Updated on 2021/04/08

写真a

 
ITO Sachio
 
Organization
Medicine, Dentistry and Pharmaceutical Sciences Assistant Professor
Position
Assistant Professor
External link

Degree

  • 修士(農学) ( 岡山大学 )

  • Ph.D in Medicine ( Okayama University )

Research Interests

  • 分子生物学

  • 分子腫瘍学

  • Molecular Biology

  • Molecular Oncology

Research Areas

  • Life Science / Molecular biology

  • Life Science / Cell biology

  • Life Science / Medical biochemistry

  • Life Science / Pathological biochemistry

Education

  • Okayama University    

    - 2001

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  • Okayama University   医学研究科   病理系病態遺伝子解析

    - 2001

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    Country: Japan

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  • Okayama University of Science   Faculty of Science   Department of Biochemistry

    - 1993

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    Country: Japan

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  • Okayama University of Science    

    - 1993

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Research History

  • - 岡山大学医歯薬学総合研究科 助教

    2004

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  • - Assistant Professor,Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,Okayama University  

    2004

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Professional Memberships

 

Papers

  • Human NINEIN polymorphism at codon 1111 is associated with the risk of colorectal cancer. Reviewed International journal

    Yukiko Yasuda, Akiko Sakai, Sachio Ito, Kaori Sasai, Akisada Ishizaki, Yoshiya Okano, Seito Kawahara, Yoshimi Jitsumori, Hiromasa Yamamoto, Nagahide Matsubara, Kenji Shimizu, Hiroshi Katayama

    Biomedical reports13 ( 5 ) 45 - 45   2020.11

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    NINEIN serves an essential role in centrosome function as a microtubule organizing center, and in the reformation of the interphase centrosome architecture following mitosis. In the present study, the association between NINEIN Pro1111Ala (rs2236316), a missense single nucleotide polymorphism, and the risk of colorectal cancer (CRC), related to smoking and alcohol consumption habits in 200 patients with CRC and 1,141 cancer-free control participants were assessed in a case-control study performed in Japan. The results showed that the NINEIN Ala/Ala genotype compared with the Pro/Pro genotype was significantly more associated with an increased risk of CRC, and the males with the Ala/Ala genotype exhibited a significantly increased risk of CRC compared with those with Pro/Pro and Pro/Ala genotypes. Stratified analyses of the Ala/Ala genotype with CRC risk further showed an increased association in never/light drinkers (<23 g of ethanol/day), in male never/light drinkers and in male patients with rectal cancer. These findings suggest that the genetic variant of the NINEIN Pro1111Ala polymorphism has a significant effect on CRC susceptibility in the Japanese population.

    DOI: 10.3892/br.2020.1352

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  • Decreased miR-200b-3p in cancer cells leads to angiogenesis in HCC by enhancing endothelial ERG expression. Reviewed International journal

    Aye Moh-Moh-Aung, Masayoshi Fujisawa, Sachio Ito, Hiroshi Katayama, Toshiaki Ohara, Yoko Ota, Teizo Yoshimura, Akihiro Matsukawa

    Scientific reports10 ( 1 ) 10418 - 10418   2020.6

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    Transcription factor ERG (erythroblast transformation-specific (ETS)-related gene) is essential in endothelial differentiation and angiogenesis, in which microRNA (miR)-200b-3p targeting site is expected by miRNA target prediction database. miR-200b is known decreased in hepatocellular carcinoma (HCC), however, the functional relation between ERG and miR-200b-3p, originating from pre-miR-200b, in HCC angiogenesis remains unclear. We investigated whether hepatocyte-derived miR-200b-3p governs angiogenesis in HCC by targeting endothelial ERG. Levels of miR-200b-3p in HCC tissues were significantly lower than those in adjacent non-HCC tissues. Poorly differentiated HCC cell line expressed lower level of miR-200b-3p compared to well-differentiated HCC cell lines. The numbers of ERG-positive endothelial cells were higher in HCC tissues than in adjacent non-HCC tissues. There was a negative correlation between the number of ERG-positive cells and miR-200b-3p expression in HCC tissues. Culture supernatants of HCC cell lines with miR-200b-3p-overexpression reduced cell migration, proliferation and tube forming capacity in endothelial cells relative to the control, while those with miR-200b-3p-inhibition augmented the responses. Exosomes isolated from HCC culture supernatants with miR-200b-3p overexpression suppressed endothelial ERG expression. These results suggest that exosomal miR-200b-3p from hepatocytes suppresses endothelial ERG expression, and decreased miR-200b-3p in cancer cells promotes angiogenesis in HCC tissues by enhancing endothelial ERG expression.

    DOI: 10.1038/s41598-020-67425-4

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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 OKAYAMA71 ( 1 ) 59 - 68   2017.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:OKAYAMA UNIV MED SCHOOL  

    Human RAD17 acts as an activator of checkpoint signals in response to DNA damage. Here we evaluated the association of hRAD17 Leu546Arg (rs1045051), a missense single nucleotide polymorphism, with the risk of colorectal cancer (CRC) in relation to smoking and alcohol consumption habits in 212 CRC patients and 1,142 cancer-free controls in a case-control study conducted in Japan. The results showed that the hRAD17 Leu/Arg genotype compared to the Leu/Leu genotypes was significantly associated with the protective effect on CRC risk with the adjusted odds ratio (OR) of 0.68 [95% confidence interval (CI): 0.49-0.95, p=0.024], and the males with the Arg/Arg genotype had a greater risk of CRC compared to those with the Leu/Leu and Leu/Arg genotypes (OR=1.87, 95% CI 1.03-3.40, p=0.04). In stratified studies, the protective effect of the Leu/Arg genotype on CRC risk was markedly higher in the light smokers (&lt; 20 pack years) (OR=0.61, 95% CI 0.40-0.94, p=0.024) and the rectal cancer patients (OR=0.49, 95% CI 0.31-0.78, p=0.003). The risk of the Arg/Arg genotype was associated with heavy smoking (&gt;= 20 pack-years) (OR=2.24, 95% CI 1.09-4.61, p=0.03). These findings suggest that the genetic variant of hRAD17 Leu546Arg polymorphism has a significant effect on CRC susceptibility in Japanese.

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  • Unique circulating microRNAs in relation to EGFR mutation status in Japanese smoker male with lung adenocarcinoma Reviewed

    Sachio Ito, Yoshihiro Kamoto, Akiko Sakai, Kaori Sasai, Tatsuro Hayashi, Shinichi Toyooka, Hiroshi Katayama

    Oncotarget8 ( 70 ) 114685 - 114697   2017

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Impact Journals LLC  

    The incidence of lung adenocarcinoma has been increasing recently in smokers. The molecular target therapy has been developed for lung adenocarcinoma patients harboring EGFR gene mutation. However, the treatment modalities for patients without mutation are currently limited. Thus, analysis of EGFR gene mutation status at early stage is important strategy to classify the patients for improving treatments and prognosis efficiently. This study aimed to identify microRNA (miRNA) signature in relation to mutation status in EGFR gene in early stage of lung adenocarcinoma male patients with smoking history. MiRNA profiles were assessed by microarray in paired plasma and tissue pooled from 10 EGFR wild type (EGFR-wt) and 10 EGFR mutated (EGFR-mut) patients. Expressions of selected miRNAs were verified further by real-time qRT-PCR in 83 plasma samples consisting of 55 EGFR-wt patients and 28 EGFR-mut patients and their correlation with clinicopathological parameters and EGFR gene mutation status were evaluated. We found that seven miRNAs (miR-16-5p, miR-23a-3p, miR-103a-3p, miR122-5p, miR-223-3p, miR-346 and miR-451a) were differentially expressed in stage I and stage I+II. Especially, miR-23a-3p was only miRNA shown higher expression in EGFR-wt patients than EGFR-mut patients. Thus, our findings could be useful non-invasive biomarkers to differentiate mutation status in EGFR gene in smoker lung adenocarcinoma male patients.

    DOI: 10.18632/oncotarget.21425

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  • Genetic polymorphism at codon 546 of the human RAD17 contributes to the risk for esophageal squamous cell carcinoma Reviewed

    Yukiko Yasuda, Akiko Sakai, Sachio Ito, Yuichiro Mita, Takayuki Sonoyama, Shunsuke Tanabe, Yasuhiro Shirakawa, Yoshio Naomoto, Hiroshi Katayama, Kenji Shimizu

    International Journal of Molecular Epidemiology and Genetics7 ( 1 ) 58 - 66   2016

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

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

    PLOS ONE10 ( 9 )   2015.9

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    Micro RNAs (miRNAs) regulate the expression of target genes posttranscriptionally by pairing incompletely with mRNA in a sequence-specific manner. About 30% of human genes are regulated by miRNAs, and a single miRNA is capable of reducing the production of hundreds of proteins by means of incomplete pairing upon miRNA-mRNA binding. Lately, evidence implicating miRNAs in the development of lung cancers has been emerging. In particular, miR-19a, which is highly expressed in malignant lung cancer cells, is considered the key miRNA for tumorigenesis. However, its direct targets remain underreported. In the present study, we focused on six potential miR-19a target genes selected by miRNA target prediction software. To evaluate these genes as direct miR-19a target genes, we performed luciferase, pull-down, and western blot assays. The luciferase activity of plasmids with each miR-19a-binding site was observed to decrease, while increased luciferase activity was observed in the presence of anti-miR-19a locked nucleic acid (LNA). The pull-down assay showed biotinylated miR-19a to bind to AGO2 protein and to four of six potential target mRNAs. Western blot analysis showed that the expression levels of the four genes changed depending on treatment with miR-19a mimic or anti-miR-19a-LNA. Finally, FOXP1, TP53INP1, TNFAIP3, and TUSC2 were identified as miR-19a targets. To examine the function of these four target genes in lung cancer cells, LK79 (which has high miR-19a expression) and A549 (which has low miR-19a expression) were used. The expression of the four target proteins was higher in A549 than in LK79 cells. The four miR-19a target cDNA expression vectors suppressed cell viability, colony formation, migration, and invasion of A549 and LK79 cells, but LK79 cells transfected with FOXP1 and TP53INP1 cDNAs showed no difference compared to the control cells in the invasion assay.

    DOI: 10.1371/journal.pone.0137887

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  • Truncated SSX Protein Suppresses Synovial Sarcoma Cell Proliferation by Inhibiting the Localization of SS18-SSX Fusion Protein Reviewed

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

    PLOS ONE8 ( 10 )   2013.10

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    Synovial sarcoma is a relatively rare high-grade soft tissue sarcoma that often develops in the limbs of young people and induces the lung and the lymph node metastasis resulting in poor prognosis. In patients with synovial sarcoma, specific chromosomal translocation of t(X; 18) (p11.2; q11.2) is observed, and SS18-SSX fusion protein expressed by this translocation is reported to be associated with pathogenesis. However, role of the fusion protein in the pathogenesis of synovial sarcoma has not yet been completely clarified. In this study, we focused on the localization patterns of SS18-SSX fusion protein. We constructed expression plasmids coding for the full length SS18-SSX, the truncated SS18 moiety (tSS18) and the truncated SSX moiety (tSSX) of SS18-SSX, tagged with fluorescent proteins. These plasmids were transfected in synovial sarcoma SYO-1 cells and we observed the expression of these proteins using a fluorescence microscope. The SS18-SSX fusion protein showed a characteristic speckle pattern in the nucleus. However, when SS18-SSX was co-expressed with tSSX, localization of SS18-SSX changed from speckle patterns to the diffused pattern similar to the localization pattern of tSSX and SSX. Furthermore, cell proliferation and colony formation of synovial sarcoma SYO-1 and YaFuSS cells were suppressed by exogenous tSSX expression. Our results suggest that the characteristic speckle localization pattern of SS18-SSX is strongly involved in the tumorigenesis through the SSX moiety of the SS18-SSX fusion protein. These findings could be applied to further understand the pathogenic mechanisms, and towards the development of molecular targeting approach for synovial sarcoma.

    DOI: 10.1371/journal.pone.0077564

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  • EGFRチロシンキナーゼ阻害薬耐性肺癌細胞に対するmicroRNA-7発現プラスミドのリポソームを用いた導入による克服の検討 Reviewed

    頼 冠名, 瀧川 奈義夫, 伊藤 佐智夫, 柏原 宏美, 市原 英基, 保田 立二, 清水 憲二, 谷本 光音, 木浦 勝行

    岡山医学会雑誌124 ( 3 ) 207 - 210   2012.12

  • 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 oncology138 ( 9 ) 1501 - 9   2012.9

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    PURPOSE: We investigated the miRNA profile in peripheral nerve tumors and clarified the involvement of miRNA in the development and progression of MPNST in comparison with neurofibroma (NF). In addition, we attempted to seek associations between the miRNA and their potential targets in MPNST. METHODS: Global miRNA expression profiling was investigated for clinical samples of 6 MPNSTs and 6 NFs. As detected by profiling analysis, the expressions of miR-21 in clinical samples of 12 MPNSTs, 11 NFs, and 5 normal nerves, and 3 MPNST cell lines were compared using quantitative real-time reverse transcription PCR. MPNST cell line (YST-1) was transfected with miR-21 inhibitor to study its effects on cell proliferation, caspase activity, and the expression of miR-21 targets. RESULTS: Analysis of miRNA expression profiles in MPNST and NF revealed significantly altered expression levels of nine miRNAs, one of those, miR-21, and its putative target, programmed cell death protein 4 (PDCD4), were selected for further studies. miR-21 expression level in MPNST was significantly higher than that in NF (P < 0.05). In MPNST cells, transfection of miR-21 inhibitor significantly increased caspase activity (P < 0.01), significantly suppressed cell growth (P < 0.05), and upregulated protein level of PDCD4, indicating that miR-21 inhibitor could induce cell apoptosis of MPNST cells. CONCLUSIONS: These results suggest that miR-21 plays an important role in MPNST tumorigenesis and progression through its target, PDCD4. MiR-21 and PDCD4 may be candidate novel therapeutic targets against the development or progression of MPNSTs.

    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

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

    PLOS ONE7 ( 8 )   2012.8

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    The miR-17-92 cluster encodes 7 miRNAs inside a single polycistronic transcript, and is known as a group of oncogenic miRNAs that contribute to tumorigenesis in several cancers. However, their direct targets remain unclear, and it has been suggested that a single miRNA is capable of reducing the production of hundreds of proteins. The majority of reports on the identification of miRNA targets are based on computational approaches or the detection of altered mRNA levels, despite the fact that most miRNAs are thought to regulate their targets primarily by translational inhibition in higher organisms. In this study, we examined the target profiles of miR-19a, miR-20a and miR-92-1 in MCF-7 breast cancer cells by a quantitative proteomic strategy to identify their direct targets. A total of 123 proteins were significantly increased after the endogenous miR-19a, miR-20a and miR-92-1 were knocked down, and were identified as potential targets by two-dimensional electrophoresis and a mass spectrometric analysis. Among the upregulated proteins, four (PPP2R2A, ARHGAP1, IMPDH1 and NPEPL1) were shown to have miR-19a or miR-20a binding sites on their mRNAs. The luciferase activity of the plasmids with each binding site was observed to decrease, and an increased luciferase activity was observed in the presence of the specific anti-miRNA-LNA. A Western blot analysis showed the expression levels of IMPDH1 and NPEPL1 to increase after treatment with anti-miR-19a, while the expression levels of PPP2R2A and ARHGAP1 did not change. The expression levels of IMPDH1 and NPEPL1 did not significantly change by anti-miR-19a-LNA at the mRNA level. These results suggest that the IMPDH1 and NPEPL1 genes are direct targets of miR-19a in breast cancer, while the exogenous expression of these genes is not associated with the growth suppression of MCF-7 cells. Furthermore, our proteomic approaches were shown to be valuable for identifying direct miRNA targets.

    DOI: 10.1371/journal.pone.0044095

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

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

    PROTEOMICS11 ( 17 ) 3531 - 3539   2011.9

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    MicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally repress the expression of target genes. Many miRNAs have been implicated in a number of diseases, including cancers. The miR-17-92 miRNA cluster is known as a body of oncogenic miRNAs, and has been shown to be overexpressed in several cancers, including lung cancer. Although the overexpression of miR-17-92 is clearly implicated in the development of lung cancer, only a few direct targets for the miR-17-92 cluster have been identified thus far. In this study, we examined miR-17-92 target profiles in SBC-3 small-cell lung cancer cells using a quantitative proteomic strategy to identify direct targets of the miR-17-92 cluster. By knocking down the expression of endogenous miR-19a, miR-20a and miR-92-1, which are contained in the cluster, 112 up-regulated proteins were detected and also identified as potential targets of these miRNAs. Among these candidate targets, we validated one direct target, RAB14. In conclusion, these findings suggest that proteomic approaches are valuable for identifying direct miRNA targets, and we were able to identify a novel direct target for the miR-92-1 using our proteomic strategy.

    DOI: 10.1002/pmic.201000501

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  • Liposomal Delivery of MicroRNA-7-Expressing Plasmid Overcomes Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor-Resistance in Lung Cancer Cells Reviewed

    Kammei Rai, Nagio Takigawa, Sachio Ito, Hiromi Kashihara, Eiki Ichihara, Tatsuji Yasuda, Kenji Shimizu, Mitsune Tanimoto, Katsuyuki Kiura

    MOLECULAR CANCER THERAPEUTICS10 ( 9 ) 1720 - 1727   2011.9

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    Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have been strikingly effective in lung cancers harboring activating EGFR mutations. Unfortunately, the cancer cells eventually acquire resistance to EGFR-TKI. Approximately 50% of the acquired resistance involves a secondary T790M mutation. To overcome the resistance, we focused on EGFR suppression using microRNA-7 (miR-7), targeting multiple sites in the 30-untranslated region of EGFR mRNA. Two EGFR-TKI-sensitive cell lines (PC-9 and H3255) and two EGFR-TKI-resistant cell lines harboring T790M (RPC-9 and H1975) were used. We constructed miR-7-2 containing miR-7-expressing plasmid. After transfection of the miR-7-expressing plasmid, using cationic liposomes, a quantitative PCR and dual luciferase assay were conducted to examine the efficacy. The antiproliferative effect was evaluated using a cell count assay and xenograft model. Protein expression was examined by Western blotting. The miR-7 expression level of the transfectants was approximately 30-fold higher, and the luciferase activity was ablated by 92%. miR-7 significantly inhibited cell growth not only in PC-9 and H3255 but also in RPC-9 and H1975. Expression of insulin receptor substrate-1 (IRS-1), RAF-1, and EGFR was suppressed in the four cell lines. Injection of the miR-7-expressing plasmid revealed marked tumor regression in a mouse xenograft model using RPC-9 and H1975. EGFR, RAF-1, and IRS-1 were suppressed in the residual tumors. These findings indicate promising therapeutic applications of miR-7-expressing plasmids against EGFR oncogene-addicted lung cancers including T790M resistance by liposomal delivery. Mol Cancer Ther; 10(9); 1720-7. (C)2011 AACR.

    DOI: 10.1158/1535-7163.MCT-11-0220

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  • EGFR mutation status in pleural fluid predicts tumor responsiveness and resistance to gefitinib Reviewed

    Junichi Soh, Shinichi Toyooka, Shuji Ichihara, Hiroshi Suehisa, Naruyuki Kobayashi, Sachio Ito, Masaomi Yamane, Motoi Aoe, Yoshifumi Sano, Katsuyuki Kiura, Hiroshi Date

    LUNG CANCER56 ( 3 ) 445 - 448   2007.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER IRELAND LTD  

    It has been reported that the threonine-to-methionine substitution at amino acid position 790 (T790M) of the epidermal growth factor receptor (EGFR) gene is correlated with acquired resistance to gefitinib. We previously reported that there was some population that harbored the EGFR T790M mutation as a minor clone of tumor cells prior to drug treatment, may be causing resistance to gefitinib during treatment. This fact also suggests that the detection of the EGFR T790M mutation prior to treatment may predict the development of resistance. We also showed that pleural fluid is a useful specimen for detection of EGFR mutation using sensitive assays. In this study, we reported a female patient who was treated with gefitinib because an EGFR L858R mutation was found in her pleura[ fluid. Our patient showed partial response to gefitinib, but she had progressive disease only 4 months after the start of treatment. Furthermore, the EGFR T790M mutation was detected in the pleural fluid before gefitinib treatment by the mutant-enriched PCR assay. Our findings confirmed that the EGFR T790M mutation was occasionally present as a minor population in tumor cells before treatment and caused resistance after gefitinib administration. The detection of a small fraction of T790M-positive alleles may be useful to predict the clinical course of the gefitinib-treated non-small-cell lung cancer patients. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.lungcan.2007.01.014

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

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

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE18 ( 6 ) 1153 - 1158   2006.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:PROFESSOR D A SPANDIDOS  

    The molecular pathogenesis of osteosarcoma is very complicated and associated with chaotic abnormalities on many chromosomal arms. We analyzed 12 cases of osteosarcomas with comparative genomic hybridization (CGH) to identify chromosomal imbalances, and detected highly frequent chromosomal alterations in chromosome 6q, 8p, 10p and 10q. To define the narrow rearranged region on chromosome 6 with higher resolution, loss of heterozygosity (LOH) analysis was performed with 21 microsatellite markers. Out of 31 cases, 23 cases (74%) showed allelic loss at least with one marker on chromosome 6q. We identified two distinct commonly deleted regions on chromosome 6 using markers D6S1565 located at 6q16 and 6q23MS1 at 6q23. The expression analysis of genes located at the deleted region was performed, and the decreased mRNA expression of the CCNC gene, one of the regulators of cell cycle, was detected. Growth of osteosarcoma cell line was significantly suppressed after the CCNC cDNA transfection. Fine mapping of the deleted region containing a possible tumor suppressor gene and the transfection assay suggest that the CCNC is a candidate tumor suppressor gene.

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

    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 RESEARCH66 ( 16 ) 7854 - 7858   2006.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:AMER ASSOC CANCER RESEARCH  

    The threonine-to-methionine substitution at amino acid position 790 (T790M) of the epidermal growth factor receptor (EGFR) gene has been reported in progressing lesions after gefitinib treatment in non-small cell lung cancer (NSCLC) that causes sensitive tumors to become resistant to gefitinib. Alternatively, the EGFR T790M mutation might be present in small fractions of tumor cells before drug treatment, and the tumor cells harboring the T790M mutation might be enriched during the proliferation after drug treatment. We developed a mutant-enriched PCR assay to detect small fractions of cells with T790M mutation and used this technique to detect mutations in 280 NSCLCs, including gefitinib-treated 95 cases. Although the direct sequencing detected only I T790M mutant case, the mutant-enriched PCR (confirmed to enrich one mutant out of 1 X 10(3) wild-type alleles) detected 9 additional cases among 280 cases. As linkage to clinicopathologic factors, the T790M mutation showed no bias for sex, smoking status, or histology but was significantly more frequent in advanced tumors (9 of III cases) than in early-stage tumors (I of 169 cases; P = 0.0013). Among gefitinib-treated cases, gefitinib-sensitive mutations were found in 30 cases. The T790M mutation was present in 3 of 7 no-responders with the gefitinib-sensitive mutation and was not present in 19 responders (P = 0.014). Our results indicate that the T790M mutation is sometimes present in a minor population of tumor cells during the development of NSCLC and suggest that the detection of small fractions of T790M mutant alleles may be useful for predicting gefitinib resistance of NSCLCs with sensitive EGFR mutations.

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

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

    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 RESEARCH12 ( 1 ) 43 - 48   2006.1

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    Purpose: Mutations in the epidermal growth factor receptor (EGFR) gene have been reported to be present in non-small cell lung cancer (NSCLC) and related to the responsiveness of tumors to EGFR tyrosine kinase inhibitors, suggesting its usefulness as a biomarker. Because clinical samples contain tumor and normal cells or genes, a highly sensitive assay for detecting mutation is critical for clinical applications.
    Experimental Design: The mutant-enriched PCR is a rapid and sensitive assay with selective restriction enzyme digestion. We developed the mutant-enriched PCR assay targeting exons 19 and 21 of EGFR and applied the developed assay to detect mutations in 108 cases of surgically resected specimens of NSCLCs,18 samples of computed tomography (CT)-guided needle lung biopsies, and 20 samples of pleural fluid. In addition, results were then compared with those from direct sequencing and a nonenriched PCR assay.
    Results: The mutant-enriched PCR that was proved to enrich one mutant of 2 x 103 normal genes detected mutations in 37 cases of 108 resected tumors, seven samples of CT-guided lung biopsies, and seven samples of pleural fluid. Among mutant cases, four resected tumors, two CT-guided lung biopsies, and two pleural fluid were identified as additional mutant cases by the mutant-enriched PCR, which were considered normal based on nonenriched assays.
    Conclusions: Our results indicate that EGFR mutations are readily detectable by mutant-enriched PCR in various clinical samples. Thus, mutant-enriched PCR may provide a valuable method of potentially detecting a small fraction of mutant genes in heterogeneous specimens, indicating its possible use in clinical application for NSCLC.

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

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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. Reviewed International journal

    Levent B Beder, Mehmet Gunduz, Mamoru Ouchida, Esra Gunduz, Akiko Sakai, Kunihiro Fukushima, Hitoshi Nagatsuka, Sachio Ito, Noriyasu Honjo, Kazunori Nishizaki, Kenji Shimizu

    Journal of cancer research and clinical oncology132 ( 1 ) 19 - 27   2006.1

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    PURPOSE: Aims of the study are to narrow-down the hotspot region on 10q21 defined by previous genome-wide loss of heterozygosity (LOH) analysis in head and neck squamous cell carcinomas (HNSCC) and to define candidate tumor suppressor genes (TSG) concerned with 10q21. MATERIALS AND METHODS: LOH analysis was carried out with ten polymorphic microsatellite markers. Expression analysis was performed by semi-quantitative RT-PCR, and mutation analysis by PCR and direct sequencing. RESULTS: LOH analysis on 10q21 in 52 HNSCC indicated distinctive and frequent allelic loss at D10S589 (42%). Among flanking genes, we found the RHOBTB1 gene as a candidate TSG, since an intragenic marker demonstrated the highest LOH (44%). Expression analysis revealed down-regulation of RHOBTB1 mRNA in 37% of tumors. Interestingly, all the five tumors that showed decreased expression of RHOBTB1 were accompanied with LOH, supporting the haploinsufficiency and class 2 TSG characteristics of RHOBTB1. No pathogenic mutation of RHOBTB1 was found. Furthermore, another gene within the region, EGR2, was also taken under scope. LOH frequencies around the EGR2 gene were relatively low (23 and 33%). Albeit semi-quantitative expression analysis of EGR2 demonstrated downregulation in 45% of tumor samples, no relation was found between the expression levels and LOH status. CONCLUSION: Frequent allelic loss and decreased expression of RHOBTB1 suggested that this gene has a role in tumorigenesis of a subset of HNSCC.

    DOI: 10.1007/s00432-005-0033-0

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

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

    LABORATORY INVESTIGATION84 ( 11 ) 1484 - 1490   2004.11

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    Synovial sarcomas are soft-tissue tumors predominantly affecting children and young adults. They are molecular-genetically characterized by the SYT-SSX fusion gene generated from chromosomal translocation t(X; 18) (p11.2; q11.2). When we screened new gene products that interact with SYT or SSX proteins by yeast two-hybrid assay, we found that mSin3A, a component of the histone deacetylase complex, interacts with SYT but not with SSX. These results were confirmed by mammalian two-hybrid and pull-down assays. Analyses with sequential truncated proteins revealed a main mSin3A-interaction region on the SYT amino-terminal 93 amino acids, and another one on the region between 187th amino acid and break point. In luciferase assay, mSin3A repressed the transcriptional activity of reporter promoter mediated by SYT and hBRM/BRG1. Our results suggest that the histone deacetylase complex containing mSin3A may regulate the transcriptional activation mediated by SYT.

    DOI: 10.1038/labinvest.3700174

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

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

    ONCOLOGY REPORTS12 ( 4 ) 789 - 795   2004.10

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    Certain tumor suppressor genes (TSG) residing on human chromosome 10q are implicated in astrocytic tumors. We thoroughly examined loss of heterozygosity (LOH) on chromosome 10q in astrocytic tumors to determine the extent of deletion and their relation to prognostic variables of patients. We analyzed 63 astrocytic tumors, including 9 diffuse astrocytomas, 36 anaplastic astrocytomas, and 18 glioblastomas. DNAs from tumors and leukocytes were analyzed for LOH at 18 microsatellite loci by polymerase chain reaction using fluorescence-labeled primers. Then correlation between LOH and clinicopathological variables was examined statistically. Twenty-four (66.7%) anaplastic astrocytomas and 15 (83.3%) glioblastomas had at least one LOH on chromosome 10q. However, diffuse astrocytomas exhibited no LOH. Nineteen tumors (10 anaplastic astrocytomas and 9 glioblastomas) were believed to have a total loss of one chromosome 10. Analyses on 20 tumors with interstitial LOH revealed that most of the high LOH regions matched the location of known TSGs, while some novel LOH regions were found preferentially in anaplastic astrocytoma. The median survivals of the total, partial, and no loss groups were 10.1, 14.8, and 46.8 months, respectively, indicating a significant difference in the survivals of these groups (P=0.0289). Thus, analyzing chromosome 10q loss is helpful for diagnosing malignancy in astrocytic tumors and for predicting patients' survival. Our data also suggested that there are novel TSGs for anaplastic astrocytoma at 10q24 and 10q26.

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

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

    INTERNATIONAL JOURNAL OF ONCOLOGY25 ( 3 ) 685 - 691   2004.9

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    CDH13 (H-cadherin) is a member of the cadherin superfamily, which plays an important role in cell recognition and adhesion. We examined the expression and methylation status of the CDH13 gene in diffuse large B cell lymphomas (B-DLCLs). We found decreased expression of the CDH13 gene in all of 6 hematopoietic cell lines by reverse transcription-polymerase chain reaction (RT-PCR). Promoter hypermethylation of the gene was detected in all 6 cell lines and in 13 of 19 (68%) B-DLCL samples by methylation-specific PCR. Interestingly, the methylation frequency of the CDH13 gene was comparable to those of the tumor suppressor genes p15 (68%) and p16 (74%) detected in B-DLCLs. Sequencing of bisulfite-treated DNA revealed hyper-methylation of the CpG islands of the CDH13 promoter in B-DLCLs and the cell lines. Treatment with 5-aza-2'-deoxycytidine restored CDH13 gene expression in a cell line in which promoter hyper-methylation and impaired expression of the CDH13 gene were observed. Loss of heterozygosity (LOH) around the CDH13 genes on chromosome 16q24 was detected in 6 of 15 (40%) informative cases with microsatellite marker D16S507 and in 6 of 15 (40%) cases with D16S422 in B-DLCLs. In all of 4 B-DLCL cases which showed both promoter methylation and LOH at the two marker loci, expression of the CDH13 gene was significantly low. These results suggest that silencing of the CDH13 gene by aberrant promoter methylation and allelic deletion is associated with tumorigenesis in a subset of B-DLCL.

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

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

    UROLOGY64 ( 1 ) 176 - 181   2004.7

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    Objectives. To report our development of a new application of the inter-AN long polymerase chain reaction (PCR) for genomic scanning to screen for tumor-specific alterations in tumor DNA. Using this method, we detected a rearranged chromosomal region in renal cell carcinomas (RCCs). We then examined tumor-specific allelic loss in this region using microsatellite markers and determined whether a relationship was present between this allelic loss and the clinicopathologic features of the patients.
    Methods. The inter-Alu long PCR genomic scan method was performed using RCC DNA samples and primers specific for a minor subset of the human repeat sequence Alu. We analyzed DNA samples from 42 pairs of matched normal and nonpapillary RCC tissues with seven microsatellite markers.
    Results. The inter-Alu long PCR genomic scan method revealed an altered DNA region on chromosome 14q24-31, which is the location of several putative tumor suppressor genes. At least one of seven microsatellite markers on chromosome 14q24-31 showed loss of heterozygosity in 23 (54.8%) of 42 informative cases of RCC. The prevalent loss region was confined to a 2-Mb region around D14S67. We found a positive correlation between the presence of the loss of heterozygosity on 14q24-31 and tumor stage (P &lt; 0.05). We also found that cases with allelic loss at 14q24-31 had a poor prognosis (P = 0.045).
    Conclusions. Our inter-Alu long PCR genomic scan method is a powerful method for the screening of DNA alterations, and our data suggest that the chromosome 14q24-31 region contains likely tumor suppressor genes associated with the progression of RCC. (C) 2004 Elsevier Inc.

    DOI: 10.1016/j.urology.2004.03.015

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

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

    LABORATORY INVESTIGATION83 ( 1 ) 99 - 105   2003.1

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    Head and neck squamous cell carcinoma (HNSCC) is a frequent malignancy with a poor survival rate. Identifying the tumor suppressor gene (TSG) loci by genomic studies is an important step to uncover the molecular mechanisms involved in HNSCC pathogenesis. We therefore performed comprehensive analyses on loss of heterozygosity (LOH) using a genome-wide panel of 191 microsatellite markers in 22 HNSCC samples. We found 53 markers with significantly high LOH (&gt;30%) on 21 chromosomal arms; the highest values of those were observed on 3p, 9p, 13q, 15q, and 17p, corresponding to D3S2432 (67%), D9S921-D9S925 (67%) and GATA62F03 (86%), D13S1493 (60%), D15S211 (62%), and D17S1353 (88%), respectively. Fifteen hot spots of LOH were defined in 13 chromosomal arms: 2q22-23, 4p15.2, 4q24-25, 5q31, Sp23, 9p23-24, 9q31.3, 9q34.2, 10q21, 11q21-22.3, 14q11-13, 14q22.3, 17p13, 18q11, and 19q12 as loci reported previously in HNSCCs. Furthermore, we identified five novel hot spots of LOH on three chromosomal arms in HNSCC at 2q33 (D2S1384), 2q37 (D2S125), 8q12-13 (D8S1136), 8q24 (D8S1128), and 15q21 (D15S211). In conclusion, our comprehensive allelotype analyses have unveiled and confirmed a total of 20 possible TSG loci that could be involved in the development of HNSCC. These results provide useful clues for identification of putative TSGs involved in HNSCC by fine mapping of the suspected regions and subsequent analysis for functional genes.

    DOI: 10.1097/01.LAB.0000047489.26246.E1

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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. Reviewed International journal

    Mehmet Gunduz, Mamoru Ouchida, Kunihiro Fukushima, Sachio Ito, Yoshimi Jitsumori, Tomoko Nakashima, Noriyuki Nagai, Kazunori Nishizaki, Kenji Shimizu

    Oncogene21 ( 28 ) 4462 - 70   2002.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    Loss of heterozygosity (LOH) has been frequently detected at chromosome 7q31 region in human head and neck squamous cell carcinomas (HNSCC) and many other cancers, suggesting the existence of tumor suppressor genes (TSG). We analysed LOH at 7q31 region in 49 HNSCC by using six polymorphic microsatellite markers and found allelic deletion in 48% (22/46) of the informative cases. We detected two preferentially deleted regions, one is around D7S643 and the other around D7S486. When we redefined the map of 7q31 region according to the contiguous sequences, a recently identified gene, ING3, was found in the proximity of D7S643. ING3 protein harbors the PHD domain highly homologous among ING family proteins, in which we previously found mutations in a related gene, ING1. As only one missense mutation of the ING3 gene was found in HNSCC, we examined the expression level. Reverse-transcription-PCR analysis demonstrated decreased or no expression of ING3 mRNA in 50% of primary tumors as compared with that of matched normal samples. Especially, about 63% of tongue and larynx tumors showed the decrease and a tendency of higher mortality was observed in cases with decreased ING3 expression. All these findings suggest a possibility that the ING3 gene functions as a TSG in a subset of HNSCC.

    DOI: 10.1038/sj.onc.1205540

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

    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-ONCOLOGY58 ( 2 ) 107 - 114   2002.6

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    We thoroughly examined loss of heterozygosity (LOH) around three candidate tumor suppressor genes on chromosome 10q to determine whether LOH of each tumor suppressor gene is associated with the previously defined clinical prognostic indices. We also examined whether LOH can help predict prognostic variables in astrocytomas.
    We selected samples from 40 astrocytomas (grades 2-4), performed Ki-67 immunostaining, and counted positive cells. Using DNA from aliquots of tumor blocks and leukocytes, we investigated LOH around the PTEN, NEURL, and DMBT1 genes (10q23.3-26.1) with the silver staining procedure. We then statistically evaluated the relationship among histological features, regional LOH on chromosome 10q, and survival. The mean survival period for patients with LOH around PTEN was 7.2 months after surgery, while that for patients without LOH around PTEN was 21.4 months. Thus, LOH around PTEN was closely associated with a reduced overall survival (p = 0.0020) but LOH at NEURL or DMBT1 was not (p &gt; 0.05).
    The combined features of an increase in histological grading and Ki-67-positive cells and the presence of LOH around PTEN significantly correlated with poor prognosis. These factors may be useful predictors of survival, and LOH analysis of tumor suppressor genes on chromosome 10q can contribute greatly to the treatment of patients with astrocytoma.

    DOI: 10.1023/A:1016017711033

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  • Rapid and sensitive detection of physical status of human papillomavirus type 16 DNA by quantitative real-time PCR Reviewed

    S Nagao, M Yoshinouchi, Y Miyagi, A Hongo, J Kodama, S Itoh, T Kudo

    JOURNAL OF CLINICAL MICROBIOLOGY40 ( 3 ) 863 - 867   2002.3

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    A rapid quantitative real-time PCR method was employed to quantify the copy number of E2 and E6 genes for analysis of the physical status of human papillomavirus type 16 (HPV-16) DNA. Significant differences with respect to both copy numbers were found when more than 40% of HPV- 161 DNA was integrated with disruption of the E2 gene in an experimental model. The physical status of HPV-16 DNA in 50 clinical samples was exclusively episomal in 21 cases (42%), concomitant in 14 cases (28%), and integrated in 15 cases (30%). The prevalence of integrated and/or concomitant forms of HPV-16 DNA increased with progression of cervical disease. Four of 11 cervical intraepithelial neoplasia involved integrated forms of HPV-16 DNA partially or exclusively. This rapid, sensitive technique is useful in the analysis of the physical status of HPV DNA.

    DOI: 10.1128/JCM.40.3.863-867.2002

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

    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 INVESTIGATION81 ( 11 ) 1565 - 1573   2001.11

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    E2F is a family of transcription factors implicated in the regulation of gene expression required for progression through the G(1)-S transition. We have previously detected tumor-specific mutations at a trinucleotide repeat coding sequence of E2F-4 gene in a subset of human sporadic colorectal cancers. The purpose of this study was to investigate the potential functional consequences of these E2F-4 mutations. We transfected NIH3T3 fibroblasts with expression constructs containing wild-type as well as mutant E2F-4 cDNA, and the effect of the E2F-4 mutations on proliferation was examined. Alteration in transactivation of the E2F consensus promoter sequence was also examined by transient cotransfection of a E2F-4 with a DP-2 construct into cultured human cells. Transfected cell clones overexpressing mutant E2F-4 grew more rapidly and showed higher proliferative activity by increased immunohistochemical staining for proliferating cell nuclear antigen (PCNA). All three mutant forms of E2F-4 showed elevated transactivation of the E2F consensus promoter sequence. Thus, expression of mutant E2F-4s confers a growth advantage in vivo, and this effect may be related to the acquisition of a neoplastic phenotype.

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

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

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS280 ( 3 ) 656 - 663   2001.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    We have cloned a novel cDNA encoding a protein with eight WD repeat motifs and a domain similar to collagen. As the predicted size of the protein was 146 kDa, the gene was named WDC146. Here, we characterized the genomic structure, gene products, and the expression profiles. The human WDC146 gene had 22 exons spanning over 105 kb, and these exons were distributed in three islands intervened by two long introns of around 40 kb. A minimum promoter region was identified within a 0.5 kb 5'-upstream region of exon 1. WDC146 mRNA was most highly expressed in human testis on Northern blot analysis. In mouse tissues, the highest expression was also observed in testis. By in situ hybridization on rat tissues, WDC146 mRNA was detected preferentially in the pachytene stage of spermatocytes in testis, and weakly in white pulp/marginal band of spleen and in cortex of thymus. WDC146 protein was found to be localized in nucleus. These data implied that WDC146 protein may play important roles in the mechanisms of cytodifferentiation and/or DNA recombination. (C) 2001 Academic Press.

    DOI: 10.1006/bbrc.2000.4163

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  • Analysis by multiplex PCR of the physical status of human papillomavirus type 16 DNA in cervical cancers Reviewed

    M Yoshinouchi, A Hongo, K Nakamura, J Kodama, S Itoh, H Sakai, T Kudo

    JOURNAL OF CLINICAL MICROBIOLOGY37 ( 11 ) 3514 - 3517   1999.11

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    Integration of human papillomavirus (HPV) DNA occurs early in cancer development and is an important event in malignant transformation of cervical cancer. Integration of HPVs preferentially disrupts or deletes the E2 open reading frame, which results in the loss of its expression, The preferential disruption of the E2 gene causes the absence of the E2 gene sequences in the PCR product following integration. Twenty-two carcinomas positive for HPV type 16 (HPV-16) DNA mere first tested far the disruption of the E2 gene by PCR. A specific fragment of the E2 gene was not amplified in 10 cases, suggesting integration of HPV DNA into the host genome. Next, multiplex PCR for the RPV E2 and E6 genes was carried out in the remaining 12 cases. Copy numbers of both genes should he equivalent in episomal forms, while the E2 gene copy number will be smaller than that for E6 following the preferential disruption of the E2 gene in concominant forms. Although relative ratios of HPV E2 to E6 PCR products (E2/E6 ratios) ranged from 1.40 to 2.34 in 10 of 12 cases, multiplex PCR products from 2 cases displayed extremely low ratios of 0.69 and 0.61, Southern blot hybridization with an HPV-16 probe revealed that only in these two cases was both episomal and integrated HPV DNA being carried simultaneously. Thus, multiplex PCR for the E2 and E6 genes of HPV-16 DNA following PCR for the E2 gene can distinguish the pure episomal form from a mixed form of episomal and integrated HPV DNA, Clinical application of this technique mill help researchers to understand the implication of the integration of HPV DNA for cervical carcinogenesis and cervical cancer progression.

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  • A431細胞の上皮間葉転換におけるマトリックス分解酵素の解析

    大月孝志, 障子友理, 兒玉慎太郎, YAN Wanyu, HATIPOGLU, Omer Faruk, 西村拓人, 立木美穂, 稲垣純子, 伊藤左智夫, 片山博志, 廣畑聡

    日本分子生物学会年会プログラム・要旨集(Web)42nd   2019.12

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  • 細胞分裂期制御タンパク質による新規転写調節機構の解明

    笹井香織, TREEKITKARNMONGKOL Warapen, 伊藤佐智夫, MAITY Sankar N, SEN Subrata, 片山博志

    日本分子生物学会年会プログラム・要旨集(Web)41st   2018.11

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  • 肺癌における癌遺伝子候補MYNNとp53の統合的解析

    伊藤佐智夫, 邱艶艶, 堺明子, 殷佩浩, 片山博志

    日本分子生物学会年会プログラム・要旨集(Web)41st   2018.11

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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年度   [1LBA - 051]   2017.12

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  • EGFR変異陰性喫煙男性肺腺癌患者に特化した早期疾患診断のためのmicroRNA発現プロファイル解析

    伊藤 佐智夫, 加本 佳大, 堺 明子, 笹井 香織, 片山 博志

    生命科学系学会合同年次大会2017年度   [1LBA - 046]   2017.12

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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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  • 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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  • 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87回   [3P - 410]   2014.10

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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72回   267 - 267   2013.10

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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72回   277 - 277   2013.10

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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86回   3P - 426   2013.9

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  • in vitro pull-down法によるmiR-19aの標的遺伝子の同定(Identification of target genes for miR-19a by in vitro pull-down method)

    山本 久美子, 伊藤 佐智夫, 大内田 守

    日本癌学会総会記事71回   533 - 533   2012.8

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  • Multiple molecular targeting effects by miR-7 in EGFR tyrosine kinase inhibitor-resistant lung cancer xenograft models

    Kammei Rai, Nagio Takigawa, Sachio Ito, Katsuyuki Kiura, Tateji Yasuda, Kenji Shimizu, Mitsune Tanimoto

    CANCER RESEARCH71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-1158

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  • プロテオーム解析による癌細胞でのmiR-17-92 clusterの新規標的タンパク質の同定(Identification of target genes of miR-17-92 cluster by proteomic analysis)

    大内田 守, 神崎 浩孝, 伊藤 佐智夫, 山本 久美子, 田丸 聖治, 清水 憲二

    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83回・33回   2P - 0843   2010.12

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  • 標識ds-miRNAを用いたin vitroプルダウンアッセイによる肺癌細胞におけるmicroRNA-183の真の標的の同定(Identification of true targets of MicroRNA-183 in lung cancer cells using labeled ds-miRNA in vitro pull-down assay)

    伊藤 佐智夫, 花房 裕子, 大内田 守, 清水 憲二

    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83回・33回   2P - 0842   2010.12

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  • 肺癌における標識microRNA-183を用いた標的遺伝子の同定(Identification of true targets of MicroRNA-183 using labeled miRNA in lung cancer cells)

    伊藤 佐智夫, 大内田 守, 清水 憲二

    日本癌学会総会記事69回   174 - 174   2010.8

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  • micro RNA 7発現プラスミドによるEGFR依存性腫瘍におけるin vivoでの著明な抗腫瘍効果(Dramatic anti-proliferative effect of designed miR-7 expressing plasmid against EGFR oncogene addicted tumors)

    頼 冠名, 瀧川 奈義夫, 伊藤 佐智夫, 木浦 勝行, 清水 憲二, 谷本 光音

    日本癌学会総会記事69回   180 - 180   2010.8

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  • 癌細胞におけるmiR-17-92 clusterの新規標的タンパク質のプロテオーム解析(Proteomic analysis of target proteins of miR-17-92 cluster in cancer cells)

    大内田 守, 神崎 浩孝, 伊藤 佐智夫, 清水 憲二

    日本癌学会総会記事69回   175 - 175   2010.8

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  • Lipofection of the designed plasmid expressing microRNA-7 has antitumor effect in gefitinib-resistant lung adenocarcinoma in vivo

    Kammei Rai, Nagio Takigawa, Sachio Ito, Hiromi Kashihara, Eiki Ichihara, Katsuyuki Kiura, Tatsuji Yasuda, Kenji Shimizu, Mitsune Tanimoto

    CANCER RESEARCH70   2010.4

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    DOI: 10.1158/1538-7445.AM10-4041

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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 RESEARCH70   2010.4

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    DOI: 10.1158/1538-7445.AM10-LB-246

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  • EGFRチロシンキナーゼ阻害剤感受性株、耐性株に対するMicroRNA-7による腫瘍形成抑制効果の検討

    頼 冠名, 瀧川 奈義夫, 伊藤 佐智夫, 保田 立二, 清水 憲二, 谷本 光音, 木浦 勝行

    肺癌49 ( 5 ) 696 - 696   2009.10

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  • ゲフィチニブ感受性および耐性細胞株の上皮成長因子受容体に対するMicro-RNA 7による抑制効果(MicroRNA-7 downregulates epidermal growth factor receptor in gefitinib resistant lung adenocarcinoma cells)

    頼 冠名, 瀧川 奈義夫, 伊藤 佐智夫, 木浦 勝行, 保田 立二, 清水 憲二, 谷本 光音

    日本癌学会総会記事68回   238 - 239   2009.8

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  • プロテオーム解析による肺癌におけるmiR-17-92の直接的な新規標的タンパク質の同定(Proteomic analysis of miR-17-92-overexpressing lung cancer cell line aimed to identify novel immediate target protein)

    神崎 浩孝, 大内田 守, 伊藤 佐智夫, 田丸 聖治, 花房 裕子, 清水 憲二

    日本癌学会総会記事68回   146 - 146   2009.8

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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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  • 乳癌におけるmiRNA clusterの新規標的タンパク質の検討(Identification of novel target proteins of miRNA cluster in breast cancer)

    大内田 守, 神崎 浩孝, 伊藤 佐智夫, 田丸 聖治, 花房 裕子, 清水 憲二

    日本癌学会総会記事68回   147 - 147   2009.8

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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 RESEARCH69   2009.5

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  • MicroRNA-7 downregulates epidermal growth factor receptor in both gefitinib-sensitive and -resistant lung adenocarcinoma cells

    Kammei Rai, Nagio Takigawa, Sachio Ito, Katsuyuki Kiura, Masayuki Yasugi, Daijiro Harada, Nobuaki Ochi, Tatsuji Yasuda, Kenji Shimizu, Mitsune Tanimoto

    CANCER RESEARCH69   2009.5

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

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

    Abstracts for Annual Meeting of Japanese Proteomics Society2009 ( 0 ) 80 - 80   2009

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    DOI: 10.14889/jhupo.2009.0.80.0

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  • 骨肉腫における6q16-23の高頻度染色体欠失の研究(High frequent allelic loss of chromosome 6q16-23 in osteosarcoma: Involvement of cyclin C in osteosarcoma)

    大畑 範英, 吉田 晶, 伊藤 佐智夫, 国定 俊之, 森本 裕樹, 神崎 浩孝, 尾崎 敏文, 清水 憲二, 大内田 守

    日本癌学会総会記事66回   345 - 345   2007.8

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  • 食道癌におけるWWOX・ATR遺伝子のSNPs及びLOH解析

    保田 雪子, 花房 裕子, 伊藤 佐智夫, 堺 明子, 大内田 守, 清水 憲二, 白川 靖博, 猶本 良夫, 田中 紀章, 中地 敬

    日本癌学会総会記事63回   167 - 167   2004.9

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  • 滑膜肉腫におけるSYT-SSX蛋白結合因子の解析

    大内田 守, 伊藤 達男, 尾崎 敏文, 伊藤 佐智夫, 大畑 範英, 吉田 晶, 清水 憲二

    日本癌学会総会記事63回   370 - 370   2004.9

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  • 腎癌患者における14q24-31の染色体欠失と予後不良の相関性(POSITIVE CORRELATION BETWEEN ALLELIC LOSS AT CHROMOSOME 14q24-31 AND POOR PROGNOSIS OF PATIENTS WITH RENAL CELL CARCINOMA)

    伊藤 佐智夫, 賀来 春紀, 江原 伸, 大内田 守, 那須 保友, 津島 知靖, 公文 裕巳, 清水 憲二

    日本癌学会総会記事63回   362 - 362   2004.9

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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(LOH analysis of 16q24 and prevalent hyper-methylation of the CDH13 gene promoter in malignant B cell lymphomas)

    大釜 陽一郎, 大内田 守, 吉野 正, 伊藤 佐智夫, 石丸 文彦, 原田 実根, 谷本 光音, 清水 憲二

    日本癌学会総会記事63回   177 - 177   2004.9

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  • 新規ヒト遺伝子OSZFはmSin3Aを介して転写制御する(OSZF, a novel human protein, recruits mSin3A corepressor to mediate transcriptional repression)

    伊藤 佐智夫, 大内田 守, 内藤 訓子, 清水 憲二

    日本癌学会総会記事62回   302 - 302   2003.8

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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77 ( 8 ) S1086 - S1086   2003.8

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  • SYT蛋白とSSX蛋白のyeast two hybrid assayを用いた機能解析

    伊藤 達男, 大内田 守, 尾崎 敏文, 国定 俊之, 森本 裕樹, 大畑 範英, 中川 寧子, 吉田 晶, 伊藤 佐智夫, 清水 憲二

    日本癌学会総会記事62回   536 - 536   2003.8

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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

    高尾 聡一郎, 大同 茂, 田宮 隆, 寺田 欣矢, 市川 智継, 小野 泰裕, 伊藤 佐智夫, 大内田 守, 伊達 勲, 清水 憲二

    日本癌学会総会記事62回   479 - 479   2003.8

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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77 ( 6 ) S823 - S823   2003.6

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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

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

    日本癌学会総会記事61回   395 - 395   2002.10

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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 Pathology19 ( Suppl. ) 96 - 96   2002.5

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  • BTB/POZdomainとZinc-Fingerをもつ新規ヒト遺伝子,OSZFの解析

    伊藤 佐智夫, 内藤 訓子, 大内田 守, 清水 憲二

    日本癌学会総会記事60回   307 - 307   2001.9

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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60回   345 - 345   2001.9

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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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  • WDC-146(新規WD-40リピートタンパク)mRNAのラット精巣における発現

    野村 貴子, 伊藤 佐智夫, 境 明子, 三木 友香理, 森 英樹, 佐々木 順造

    解剖学雑誌75 ( 1 ) 63 - 63   2000.2

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Presentations

  • Integrated analysis of oncogene candidate MYNN and p53 in lung cancer

    ITO Sachio

    The 41th Annual Meeting of the Molecular Biology Society of Japan  2018.11 

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  • Unique Circulating MicroRNAs in Relation to EGFR Mutation Status in Japanese Smoker Make with Lung Adenocarcinoma

    ITO Sachio

    The 40th Annual Meeting of the Molecular Biology Society of Japan  2017.12 

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  • 肺癌に関わるmiR-19aの標的遺伝子解析

    第75回日本癌学会学術総会  2016 

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

    The 75th Annual Meeting of the Japanese Cancer Association  2016 

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  • 肺癌におけるmiR19a新規標的遺伝子の機能解析

    第38回日本分子生物学会年会  2015 

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  • Functional analysis of miR-19a novel target genes in lung cancer

    The 38th Annual Meeting of the Molecular Biology Society of Japan  2015 

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  • 肺癌細胞株におけるmiR19a標的遺伝子の機能解析

    第37回日本分子生物学会年会  2014 

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  • Functional analysis of miR-19a target genes in lung cancer cells.

    The 37th Annual Meeting of the Molecular Biology Society of Japan  2014 

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  • Novel Direct Targets of miR-19a Identified in Breast Cancer Cells by a Quantitative Proteomic Approach

    The 35th Annual Meeting of the Molecular Biology Society of Japan  2012 

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  • in vitro pull-down法によるmiR-19a標的遺伝子の同定

    第71回日本癌学会学術総会  2012 

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  • 乳癌におけるmiR17-92 cluster の新規標的タンパク質の検討

    第35回日本分子生物学会年会  2012 

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  • Identification of Direct Targets of MicroRNA-29a in Esophageal Cancer Cells

    第35回日本分子生物学会年会  2012 

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  • miR-19a標的遺伝子の探索と同定

    第35回日本分子生物学会年会  2012 

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  • Search and Identification of Target genes for miR-19a

    The 35th Annual Meeting of the Molecular Biology Society of Japan  2012 

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  • Identification of Target genes for miR-19a by in vitro pull-down method

    The 71th Annual Meeting of the Japanese Cancer Association  2012 

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  • Identification of direct targets of MicroRNA-29a in Esophageal squamous carcinoma

    第34回日本分子生物学会年会  2011 

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

    第34回日本分子生物学会年会  2011 

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  • Proteomic analysis of target genes of miR-17-92 cluster in lung cancer

    第34回日本分子生物学会年会  2011 

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  • Identification of direct targets of MicroRNA-29a in Esophageal squamous carcinoma

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

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  • Proteomic analysis of target proteins of miR17-92 cluster in cancer cells

    69th Annual Meeting of the Japanese Cancer Association  2010 

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  • microRNA7発現プラスミドによるEGFR依存性腫瘍におけるin vivoでの著明な抗腫瘍効果

    第69回日本癌学会学術総会  2010 

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  • Identification of true targets of microRNA-183 in lung cancer cells using labeled ds-miRNA in vitro pull-down assay

    第33回 日本分子生物学会年会  2010 

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

    第33回 日本分子生物学会年会  2010 

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  • 癌細胞におけるmiR-17-92 clusterの新規標的タンパク質のプロテオーム解析

    第69回日本癌学会学術総会  2010 

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  • 肺癌における標識microRNA183を用いた標的遺伝子の同定

    第69回日本癌学会学術総会  2010 

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  • Identification of true targets of MicroRNA183 using labeled miRNA in lung cancer cells

    69th Annual Meeting of the Japanese Cancer Association  2010 

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  • Dramatic anti-proliferative effect of designed miR-7 expressing plasmid against EGFR oncogene addicted tumors in vivo.

    69th Annual Meeting of the Japanese Cancer Association  2010 

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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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  • Lipofection of the designed plasmid expressing microRNA-7 has antitumor effect in gefitinib-resistant lung adenocarcinoma in vivo

    AACR 100th Annual Meeting 2009  2010 

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

    JHUPO 2009 (7th Japan Human Proteome Organization Conference2009)  2009 

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  • ゲフィチニブ感受性および耐性細胞株の上皮成長因子受容体に対するMicro-RNA7による抑制効果

    第68回日本癌学会学術総会  2009 

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  • プロテオミクス解析によるmiR17-92 clusterの新規標的遺伝子の同定

    第32回日本分子生物学会年会  2009 

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  • MicroRNA expression profiling in human tumors

    第32回日本分子生物学会年会  2009 

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

    The 8th HUPO World Congress C286.  2009 

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  • プロテオーム解析による肺癌におけるmiR17-92の直接的な新規標的タンパク質の同定

    第68回日本癌学会学術総会  2009 

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  • 乳癌におけるmiRNA clusterの新規標的タンパク質の検討

    第68回日本癌学会学術総会  2009 

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

    The 32th Annual Meeting of theMolecular Biology Society of Japan  2009 

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

    100th AACR Annual Meeting 2009. No. 2649.  2009 

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  • MicroRNA-7 downregulates epidermal growth factor receptor in both gefitinib-sensitive and -resistant lung adenocarcinoma cells

    AACR 100th Annual Meeting 2009  2009 

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  • miR-17-92 cluster の肺癌における新規標的タンパク質の同定を目的としたプロテオーム解析

    日本ヒトプロテオーム機構 第7回大会  2009 

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  • Proteomic analysis of miR17-92-overexpressing lung cancer cell line aimed to identihy novel immediate target protein

    68th Annual Meeting of the Japanese Cancer Association  2009 

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  • Identification of novel target proteins of miRNA cluster in breast cancer

    68th Annual Meeting of the Japanese Cancer Association  2009 

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  • MicroRNA-7 downregulates epidermal growth factor receptor in gefitinib resistant lung adenocarcinoma cells

    68th Annual Meeting of the Japanese Cancer Association  2009 

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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 合同大会  2008 

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  • MicroRNA expression profiling in human esophageal cancer

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

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  • OSZF, a novel human oncoprotein, recruits mSin3A corepressor to mediate transcriptional repression

    20th IUBMB International Congress of Biochemistry and Molecular Bioligy 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 Bioligy and 11th FAOBMB Congress  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の相互作用

    第28回日本分子生物学会年会  2005 

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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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  • 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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  • 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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  • Positive 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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  • 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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  • 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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  • 腎癌患者における14q24-31の染色体欠失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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  • 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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  • 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

    第26回日本分子生物学会年会  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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  • 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年9月25〜27日(名古屋国際会議場)  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年9月25〜27日(名古屋国際会議場)  2003 

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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

    American Association for Cancer Research 93td Annual Meeting  2002 

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  • 新規ヒト遺伝子OSZFはmSin3Aを介して転写抑制する。

    第25回日本分子生物学会年会  2002 

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  • 新規癌遺伝子hBRMの頭頸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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  • 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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  • Astrocytic tumorにおける10番染色体長腕の遺伝子異常と悪性度との関係

    第61回日本癌学会総会  2002 

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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

    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2回若手研究者ワークショップ  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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Research Projects

  • 新規RNAメタボリズム調節機構とその破綻による膠芽腫進行メカニズムの解明

    2017 - 2020

    基盤研究(C) 

    片山 博志

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    Grant type:Competitive

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  • 癌遺伝子候補MYNNとp53の統合的解析と肺癌発症メカニズムの解明

    2016 - 2019

    基盤研究(C) 

    伊藤 佐智夫

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    Authorship:Principal investigator  Grant type:Competitive

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  • 関節破壊を制御するマイクロRNAの統合的解析と軟骨における機能解析

    2014 - 2017

    基盤研究(B) 

    廣畑 聡

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    Grant type:Competitive

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  • 肺癌に関わるmiRNAクラスターの標的遺伝子群の同定と肺癌発症機構の解析

    2012 - 2016

    基盤研究(C) 

    大内田 守

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    Grant type:Competitive

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  • ビオチン標識miRNAを用いたプルダウン法による食道癌関連遺伝子の同定と機能解析

    2010 - 2012

    基盤研究(C) 

    伊藤 佐智夫

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    Authorship:Principal investigator  Grant type:Competitive

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  • 食道癌における発癌/抑制に関与するmicroRNAの同定とその機能解析

    2007 - 2008

    若手研究(B) 

    伊藤 佐智夫

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    Authorship:Principal investigator  Grant type:Competitive

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  • 胃癌における遺伝的発癌高リスクグループの遺伝的素因に関する研究

    2002 - 2003

    若手研究(B) 

    伊藤 佐智夫

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    Authorship:Principal investigator  Grant type:Competitive

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Class subject in charge

  • Research Projects and Practicals: Molecular Genetics I (2020academic year) special  - その他

  • Lecture and Research Projects: Molecular Genetics I (2020academic year) special  - その他

  • Lecture and Research Projects: Molecular Genetics II (2020academic year) special  - その他

  • Lecture and Research Projects: Molecular Genetics II (2020academic year) special  - その他

  • Practice in Biochemistry and Molecular Biology (2020academic year) special  - その他

  • New development of gene engineering (2020academic year) Third semester  - 木3,木4

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