn1a mutant rats, however, they did not last more than 30 minutes which are often observed in acute encephalopathy in human. Various behavioral tests and pathological examinations of the brain were conducted after provoked seizures. They showed no cognitive impairment and motor disturbance. Pathological tests exhibited no brain edema nor inflammation.

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  • Epigenetic abnormalities during onset and progression of adult T-cell leukemia/lymphoma (ATL)

    Grant number:25460437  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    Oka Takashi, ITO SACHIO, OUCHIDA MAMORU, YOSHINO TADASHI

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    Grant amount:\5200000 ( Direct expense: \4000000 、 Indirect expense:\1200000 )

    We investigated the epigenetic mechanism of onset and progression of non-Hodgikin lymphoma as well as adult T-cell leukemia/lymphoma (ATL). We found that epigenetic abnormalities including unbalanced expression of Polycomb Repressive Complex (PRC) molecules, aberrant expression of miRNA and mRNA and also aberrant DNA methylation are playing the important role in the pathogenesis of ATL. Ezh2 was strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2 in aggressive lymphoma variants as well as ATL. Tax protein expression induced epigenetic heterogeneity with expanding the global DNA methylation profile to generate various epigenetic clones, suggesting that Tax-mediated epigenetic clonal heterogeneity and diversity may contribute to induce leukemic transformation and more aggressive clonal progression.

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  • Direct target genes of miRNAs involved in lung cancer

    Grant number:24591905  2012.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    Ouchida Mamoru, OKA Takashi, ITO Sachio

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    Grant amount:\5330000 ( Direct expense: \4100000 、 Indirect expense:\1230000 )

    Lately, miR-17-92, which is highly expressed in malignant lung cancer cells, is considered the key miRNA for tumorigenesis. However, its direct targets remain under reported. We identified the FOXP1, TP53INP1, TNFAIP3, and TUSC2 genes as miR-19a targets, using luciferase, pull-down, and western blot assays. The four miR-19a target cDNA expression vectors suppressed cell viability, colony formation, migration, and invasion of lung cancer cells.

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  • clarification of the mechanism of proteinuria with conditional knockout mice

    Grant number:24659499  2012.04 - 2013.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research  Grant-in-Aid for Challenging Exploratory Research

    KUNIHIKO AYA, OUCHIDA Mamoru

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    Grant amount:\3770000 ( Direct expense: \2900000 、 Indirect expense:\870000 )

    To clarify the mechanism of proteinuria, we identified the transport protein which binds to podocin and expresses in podocyte on previous grant-in-aid. We made podocyte-specific conditional knockout mice to examine the in-vivo function of this molecule and start analysis on this grant-in-aid.

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  • Identification and functional analysis of esophageal cancer-related genes by pull-down method using biotin-labeled miRNA

    Grant number:22591433  2010 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    ITO Sachio, OKA Takashi, OUCHIDA Mamoru

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

    In order to identify possible predictive markers, We performed the identification of miRNA related to the degree of differentiation-grade and malignancy by the profiling of esophageal cancer cell lines and esophageal cancer clinical specimens. In poorly differentiated cells, miR-29a and let-7b were overexpressed. We identified target genes of these miRNAs using in vitro pull-down method, and found some candidates of target genes related to tumor suppressor and apoptosis. Our results suggest that these miRNAs are involved in esophageal cancer progression.

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  • Comprehensive analyses of epigenetic abnormalities inadult T-cell leukemia/lymphoma (ATLL)

    Grant number:22590312  2010 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OKA Takashi, YOSHINO Tasashi, OUCHIDA Mamoru

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    We investigated the epigenetic mechanism of onset and progression of non-Hodgikinlymphoma as well as adult T-cell leukemia/lymphoma (ATLL). We found that epigenetic abnormalities including unbalanced expression of Polycomb Repressive Complex (PRC) molecules, aberrant expression of miRNA and mRNA and also aberrant DNA methylation are playing the important role in the pathogenesis of ATLL.

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  • Establishment of a genetic diagnosis system for cancer predispositionand its application to cancer prevention.

    Grant number:22300346  2010 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    SHIMIZU Kenji, SHINAGAWA Katuji, TOYOOKA Shinichi, OUCHIDA Mamoru, SAKAI Akiko, ITO Sachio

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    Grant amount:\17160000 ( Direct expense: \13200000 、 Indirect expense:\3960000 )

    We have aimed to clarify the nature of genetic predisposition for sporadic cancers, influenced by genetic polymorphisms, such as single-nucleotide polymorphism (SNP). By analyzing about 8,000 specimens, we found 53 SNP are related with at least one of 17 major cancers in Japan. Stratification of the data of the multiplied OR of overlapping SNP for each cancer and each individual revealed that about 15% and 1% of the Japanese represent the high- and the highest risk-group for most cancers, respectively. Other major findings are, about half of the SNPs at risk were replicated between two case/control data sets on 4 kinds of cancers, Risk-SNP combinations were largely different between genders, some SNPs were identified as those closely associated with cancer-progression or occurrence of specific gene alterations.

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  • 転写調節制御による慢性疼痛治療技術の開発研究

    2010

    産学が連携した研究開発成果の展開 研究成果展開事業 研究成果最適展開支援プログラム(A-STEP) 探索タイプ 

    大内田 守

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    申請者は疼痛シグナル伝達遺伝子の発現をデコイDNAで選択的に抑制する慢性疼痛治療剤を開発した。本課題の目標は当該遺伝子発現を制御する転写因子の検出である。疼痛刺激に反応するプロモーター領域の同定と、その領域に結合する35個の転写調節因子の結合サイトの検出に成功した。しかし、蛋白解析においては非特異的吸着蛋白の存在という予期せぬ事態となり、目標達成には時間不足であった。今後は本研究を継続し、疼痛刺激特異的な転写因子の抑制技術による疼痛緩和、デコイDNAを利用した疼痛緩和、その受容体蛋白を応用した疼痛緩和、これらの技術を総合的に組み合わせることにより効果的な慢性疼痛の治療法を開発する計画である。

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  • Genetic modifiers of an intractable epilepsy with channel gene mutations

    Grant number:21390312  2009 - 2011

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    OMORI Iori, OUCHIDA Mamoru, MASHIMO Tomoji

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    Grant amount:\17160000 ( Direct expense: \13200000 、 Indirect expense:\3960000 )

    Dravet syndrome is an intractable epileptic syndrome beginning in the first year of life. De novo mutations of SCN1A, which encode the Na_v1. 1 neuronal voltage-gated sodium channel, are considered the major cause of Dravet syndrome. In this study, we investigated genetic modifiers of this syndrome.
    We performed a mutational analysis of all coding exons of CACNA1A in 48 subjects with Dravet syndrome. Nine CACNA1A variants, including six novel ones, were detected in 21 of 48 subjects(43. 8%). The electrophysiological properties of four of the five novel Ca_v2. 1 variants exhibited biophysical changes consistent with gain-of-function.

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  • identification of proteins interacting with causative molecules for hereditary nephrotic syndrome and analysis of pathogenesis of it.

    Grant number:21591387  2009 - 2011

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    AYA Kunihiko, OUCHIDA Mamoru

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    We identified transport protein x bounded to podocin, important molecule for proteinuria, with immunoprecipitation and LC/MS. The double staining with endothelial marker and anti-x antibody indicated that protein x was expressed in podocyte. When protein x was suppressed with siRNA in cells, podocin expression along cell membrane was much lower than control and cell shape was changed. Overexpression of protein x improved expression of mutated podocin along cell membrane. These data indicated protein x play role in membrane trafficking of podocin.

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  • 難治性疼痛治療薬の持続性向上に関する開発研究

    2009

    産学が連携した研究開発成果の展開 研究成果展開事業 地域事業 地域イノベーション創出総合支援事業 シーズ発掘試験 

    大内田 守

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    Authorship:Principal investigator 

    末期癌や糖尿病、交通事故や手術後の後遺症でみられる慢性的な耐え難い痛みは末梢神経および中枢神経系の圧迫、変性、損傷に起因している。これは創傷などによる初期の痛みとは異なり、創傷が治癒した後に新たに発生する痛みで、急性痛で有効な非ステロイド系消炎鎮痛剤や麻薬系鎮痛薬等の薬剤が効きにくく決定的な治療法がない。本課題は難治性疼痛治療薬の実用化に向けた技術開発であり、当該治療薬の持続期間の延長・向上を目指した研究である。

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  • Studies in targets of SYT-SSX fusion protein in synovial sarcoma.

    Grant number:20591756  2008 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OUCHIDA Mamuru

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    The aim of this study was identification of the target genes transcriptionally regulated by SYT-SSX fusion protein in synovial sarcomas. We found about 300 candidate targets by chromatin immunoprecipitation assay, DNA cloning and sequencing. We have screened the reagents which can block and inhibit the localization of SYT-SSX fusion protein in synovial sarcoma cells, to find new targeted therapy agents for synovial sarcoma.

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  • 急性脳炎・脳症の罹患リスクの判定技術の改良・開発

    2008

    産学が連携した研究開発成果の展開 研究成果展開事業 地域事業 地域イノベーション創出総合支援事業 シーズ発掘試験 

    大内田 守

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    Authorship:Principal investigator 

    急性脳炎・脳症の中でもインフルエンザ脳症は主に6歳以下の子供が罹り、日本で毎年300人前後の患者が発生している。脳症発症後1?2日で死に至ることもあり、死亡率は30%、後遺症も25%の患者に認められる重篤な疾患である。できる限り早く治療を始めたほうが軽く済むが、インフルエンザに感染した際に誰が急性脳症に進行するか不明である。本課題は急性脳炎・脳症の罹患危険度検査法の実用化に向けての改良と検出効率の向上を目指す研究である。

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  • Analyses of epigenetic mechanism of lymphomagenesis/leukemogenesis

    Grant number:19590349  2007 - 2008

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OKA Takashi, YOSHINO Tadashi, OUCHIDA Mamoru

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    Grant amount:\4420000 ( Direct expense: \3400000 、 Indirect expense:\1020000 )

    悪性腫瘍の発症機構に関する研究は、これまで癌遺伝子、癌抑制遺伝子の構造異常などを伴うゼネテイックな変化に注目して研究が進められてきた。それに対し近年遺伝子の構造異常を伴わないエピジェネテイックな機構による発癌が注目されてきている。我々は造血器腫瘍の発症機構をとくにエピジェネテイックな機構に注目し解析を行い、HTLV-I, H.pyloriの感染によって異常なDNAメチル化が誘導・蓄積することが造血器腫瘍発症に重要であることを見いだした。これらの知見を元に造血器腫瘍を高感度に早期発見・早期診断することが可能になると期待される。

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  • 難治性小児てんかんの早期発見技術の開発

    2007

    産学が連携した研究開発成果の展開 研究成果展開事業 地域事業 地域イノベーション創出総合支援事業 シーズ発掘試験 

    大内田 守

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    1歳未満の小児の約8%には熱性痙攣がみられる。一般に、熱性痙攣は6歳までに治癒し積極的な治療を必要としないことが多いが、その良性経過を示す患者の中にはDravet症候群という難治てんかん患者が混在している。Dravet症候群患者は何度も痙攣を繰り返し、てんかん重積など危険な状態をもたらすため、早期に専門医の治療を必要とする。本課題は1歳未満の病初期に良性の熱性痙攣の中から難治てんかん患者を早期に選別する方法の実用化に向けての改良と検出効率の向上を目指す研究である。

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  • Molecular mechanism of loss-of-function SCN1A mutations associated with epilepsy

    Grant number:18591154  2006 - 2008

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OOMORI Iori, MATSUI Hideki, OUCHIDA Mamoru

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    Grant amount:\3850000 ( Direct expense: \3400000 、 Indirect expense:\450000 )

    難治てんかんの一種である乳児重症ミオクロニーてんかんに認められる電位依存性ナトリウムチャネル・1サブユニット(Na_v1.1)をコードするSCN1A遺伝子変異をもとに、その機能喪失メカニズムを解明した。変異の種類により、蛋白は合成されているが細胞膜へ移行できない障害とチャネル蛋白は膜に移行してきているがナトリウムイオンを透過することができない障害があることが推測された。蛋白が細胞膜へ移行できないある種の変異については、抗てんかん薬によって膜への移行が促進されることが分かった。これらの知見は、てんかん患者の遺伝子情報から、効果の高い治療薬を選択するテーラーメイド治療の開発に資することができると思われる。

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  • がん発症前高リスクに関わるがん体質遺伝素因の実体解明と試行的コホート解析

    Grant number:18014017  2006 - 2007

    日本学術振興会  科学研究費助成事業 特定領域研究  特定領域研究

    清水 憲二, 大内田 守, 松原 長秀, 小出 典男, 堺 明子, 伊藤 佐智夫

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    Grant amount:\11100000 ( Direct expense: \11100000 )

    本研究は、日本人の肺癌、頭頸部癌、大腸癌、食道癌、胃癌、膵臓癌、乳癌、前立腺癌における「発がんのリスク関わる遺伝子多型」を広汎に検索したものである。これまでに計225遺伝子、約270 SNPを解析した結果、有意差をもって上記の癌の発癌リスクに関わるミスセンスSNPを42遺伝子で計47種発見した(高リスク:34種、保護的SNP:13種)。42遺伝子にはDNA修復遺伝子、癌抑制遺伝子、物質代謝遺伝子、染色体分配遺伝子、細胞接着遺伝子等が含まれる。これらのms-SNPの多くは複数種の癌に関係し、多いものでは約8割の癌種に影響していた。上記のうち38 SNPの発癌リスクとの相関は、本研究で初めて示されたものである。
    特筆すべきことは、本研究では対照健常人(約450検体)、癌患者(約1,300検体)共にほぼ全てのSNPを解析し、それらの重複のデータを得たことである。上記のうち、99%信頼区間も有意であった20遺伝子の24 SNPについて、癌種毎に関係する4〜7 SNPの個人別重複を数値化したところ、高リズクSNP数から保護的SNP数を差し引いた数値が上位20%に属する個人の割合は健常人で約4〜20%、癌患者で20〜60%を占めた。統計学的には、肺癌、大腸癌、食道癌についてはいずれもP値が10^<-10>〜10^<-16>、その他の癌では10^<-5>〜10^<-6>を示し、高い信頼性を示した。これらのグループの集団内発癌寄与率(PAR)は平均50%を占め、遺伝的リスクの過半を説明できることが判明した。さらに、我々は日本人の癌の約7割を占める肺癌、頭頸部癌、大腸癌、食道癌、胃癌、膵臓癌、乳癌、前立腺癌の各々について、約75%の低リスク群、25%の高リスク群、0.5-1.5%の超高リスク群を分別できる系を構築した。今後この系を前向きコホート研究で実証できれば、癌の予防と早期発見に革新的進展が実現できると期待される。

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  • Proteome analysis of SYT-SSX protein complexes in synovial sarcomas.

    Grant number:18591632  2006 - 2007

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OUCHIDA Mamoru

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    Grant amount:\3730000 ( Direct expense: \3400000 、 Indirect expense:\330000 )

    In order to understand the molecular mechanism underlying the onset of synovial sarcomas, we analyzed fit SYT-SSX protein complex in synovial sarcoma cells by protecmics methods.
    Detection of the unknown proteins the SYT-SSX protein complex;
    We male the SYT, SSX, or SYT-SSX cDNA expression plasmid to produce FLAG-lag fusion protein and GST-tag fusion protein. These plasmids were transfected into HEK293 cells. The cellular proteins were prepared, and the fusion proteins were pulled dorm by anti-tag antibody-beads, and analyzed by western blotting. We could detect tie FLAG-tagged piths, but The yeti of FLAG-tagged SYT-SSX protein was low. The almost sane result was observed in tie experiment with GST-tagged *smiths, suggesting that the ION yeti was die to tie cellular localization of SYT-SSX fusion proteins within nucleus. So, we isolated the nucleus and the nuclear proteins were eluted in high cancer &fled salt condition. The eluted nuclear proteins were mixed will cytoplasmic proteins to make total cellular protein. FLAG-lagged SYT-,SSX protein was purified from the total cellular proteins, and the puffed FLAG-tagged SYT-SSX protein was incubated and re-constructed to make the SYT-SSX protein complex. Then the complex was puled by FLAG-beads, and the proteins were applied on SDS-PAGE. We analyzed sane bands of the complex by LC-MS.
    Cellular localization analysis of SYT-SSX protein in the presence of some inhibitors. We made the SYT, SSX, and SYT-SSX cDNA expression plasmids to produce EGFP-fusion proteins. The plasmids were reverse-transfected into SYO-1 that is a synivial cell line we established. We found that the SYTT-SSX proteins localize in nucleus with speckled form. We analyzed the effect of some inhibitors on the localization of the SYT-SSX proteins.
    We established an inducible cell line that can express the SYT-SSX gene in the presence of doxicyclin, and the gene expression pattern in the induced/non-induced cells were analyzed on cDNA microarray analysis.

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  • Early-detection, diagnosis and monitoring of malignant lymphoma/leukemia.

    Grant number:17590302  2005 - 2006

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OKA Takashi, YOSHINO Tadashi, OUCIDA Mamoru, SHINAGAWA Katsuzi

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    Grant amount:\3700000 ( Direct expense: \3700000 )

    There are various kinds of hematopoietic malignancies including lymphoma and leukemia. There is wide range of spectrum in terms of prognosis. Some of them are very aggressive and hard to control. Others show slightly well prognosis. In many cases, relapse will occur after the regression of tumor cells with the treatments of chemotherapy, x-irradiation or immuno-therapy etc., if only a small number of tumor cells could survive. In order to prevent relapse and induce complete remission, development of highly sensitive, specific technology to detect tumor cells is urgently required.
    We found highly frequent gene silencing of specific genes with DNA hyper-methylation in hematopoietic malignancies. Especially, we found that some type of malignant lymphoma/leukemia show specific changes of methylation profiles and also CpG island methylator phenotype (CIMP) in accordance with the progression. In the basis of these findings, we developed a new highly sensitive, specific system to detect hematopoietic malignancies. It will be useful for the early-detection, diagnosis and monitoring of malignant lymphoma/leukemia.

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  • がん発症前高リスクに関わるがん体質遺伝素因の実体解明と試行的コホート解析

    Grant number:17015030  2005

    日本学術振興会  科学研究費助成事業 特定領域研究  特定領域研究

    清水 憲二, 大内田 守, 松原 長秀, 小出 典男, 堺 明子, 伊藤 佐智夫

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    Grant amount:\6900000 ( Direct expense: \6900000 )

    本研究では「がん体質遺伝」の実体に迫るために、がん関連候補遺伝子のミスセンス1塩基多型(ms-SNP)を広汎に検索してきた。これまでに計135遺伝子で205箇所のms-SNP候補を見出し、担がん患者(計344名)及び対照健常人集団におけるアレル分布を解析した。本年度は対照健常人検体数を約2倍に増やして(計202名)再検討した結果、昨年度までの19種と新規に8種のms-SNPが統計学的に有意なリスクを示した。この27種の内訳は、肺、頭頸部、大腸、食道、乳腺などのがんで高リスクSNPが21種(オッズ比;1.62〜14.2)と保護的SNPが6種(オッズ比;0.12〜0.61)を占め、DNAの修復/複製(7)、がん抑制(5)、染色体分配(5)、細胞周期制御(3)及びその他の機能(3)に関与する23遺伝子群であった。また27種のうち20種は複数種のがんに影響し、うち22種は本研究による新発見である。検体毎にms-SNPの重複(累積オッズ比:COR)を検討した結果、肺腺がんのリスクに関わる13種のms-SNP遺伝子型が重複し、CORが30以上を示す人は、健常人では5%で、肺腺がん患者では30%に達した(P=6.7x10^<-8>,OR=8.33)。同じく肺扁平上皮がんのリスク因子11種でCORが20以上の人は、健常人7.9%、肺扁平上皮がん患者59%であった(P=6.9x10^<-1>1,OR=16.6)。同様の傾向は頭頸部、大腸、食道などのがんでも認められ、健常人と患者群の平均CORは3〜15倍の差があった。このように、本研究で明らかになったms-SNP27種は、実際に発がんリスクの遺伝的背景となっていることが強く示唆された。以上の結果を協力病院の通院非がん患者246名について適用したところ、計34名で各種のがん発症リスクが特に高いことが判明したため、主治医による継続的フォローを開始した。

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  • Molecular Pathological analyses of aberrant expression of the proteintyrosine phosphatase SHP1 gene in terms of lymphomagenesis/leukemogenesis.

    Grant number:15590302  2003 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OKA Takashi, YOSHINO Tadashi, HAYASHI Kazuhiko, OUCHIDA Mamoru

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    Grant amount:\3700000 ( Direct expense: \3700000 )

    The studies of gene expression on a genomic scale with cDNA microarrays make it easy to measure the transcripts for every gene at once. Various types of lymphomas/leukemias have been analyzed with the cDNA microarray or macroarrays to investigate the molecular basis of lymphomagenesis/leukemogenesis. Recently, our group analyzed the expression pattern of the human NK/T cell line (NK-YS) genome by cDNA macroarray and tissue-microarray comprehensively and systematically followed by RT-PCR and Western blotting. The significant changes in the gene expression of NK-YS cell line were detected : increase in 18 and decrease in 20 genes compared to normal NK cells or peripheral blood mononuclear cells. Among these genes, we found a strong decrease in hematopoietic cell specific protein-tyrosine-phosphatase SHP1 mRNA by cDNA-macroarray and RT-PCR. Further analysis with standard immunohistochemistry and tissue-microarray, which utilized 207 paraffin-embedded specimens of various kinds of malignant lymphomas, showed that 100% of NK/T lymphoma specimens and more than 95% of various types of malignant lymphoma were negative for SHP1 protein expression. The promoter region of the SHP1 gene has been revealed to be highly methylated in patient samples of adult T cell leukemia (methylation frequency 90%), natural killer (NK)/T cell lymphoma (91%), diffuse large B-cell lymphoma (93%), MALT lymphoma (82%), mantle cell lymphoma (75%), plasmacytoma (100%) and follicular lymphoma (96%). The methylation frequency was significantly higher in high grade-MALT lymphoma cases (100%) than in low grade- MALT lymphoma cases (70%), correlating well with the frequency of no expression of SHP1 protein in high grade- (80%) and low grade-MALT lymphoma (54%). It suggests that the SHP1 gene silencing with aberrant CpG methylation relates to the lymphoma progression in addition to the malignant transformation. Furthermore, the promoter methylation of the SHP1 gene was clearly correlated with the clinical stage such as complete remission or relapse. Loss of heterozygosity with microsatellite markers near the SHP1 gene was showed in 79% of informative ALL cases. These evidences show that the SHP1 gene is a relevant novel biomarker of the wide range of hematopoietic malignancies. Additionally, the loss of SHP1 gene expression is suggested to play an important role in multistep lymphomagenesis/leukemogenesis.

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  • Functional Analysis of the mutated ion-channel gene in severe myoclonic epilepsy in infancy

    Grant number:15591110  2003 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OUCHIDA Mamoru, OHMORI Iori

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    Grant amount:\3500000 ( Direct expense: \3500000 )

    Severe myoclonic epilepsy in infancy(SMEI) is a malignant infant-onset epileptic syndrome with febrile seizures. We analyzed the voltage-gated sodium channel α1-subunit (SCN1A) gene, β1-subunit (SCN1B) gene and γ-aminobutyric acid _A receptor γ2-subunit (GABRG2) gene in DNAs from peripheral blood cells of patients with SMEI and patients with other types of epilepsy. Mutations of the SCN1A gene were detected in 83% of the patients with SMEI, although none with other types of epilepsy. The mutations included deletion, insertion, missense and nonsense mutations. We could not find any mutations of the SCN1B and GABRG2 genes in all patients. Our data suggested that the SCN1A mutations were significantly correlated with SME (p<0.0001).
    We cloned the wild type SCN1A cDNA, made the mutant type cDNAs by PCR-based mutagenesis, and constructed the SCN1A cDNA expression plasmids with Lumio-tag at the C-terminal region. When the expression plasmids were transfected into human embryonic kidney 293 cells, we found that some kinds of mutant forms are localized on cell membrane. The result suggests that the mutant forms of SCN1A may function dominant-negatively in the presence of the wild type SCN1A on the cell membrane.
    We found two alternative isoforms of SCN1A mRNA in human brain tissues, when we were cloning the cDNA for the expression system. Our analyses revealed that the isoforms loss the gate region of ion-channel, and that many mutations we detected had occurred in the region of SCN1A. These results suggest that the alternative isoforms also may negatively function for wild type of sodium ion-channel, like as a kind of mutant form.

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  • Studies on the Genetic Factors Influencing Predisposition to Cancer in High-risk Groups.

    Grant number:12213084  2000 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research on Priority Areas  Grant-in-Aid for Scientific Research on Priority Areas

    SHIMIZU Kenji, OUCHIDA Mamoru, MATSUBARA Nagahide, SAKAI Akiko, ITO Sachio

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    Grant amount:\54500000 ( Direct expense: \54500000 )

    To explore the molecular nature of "Cancer Predisposition", we have performed comprehensive analyses on the differential distribution of missense-single nucleotide polymorphism (ms-SNP) of cancer-related genes between cases and healthy controls. Since 1999, we have done case-control studies on 103 ms-SNP in 335 cancer cases and 110 healthy controls and we found that 22 SNP significantly associated with cancer-risk including lung adenocarcinoma (LAD), lung squamous cell carcinoma (LSC), head and neck cancer (HNSC), colorectal cancer (CRC) and esophageal cancer (ECC). These risk-related 22 SNP included 3 SNP previously reported (in genes ADH1B, ALDH2 and TP53) and 19 SNP thus far undescribed in the literature and distributed among 20 genes consisting of 6 DNA-repair genes, 5 tumor suppressor genes, 5 chromosome-segregation genes and 4 others. Of these 22 SNP, 16 were of high-risk (SNP-H) with odds ratio (OR) 1.87-18.0 and 6 were protective SNP (SNP-L) with OR 0.18-0.54. In respect to each cancer-type, number of the affecting SNP including common ones were follows; LAD (8 SNP-H and 4 SNP-L), LSC (7 SNP-H and 2 SNP-L), HNSC (3 SNP-H and 2 SNP-L), CRC (3 SNP-H and 3 SNP-L) and ECC (2 SNP-H). Because all analyses were performed with the same specimens, it was possible to examine individually the perfect overlapping of the genotype at risk on these 22 SNP. A cumulative odds ratio (COR) was calculated for each individual by multiplying OR of their all overlapping SNP at risk. As to the LAD risk calculated by 10 SNP, the frequency of individuals showing COR > 4.0 was 4.5% in healthy controls, whereas 39% in LAD patients (P = 5 x 10^<-9>, OR = 13.4 ). Similarly, for the LSC risk based on 7 SNP, the frequency of persons with COR > 4.0 in healthy controls was 13%, while 66% in LSC patients (P = 8.5 x 10^<-8>, OR = 12.0 ).
    Thus, our results demonstrated that many ms-SNP including those with novel findings are involved in the predisposition to cancer-incidence, suggesting the hereditary cancer-predisposition is determined, at least in part, by the sum effects of many ms-SNP in cancer-related genes. Our results suggested also that each individual's cancer-risk may be predicted by calculating COR in some cases.

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  • 骨・軟部腫瘍における融合型遺伝子変化の解析および新たな遺伝子治療開発に関する研究

    Grant number:12671417  2000 - 2002

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    川井 章, 大内田 守, 清水 憲二

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    Grant amount:\3300000 ( Direct expense: \3300000 )

    悪性骨軟部腫瘍における特異的融合遺伝子の発現を解析し、新たな診断・予後因子としての意義、その分子生物学的メカニズムを明らかにすると共に、これら腫瘍特異的遺伝子異常をターゲットとした遺伝子治療の基礎的研究を行うことを目的とする。本年度は、(1)融合遺伝子発現と組織学的診断との整合性、(2)融合遺伝子のvariationと臨床病理学的態度の関連、(3)融合遺伝子の補助診断、腫瘍モニタリング法としての有用性、(4)悪性軟部腫瘍におけるアポトーシスの頻度とその調節蛋白質の発現について検討した。
    悪性骨軟部腫瘍は組織型が多彩であり、その組織学的診断は屡々困難を伴う。特に、稀な部位に発生した悪性骨軟部腫瘍の診断には難渋することが多い。我々は、頭蓋底発生のEwing/PNET、膝関節内発生のsynovial sarcomaの診断が特異的融合遺伝子(EWS/FLI1,SYT-SSX)の解析により可能であることを報告した(J Neuro Oncol 2001,Clin Orthop 2001)。更に多施設共同研究によって、滑膜肉腫におけるSYT-SSX融合遺伝子のvariationが腫瘍の臨床経過に有意な影響を与えることを明らかにした(Cancer Res 2002)。アポトーシス関連因子は悪性腫瘍に対する新たな治療ターゲットとなりうるが、悪性軟部腫瘍におけるアポトシースについてはこれまで殆ど明らかにされていない。我々は、悪性軟部腫瘍では組織型に依存してアポトーシスが生じていること、その頻度はBcl-2蛋白の発現と逆送関していることを明らかにした(Cancer Lett 2002)。

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  • Functional analysis of a tumor suppressor candidate gene, HD-PTP, located on human chromosome 3p21

    Grant number:12670138  2000 - 2002

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    OUCHIDA Mamoru, SAKAI Akiko, SHIMIZU Kenji

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    Grant amount:\3300000 ( Direct expense: \3300000 )

    A human HD-PTP cDNA encoding a novel protein tyrosine phosphatase has been isolated in our laboratory. The phosphatase has unique features in its domain structure : a Histidine-domain containing several SH3-binding motifs, a tyrosine phosphatase domain, a C-terminal PEST motif, and an N-terminal domain similar to yeast BRO1, an apoptpsis-related mammalian AIP1 and to a RHO-binding protein, Rhophilin. The gene is located at chromosome 3p21.3, an area frequently deleted in many types of cancer, especially within the functionally defined narrow region. The gene may be a human homolog of the rat PTP-TD14 gene reported by others, which can suppress H-ras- mediated transformation. The phosphatase gene may be a candidate for one of the tumor suppressor genes located on 3p21.3.
    To analyze the function of HD-PTP through the signal transduction, we screened new proteins, which can bind with each domain of HD-PTP, by yeast two-hybrid assay. As targets of BRO-domain, rabaptin 5, which is an effector of rab 5(GTPase protein), and HC8, which is proteosome alpha subunit and regulates the life time of cell cycle-related proteins, were isolated. It has been reported that tumor suppressor gene TSC2 product (tuberin) binds to rabaptin 5, suggesting that HD-PTP may be associated in the tumorigenesis through rabaptin 5/rab5 complex. As targets of Histidine-domain, DNA repair gene SOH1 was isolated. SOH1 is known to bind with the other repair enzymes and transcriptional factors, suggesting that HD-PTP may be associated with DNA repair system through transcription.

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  • Analysis of a novel human protein WDC146 highly expressed in testis : for elucidation of the function during spermatogenesis

    Grant number:12671602  2000 - 2001

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    SAKAI Akiko, NOMURA Takako, SASAKI Junzo, OUCHIDA Mamoru

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    Grant amount:\3400000 ( Direct expense: \3400000 )

    1) WDC146 is a novel human protein of 146 kDa which is expressed highly in testis. It is composed of three domains, a WD40 domain, a collagen-like domain and a GPR-rich repeat domain, from N-terminus to C-terminus, respectively.
    2) WDC146 is highly expressed in testis both in human and mouse. The amino acid sequence showed significant homology between them overall (96%), including complete match (100%) for the region of WD40 domain. Even in Drosophila and yeast, we identified the sequence conserved in part.
    3) WDC146 showed marked expression in pachytene spermatocytes, and nuclear and perinuclear localization was observed intracellularly.
    4) The detailed analysis of the expression pattern of WDC146 during spermatogenesis is in progress, with the technical difficulty of fixation of testis applicable for in situ hybrization.
    5) WD40 domain is known to work as the platform motif as the time of protein-protein interaction. The two-hybrid screening was executed repeatedly to detect interactive protein with WDC146, but not yet succeed.
    6) Cancer-testis genes are defined as testis-specific genes also expressed in many tumors and tumor cell lines. WDC146 may be classified in them, as tumor cell lines tested all showed moderate expression of WDC146, though some tumors did not.
    7) The WDC146 gene is mapped at 2q14-21 and consists of 22 exons. Besides the intact mRNA of about 4kb, a chimeric one result from mis-splicing always detected at about 1kb size.
    8) The promoter region was identified within 0.5kb upstream region of exon 1.

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  • ヒト癌におけるミスマッチ修復遺伝子欠損の分子病態

    Grant number:11146214  1999

    日本学術振興会  科学研究費助成事業 特定領域研究(A)  特定領域研究(A)

    清水 憲二, 堺 明子, 藤原 田鶴子, 大内田 守

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    Grant amount:\1800000 ( Direct expense: \1800000 )

    【緒言】本研究では、独自に開発した遺伝子全領域同時SSCP法などの解析法を用いて、大腸癌や胃癌などのうち遺伝的不安定性を示すものを中心としてミスマッチ修復機構の欠損とその標的遺伝子変異への効果、修復欠損を起こす原因となった初発遺伝子異常はどのようなものかなどを明らかにすることを目的とした。
    【方法】1,研究検体の確保のため今までに約1,000例の腫瘍/正常組織を含む腫瘍バンクを設立した。
    2,微小な遺伝子異常検出法として遺伝子全領域同時SSCP法と蛍光標識マイクロサテライト(MS)解析法を開発し、癌に関係する遺伝子の異常解析を行った。
    【結果】これまでの本研究により、マイクロサテライトの不安定性(MI+)を示す胃癌と大腸癌の約37%に転写活性化因子で癌遺伝子ともなりうるE2F4のエキソン内マイクロサテライト変異を見い出した。またE2F4変異を持つ癌の80%以上が修復遺伝子であるhMSH3のエクソン内に1塩基フレームシフト変異を持つことを明らかにし、これらの癌ではE2F4遺伝子がhMSH3遺伝子の関与するミスマッチ修復機構の欠損の標的であることを初めて報告した。昨年度の研究で、変異型E2F4遺伝子をNIH3T3細胞で発現させると著明な増殖促進が見られることを明らかにしていたが、この効果は変異型E2F4による転写の活性化が上昇したことによることを本年度確認した。これらhMSH3,E2F4両遺伝子の変異を遺伝性非腺腫性大腸癌(HNPCC)と散発性大腸癌とで比較したところ、HNPCCではこれらの変異が有意に低く、また変異の形式がリピート数の減少を主にしており、散発性癌と大きく異なっていた。散発性のMI+癌における修復遺伝子欠損変異の成因を解明するために、DNAの修復と複製に関わるDNAポリメラーゼδ,εとPCNAなどの遺伝子の癌特異的変異を検索したが、有意な結果は得られなかった。しかし共同研究によって、DNAのミスマッチ修復に関わると思われるDNAポリメラーゼβ遺伝子の癌特異的変異を6例の胃癌において発見し、その変異は除去修復能を失活させることを報告した。また、食道癌などの検体で見られた染色体17番長腕の微小な欠失領域中にDNAの組み換え修復に関与する遺伝子が局在することをごく最近見い出した。この知見はDNAの組み換え修復に重要な役割を果たす遺伝子の半数化または異常が癌化の前提条件としてのゲノム不安定性に関与する可能性を示唆するものと考えられ、重要な発見であるため、本課題研究期間終了後も引き続き解析する予定である。

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  • Development of Systems for Comprehensive Genetic Diagnosis of Human Cancers and for Early Detection of Cancer-patients.

    Grant number:10470040  1998 - 2000

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B).  Grant-in-Aid for Scientific Research (B).

    SHIMIZU Kenji, FUJIWARA Tazuko, ODA Megumi, OUCHIDA Mamoru, KAKU Shunkou, SAKAI Akiko

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    Grant amount:\5700000 ( Direct expense: \5700000 )

    We have found a novel tumor-specific mutation in the gene encoding E2F4 transcription regulator in a subset of genetically unstable (MI+) colorectal cancers in 1996. The mutation was found to be a result of the inactivating frame-shift mutation of the hMSH3 gene, a DNA mismatch-repair gene. Thus, the E2F4 gene was identified, for the first time, as a target of the defective mismatch repair function involving hMSH3 protein. This notion has been confirmed bv many supporting papers. Relevant to this result, we have found an interstitial deletion within the human p107 gene, a close relative of the tumor suppressor gene RB, in a diffuse-large B cell lymphoma cell line. We found the deletion was raised by a recombination between two Alu-repeats encompassing about 15 kbp. By our genomic scanning method, we found a novel region of loss of heterozygosity (LOH) at chromosome 14q24-31 in about 30% of renal cell carcinomas and identified two candidate tumor suppressor genes (TSG) in this narrow region. By conventional microsatellite analysis, we found a high incidence of LOH at chromosome 13q34 in human head and neck cancers. The known candidate TSG, ING1, resides at this site. We clarified the whole genomic structure of the ING1 gene and found 3 inactivating point mutations in 3 primary head and neck cancers with 13q34 LOH.These are the first evidence indicatins that the p107 and ING1 genes function as TSG.Further, we discovered a novel protein tyrosine-phosphatase gene, HD-PTP, as a novel TSG candidate. The gene resides at chromosome 3p21.3, the region thought to contain multiple TSG for many types of human cancer. By similar approaches we found at least 10 TSG candidates at 8 chromosomal regions in 7 cancer/tumor groups. In addition to TSG, we isolated a cDNA encoding a novel POZ-Zn-Finger protein, whose expression led the recipient cells to malignant phenotype, suggesting that the gene is a novel oncogene. The gene locates on 3q26-27 and related to the known oncogene, Bcl-6.
    As to the molecular diagnosis of cancer, we reported a systematic method for detecting tumor-specific, fused-gene mRNAs in several bone/soft-tissue sarcomas. We have developed a new strategy to quantitate the amounts of free DNA in sera/plasma with a very high sensitivity (about ten thousand-fold higher than conventional methods). Cancer-specific genetic alterations, like as K-ras and p53 mutations, could be detected in these serum-DNA.Thus, promising strategies for early detection of potential cancer-patients were developed with free DNA in plasma/serum.

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  • ヒト癌におけるミスマッチ修復遺伝子欠損の分子病態

    Grant number:10165218  1998

    日本学術振興会  科学研究費助成事業 特定領域研究(A)  特定領域研究(A)

    清水 憲二, 堺 明子, 藤原 田鶴子, 大内田 守

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    Grant amount:\1900000 ( Direct expense: \1900000 )

    【緒言】本研究では、新規に創案した遺伝子全領域同時SSCP法などの解析法を用いて、大腸癌や胃癌などのうち遺伝的不安定性を示すものを中心としてミスマッチ修復機構の欠損とその標的遺伝子変異への効果、修復欠損を起こす原因となった初発遺伝子の異常はどのようなものがなどを明らかにすることを目的とした。
    【方法】1,研究検体の確保のため、今までに約1,000例の腫瘍/正常組織を含む岡山大学腫瘍バンクを設立した。2,微小な遺伝子異常検出法として遺伝子全領域同時SSCP法を開発し、癌に関係する遺伝子の異常解析を行った。
    【結果】これまでの本研究により、マイクロサテライトの不安定性(MI+)を示す胃癌と大腸癌の約37%に転写活性化因子で癌遺伝子ともなりうるE2F4のエキソン内マイクロサテライト変異を見い出した。またE2F4変異を持つ癌の80%以上が修復遺伝子であるhMSH3のエクソン内に1塩基フレームシフト変異を持つことを明らかにし、これらの癌ではE2F4遺伝子がkMSH3遺伝子の関与するミスマッチ修復機構の欠損の標的であることを初めて解明した。
    本年度の研究で、変異型E2F4遺伝子をNIH3T3細胞で発現させると著明な増殖促進が見られることを確認した。これらhMSH3,E2F4両遺伝子の変異を遺伝性非腺腫性大腸癌(HNPCC)と散発性大腸癌とで比較したところ、HNPCCではこれらの変異が有意に低く、また変異の形式が大きく異なっていた。敗発性のMI+癌における修復遺伝子欠損変異の成因を解明するために、DNAの修復と複製に関わるDNAポリメラーゼεと増殖細胞核抗原(PCNA)の両遺伝子の癌特異的変異を検索した。DNAポリメラーゼεに関しては、その校正機能を担う3′-エキソヌクレアーゼドメインを構成する7個のエキソンとイントロン構造をまず明らかにし、変異検索を行ったところ、このドメイン内にアミノ酸置換を伴う遺伝的多型を検出した。この多型は癌では約50%の頻度で検出されるが、他常人では20%以下であったことから、癌化に対する高リスク因子となりうることが示唆された。またPCNA逍伝子に関しては、RT-PCR産物を全領域同時SSCP法で解析し、数例の原発肺癌において共通な癌特異的変異を示唆する結果を得た。PCNAでは遺伝子レベルにおける確認がなされていないため未確定であるが、これらの知見はDNAの複製・修復に重要な役割を果たすDNAポリメラーゼεやPCNAの微小な遺伝子異常が癌化の前提条件としてのゲノム不安定性に関与する可能性を示すものとして、興味ある結果であると考えられる。

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  • Comprehensive Analysis of Genetic Alterations in Human Cancers by the Simultaneous Multiple SSCP Analysis on the Entire Coding Region of Each Gene.

    Grant number:08457049  1996 - 1997

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    SHIMIZU Kenji, MATSUBARA Nagahide, OUCHIDA Mamoru, OGURA Hajime

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    Grant amount:\7600000 ( Direct expense: \7600000 )

    As a prerequisite of this research, we established a tumor bank containing about 800 pairs of the specimens from a wide variety of human tumor patients during the term of this project. Using these materials, we have developed two novel approaches for detecting tumor-specific genetic alterations, one is the comprehensive genomic scanning method with inter-Alu long PCR amplification, and the other is the multiple SSCP analysis of the whole region of a gene.
    On application of these novel techniques, we found a novel tumor-specific mutation in the gene encoding E2F4 transcription regulator in a subset of genetically unstable (MI+) colorectal cancers. The mutation was decrease in CAG repeat number within a coding exon of the gene, giving rise to reduction of one or two amino acids of 13 consecutive serine residues of the E2F4 protein. The incidence of this mutation in MI+ colorectal/gastric cancers was approximately 40% in both Japan and American patients. Next, we found that the mutation appears to be a result of the inactivating frame-shift mutation of the hMSH3 gene, a DNA mismatch-repair gene implicated in the repair process of mismatch-loops of two to four nucleotides. The correlation between these two mutations was above 80 % (P = 0.0015 by Fisher's exact test). The E2F4 gene is known to behave as an active oncogene when it is overexpressed in living cells both in vivo and in vitro. Further, we got a preliminary result that the altered version of E2F4 gene is capable of stimulating cellular proliferation in rodent cell system. Thus, the E2F4 gene is identified, for the first time, as a target of the defective mismatch repair function involving hMSH3 protein, in actual human malignancies.
    As a relevant research result, we have found novel genetic alterations of the human p107 gene, a close relative of the tumor suppressor gene RB.The most clear case of the genetic alteration of the gene, detected in a diffuse-large B cell lymphoma cell line, was an interstitial deletion of a 15 kbp region containing 5 coding exons of the gene. In contrast to the RB gene, tumor-specific alteration of the p107 gene has never been identified as far. Our finding in human hematologic malignancies is the first discovery of such cases. We analyzed the entire genomic structure of the p107 gene and found that the gene spans about 90 kbp region and is composed of total 22 coding exons.
    Other results of our research projects include, 1) establishment of a general strategy for measuring gene expression by competitive PCR analysis, 2) identification of a novel activating mutation at 22nd codon of the K-ras gene in a human colon cancer, 3) discovery of a novel candidate of the tumor suppressor gene residing on chromosome 3p21, which may be related to many types of solid tumors.

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  • グリオーマにおける癌抑制遺伝子の単離と遺伝子及び遺伝子産物の分子生物学的解析

    Grant number:03857035  1991

    日本学術振興会  科学研究費助成事業 奨励研究(A)  奨励研究(A)

    大内田 守

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    Grant amount:\900000 ( Direct expense: \900000 )

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