Updated on 2024/10/02

写真a

 
SUZUKI Miho
 
Organization
Graduate School of Medicine Center for Neurological Diseases and Cance Division Assistant Professor
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Assistant Professor
External link

Degree 1

  1. 博士(理学) ( 2001.3   京都大学 ) 

Research Interests 4

  1. long non-coding RNA

  2. genome instability

  3. Transcriptional regulation

  4. DNA methylation

Research Areas 3

  1. Life Science / Molecular biology

  2. Life Science / Tumor biology

  3. Life Science / Tumor biology

Current Research Project and SDGs 1

  1. 核内RNAとエピジェネティクス制御

Research History 8

  1. Nagoya University   Graduate School of Medicine Center for Neural Disease and Cancer Division   Assistant Professor

    2018.12

  2. 名古屋大学医学系研究科   腫瘍生物学部門   助教

    2017.4

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  3. National Institute for Basic Biology

    2014.4 - 2017.3

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  4. National Institute for Basic Biology   Researcher

    2013.4 - 2014.3

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  5. National Institute for Basic Biology

    2012.4 - 2013.3

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  6. Institute for Developmental Research, Aichi Human Service Center

    2009.10 - 2012.3

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  7. Institute for Developmental Research, Aichi Human Service Center   Researcher

    2009.4 - 2009.9

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  8. University of Edinburgh   Wellcome Trust Centre   Postdoctral research fellow

    2004.7 - 2009.3

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Education 1

  1. Nagoya University

    1992.4 - 1996.3

Professional Memberships 3

  1. THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

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  2. 日本エピジェネティクス研究会

  3. 日本癌学会

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Awards 1

  1. 2021 JB審査員賞

    2021.11   日本生化学会  

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    Award type:Honored in official journal of a scientific society, scientific journal 

 

Papers 17

  1. TUG1-mediated R-loop resolution at microsatellite loci as a prerequisite for cancer cell proliferation. Reviewed

    Suzuki MM, Iijima K, Ogami K, Shinjo K, Murofushi Y, Xie J, Wang X, Kitano Y, Mamiya A, Kibe Y, Nishimura T, Ohka F, Saito R, Sato S, Kobayashi J, Yao R, Miyata K, Kataoka K, Suzuki HI, Kondo Y.

    Nature Communications   Vol. 14   page: 4521   2023.8

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: https://doi.org/10.1038/s41467-023-40243-8

  2. Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts. Reviewed

    Muraoka A, Suzuki M, Hamaguchi T, Watanabe S, Iijima K , Murofushi Y, Shinjo K, Osuka S, Hariyama Y, Ito M, Ohno K, Kiyono T, Kyo S, Iwase A, Kikkawa F, Kajiyama H, Kondo Y.

    Science Translational Medicine   Vol. 15   page: 1531   2023.6

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1126/scitranslmed.add1531

  3. Exclusive expression of KANK4 promotes myofibroblast mobility in keloid tissues

    Mayumi Oishi, Keiko Shinjo, Keisuke Takanari, Ayako Muraoka, Miho M. Suzuki, Miki Kanbe, Shinichi Higuchi, Katsumi Ebisawa, Kazunobu Hashikawa, Yuzuru Kamei, Yutaka Kondo

    Scientific Reports   Vol. 14 ( 1 )   2024.4

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    Keloids are characterized by abnormal wound healing with excessive accumulation of extracellular matrix. Myofibroblasts are the primary contributor to extracellular matrix secretion, playing an essential role in the wound healing process. However, the differences between myofibroblasts involved in keloid formation and normal wound healing remain unclear. To identify the specific characteristics of keloid myofibroblasts, we initially assessed the expression levels of well-established myofibroblast markers, α-smooth muscle actin (α-SMA) and transgelin (TAGLN), in scar and keloid tissues (n = 63 and 51, respectively). Although myofibroblasts were present in significant quantities in keloids and immature scars, they were absent in mature scars. Next, we conducted RNA sequencing using myofibroblast-rich areas from keloids and immature scars to investigate the difference in RNA expression profiles among myofibroblasts. Among significantly upregulated 112 genes, KN motif and ankyrin repeat domains 4 (KANK4) was identified as a specifically upregulated gene in keloids. Immunohistochemical analysis showed that KANK4 protein was expressed in myofibroblasts in keloid tissues; however, it was not expressed in any myofibroblasts in immature scar tissues. Overexpression of KANK4 enhanced cell mobility in keloid myofibroblasts. Our results suggest that the KANK4-mediated increase in myofibroblast mobility contributes to keloid pathogenesis.

    DOI: 10.1038/s41598-024-59293-z

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    Other Link: https://www.nature.com/articles/s41598-024-59293-z

  4. Long noncoding RNA TUG1 promotes cisplatin resistance in ovarian cancer via upregulation of DNA polymerase eta Reviewed

    Ryosuke Sonobe, Peng Yang, Miho M. Suzuki, Keiko Shinjo, Kenta Iijima, Nobuhiro Nishiyama, Kanjiro Miyata, Kazunori Kataoka, Hiroaki Kajiyama, Yutaka Kondo

    Cancer Science     2024.4

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    Publishing type:Research paper (scientific journal)   Publisher:Wiley  

    Abstract

    Chemoresistance is a major cause of high mortality and poor survival in patients with ovarian cancer (OVCA). Understanding the mechanisms of chemoresistance is urgently required to develop effective therapeutic approaches to OVCA. Here, we show that expression of the long noncoding RNA, taurine upregulated gene 1 (TUG1), is markedly upregulated in samples from OVCA patients who developed resistance to primary platinum‐based therapy. Depletion of TUG1 increased sensitivity to cisplatin in the OVCA cell lines, SKOV3 and KURAMOCHI. Combination therapy of cisplatin with antisense oligonucleotides targeting TUG1 coupled with a drug delivery system effectively relieved the tumor burden in xenograft mouse models. Mechanistically, TUG1 acts as a competing endogenous RNA by downregulating miR‐4687‐3p and miR‐6088, both of which target DNA polymerase eta (POLH), an enzyme required for translesion DNA synthesis. Overexpression of POLH reversed the effect of TUG1 depletion on cisplatin‐induced cytotoxicity. Our data suggest that TUG1 upregulation allows OVCA to tolerate DNA damage via upregulation of POLH; this provides a strong rationale for targeting TUG1 to overcome cisplatin resistance in OVCA.

    DOI: 10.1111/cas.16150

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  5. Long non-coding RNA lnc-CHAF1B-3 promotes renal interstitial fibrosis by regulating EMT-related genes in renal proximal tubular cells. Reviewed International journal

    Imai K, Ishimoto T, Doke T, Tsuboi T, Watanabe Y, Katsushima K, Suzuki M, Oishi H, Furuhashi K, Ito Y, Kondo Y, Maruyama S

    Mol Ther Nucleic Acids.   Vol. 31   page: 139 - 150   2022.12

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.omtn.2022.12.011

  6. Cancer-Specific Targeting of Taurine-Upregulated Gene 1 Enhances the Effects of Chemotherapy in Pancreatic Cancer Reviewed International journal

    Yoshihiko Tasaki, Miho Suzuki, Keisuke Katsushima, Keiko Shinjo, Kenta Iijima, Yoshiteru Murofushi, Aya Naiki-Ito, Kazuki Hayashi, Chenjie Qiu, Akiko Takahashi, Yoko Tanaka, Tokuichi Kawaguchi, Minoru Sugawara, Tomoya Kataoka, Mitsuru Naito, Kanjiro Miyata, Kazunori Kataoka, Tetsuo Noda, Wentao Gao, Hiromi Kataoka, Satoru Takahashi, Kazunori Kimura, Yutaka Kondo

    Cancer Research   Vol. 81 ( 7 ) page: 1654 - 1666   2021.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:American Association for Cancer Research (AACR)  

    Overcoming drug resistance is one of the biggest challenges in cancer chemotherapy. In this study, we examine whether targeting the long noncoding RNA taurine upregulated gene 1 (TUG1) could be an effective therapeutic approach to overcome drug resistance in pancreatic ductal adenocarcinoma (PDAC). TUG1 was expressed at significantly higher levels across 197 PDAC tissues compared with normal pancreatic tissues. Overall survival of patients with PDAC who had undergone 5-FU-based chemotherapy was shorter in high TUG1 group than in low TUG1 group. Mechanistically, TUG1 antagonized miR-376b-3p and upregulated dihydropyrimidine dehydrogenase (DPD). TUG1 depletion induced susceptibility to 5-FU in BxPC-3 and PK-9 pancreatic cell lines. Consistently, the cellular concentration of 5-FU was significantly higher under TUG1-depleted conditions. In PDAC xenograft models, intravenous treatment with a cancer-specific drug delivery system (TUG1-DDS) and 5-FU significantly suppressed PDAC tumor growth compared with 5-FU treatment alone. This novel approach using TUG1-DDS in combination with 5-FU may serve as an effective therapeutic option to attenuate DPD activity and meet appropriate 5-FU dosage requirements in targeted PDAC cells, which can reduce the systemic adverse effects of chemotherapy. SIGNIFICANCE: Targeting TUG1 coupled with a cancer-specific drug delivery system effectively modulates 5-FU catabolism in TUG1-overexpressing PDAC cells, thus contributing to a new combinatorial strategy for cancer treatment. GRAPHICAL ABSTRACT: http://cancerres.aacrjournals.org/content/canres/81/7/1654/F1.large.jpg.

    DOI: 10.1158/0008-5472.can-20-3021

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  7. Structural dynamics of DNA depending on methylation pattern Invited Reviewed

    Takeru Kameda, Miho M. Suzuki, Akinori Awazu, Yuichi Togashi

    Physical Review E   Vol. 103 ( 1 ) page: 012404   2021.1

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    Publishing type:Research paper (scientific journal)   Publisher:American Physical Society (APS)  

    DOI: 10.1103/physreve.103.012404

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    Other Link: http://harvest.aps.org/v2/journals/articles/10.1103/PhysRevE.103.012404/fulltext

  8. Establishment and characterization of cell lines from human endometrial epithelial and mesenchymal cells from patients with endometriosis Reviewed International journal

    Ayako Muraoka, Satoko Osuka, Tohru Kiyono, Miho Suzuki, Akira Yokoi, Tomohiko Murase, Kimihiro Nishino, Kaoru Niimi, Tomoko Nakamura, Maki Goto, Hiroaki Kajiyama, Yutaka Kondo, Fumitaka Kikkawa

    F&S Science   Vol. 1 ( 2 ) page: 195 - 205   2020.11

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    OBJECTIVE: To establish and characterize cell lines derived from human endometrial epithelial cells (ECs) and mesenchymal cells (MCs) from patients with and without endometriosis. DESIGN: In vitro experimental study. SETTING: University and national cancer center research institute. PATIENT(S): Two women with endometriosis and two women without endometriosis. INTERVENTION(S): Sampling of endometrial ECs and MCs. MAIN OUTCOME MEASURE(S): Establishing immortalized endometrial ECs and MCs with quantitative reverse transcription-polymerase chain reaction (qRT-PCR), immunocytochemical analysis, and RNA sequence profiling performed to characterize the immortalized cells and a cell proliferation assay, three-dimensional culture, and assays for hormone responses performed to characterize the features of ECs. RESULT(S): The qRT-PCR, immunocytochemical analysis, and Western blot analysis revealed that the ECs and MCs maintained their original features. Moreover, the immortalized cells were found to retain responsiveness to sex steroid hormones. The ECs formed a gland-like structure in three-dimensional culture, indicating the maintenance of normal EC phenotypes. The RNA sequence profiling, principal component analysis, and clustering analysis showed that the gene expression patterns of the immortalized cells were different from those of cancer cells. Several signaling pathways that were statistically significantly enriched in ECs and MCs with endometriosis were revealed. CONCLUSION(S): We successfully obtained four paired immortalized endometrial ECs and MCs from patients with and without endometriosis. Using these cells could help identify diagnostic and therapeutic targets for endometriosis. The cell lines established in this study will thus serve as powerful experimental tools in the study of endometriosis.

    DOI: 10.1016/j.xfss.2020.09.001

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  9. Autocrine HGF/c-Met signaling pathway confers aggressiveness in lymph node adult T-cell leukemia/lymphoma Reviewed International journal

    Haruhito Totani, Keiko Shinjo, Miho Suzuki, Keisuke Katsushima, Shoko Mase, Ayako Masaki, Asahi Ito, Masaki Ri, Shigeru Kusumoto, Hirokazu Komatsu, Takashi Ishida, Hiroshi Inagaki, Shinsuke Iida, Yutaka Kondo

    Oncogene   Vol. 39 ( 35 ) page: 5782 - 5794   2020.8

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    Adult T-cell leukemia/lymphoma (ATL) is an aggressive T-cell neoplasm. While ATL cells in peripheral blood (PB-ATL) are sensitive to anti-CC chemokine receptor 4 treatment, non-PB-ATLs, including lymph node ATLs (LN-ATLs), are more aggressive and resistant. We examined characteristic cytokines and growth factors that allow non-PB-ATLs to proliferate and invade compared with PB-ATLs. Protein array analysis revealed hepatocyte growth factor (HGF) and C-C motif chemokine 2 (CCL2) were significantly upregulated in non-PB-ATLs compared with PB-ATLs. The HGF membrane receptor, c-Met, was expressed in PB-ATL and non-PB-ATL cell lines, but CCR2, a CCL2 receptor, was not. Immunohistochemical analysis in clinical ATLs revealed high HGF expression in LNs, pharynx, bone marrow, and tonsils. The HGF/c-Met signaling pathway was active downstream in non-PB-ATLs. Downregulation of HGF/c-Met by siRNA or chemical inhibitors decreased in vitro and in vivo proliferation and invasion by non-PB-ATLs. Treatment with bromodomain and extra-terminal motif inhibitor suppressed HGF expression and decreased levels of histone H3 lysine 27 acetylation (H3K27Ac) and bromodomain-containing protein 4 (BRD4) binding promoter and enhancer regions, suppressing non-PB-ATL cellular growth. Our data indicate H3K27Ac/BRD4 epigenetics regulates the HGF/c-MET pathway in ATLs; targeting this pathway may improve treatment of aggressive non-PB-ATLs.

    DOI: 10.1038/s41388-020-01393-x

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    Other Link: https://www.nature.com/articles/s41388-020-01393-x

  10. A novel sensitive detection method for DNA methylation in circulating free DNA of pancreatic cancer. Reviewed International journal

    Keiko Shinjo, Kazuo Hara, Genta Nagae, Takayoshi Umeda, Keisuke Katsushima, Miho Suzuki, Yoshiteru Murofushi, Yuta Umezu, Ichiro Takeuchi, Satoru Takahashi, Yusuke Okuno, Keitaro Matsuo, Hidemi Ito, Shoji Tajima, Hiroyuki Aburatani, Kenji Yamao, Yutaka Kondo

    PloS one   Vol. 15 ( 6 ) page: e0233782 - e0233782   2020

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Public Library of Science (PLoS)  

    Despite recent advances in clinical treatment, pancreatic cancer remains a highly lethal malignancy. In order to improve the survival rate of patients with pancreatic cancer, the development of non-invasive diagnostic methods using effective biomarkers is urgently needed. Here, we developed a highly sensitive method to detect DNA methylation in cell-free (cf)DNA samples based on the enrichment of methyl-CpG binding (MBD) protein coupled with a digital PCR method (MBD-ddPCR). Five DNA methylation markers for the diagnosis of pancreatic cancer were identified through DNA methylation microarray analysis in 37 pancreatic cancers. The sensitivity and specificity of the five markers were validated in another independent cohort of pancreatic cancers (100% and 100%, respectively; n = 46) as well as in The Cancer Genome Atlas data set (96% and 90%, respectively; n = 137). MBD-ddPCR analysis revealed that DNA methylation in at least one of the five markers was detected in 23 (49%) samples of cfDNA from 47 patients with pancreatic cancer. Further, a combination of DNA methylation markers and the KRAS mutation status improved the diagnostic capability of this method (sensitivity and specificity, 68% and 86%, respectively). Genome-wide MBD-sequencing analysis in cancer tissues and corresponding cfDNA revealed that more than 80% of methylated regions were overlapping; DNA methylation profiles of cancerous tissues and cfDNA significantly correlated with each other (R = 0.97). Our data indicate that newly developed MBD-ddPCR is a sensitive method to detect cfDNA methylation and that using five marker genes plus KRAS mutations may be useful for the detection of pancreatic cancers.

    DOI: 10.1371/journal.pone.0233782

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  11. Pathogenic Epigenetic Consequences of Genetic Alterations in IDH-Wild-Type Diffuse Astrocytic Gliomas. Reviewed International journal

    Fumiharu Ohka, Keiko Shinjo, Shoichi Deguchi, Yusuke Matsui, Yusuke Okuno, Keisuke Katsushima, Miho Suzuki, Akira Kato, Noboru Ogiso, Akane Yamamichi, Kosuke Aoki, Hiromichi Suzuki, Shinya Sato, Nirmala Arul Rayan, Shyam Prabhakar, Jonathan Göke, Teppei Shimamura, Reo Maruyama, Satoru Takahashi, Akio Suzumura, Hiroshi Kimura, Toshihiko Wakabayashi, Hui Zong, Atsushi Natsume, Yutaka Kondo

    Cancer research   Vol. 79 ( 19 ) page: 4814 - 4827   2019.10

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    Gliomas are classified by combining histopathologic and molecular features, including isocitrate dehydrogenase (IDH) status. Although IDH-wild-type diffuse astrocytic glioma (DAG) shows a more aggressive phenotype than IDH-mutant type, lack of knowledge regarding relevant molecular drivers for this type of tumor has hindered the development of therapeutic agents. Here, we examined human IDH-wild-type DAGs and a glioma mouse model with a mosaic analysis with double markers (MADM) system, which concurrently lacks p53 and NF1 and spontaneously develops tumors highly comparable with human IDH-wild-type DAG without characteristic molecular features of glioblastoma (DAG-nonMF). During tumor formation, enhancer of zeste homolog (EZH2) and the other polycomb repressive complex 2 (PRC2) components were upregulated even at an early stage of tumorigenesis, together with an increased number of genes with H3K27me3 or H3K27me3 and H3K4me3 bivalent modifications. Among the epigenetically dysregulated genes, frizzled-8 (Fzd8), which is known to be a cancer- and stem cell reprogramming-related gene, was gradually silenced during tumorigenesis. Genetic and pharmacologic inhibition of EZH2 in MADM mice showed reactivation of aberrant H3K27me3 target genes, including Fzd8, together with significant reduction of tumor size. Our study clarifies a pathogenic molecular pathway of IDH-wild-type DAG-nonMF that depends on EZH2 activity and provides a strong rationale for targeting EZH2 as a promising therapeutic approach for this type of glioma. SIGNIFICANCE: EZH2 is involved in the generation of IDH-wild-type diffuse astrocytic gliomas and is a potential therapeutic target for this type of glioma. GRAPHICAL ABSTRACT: http://cancerres.aacrjournals.org/content/canres/79/19/4814/F1.large.jpg.

    DOI: 10.1158/0008-5472.CAN-19-1272

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  12. The Ciona intestinalis cleavage clock is independent of DNA methylation Reviewed

    Miho M. Suzuki, Tomoko Mori, Noriyuki Satoh

    GENOMICS   Vol. 108 ( 3-4 ) page: 168 - 176   2016.10

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

    The initiation of embryonic gene expression in ascidian embryos appears to be tightly regulated by the number of DNA replication cycles. DNA methylation is thought to contribute to the clock mechanism that counts the rounds of DNA replication. We used mass spectrometry and whole genome bisulfite sequencing to characterize DNA methylation changes that occur in early developmental stages of the ascidian, Ciona intestinalis. We found that global DNA methylation in early Ciona development was static, and a base-wise comparison between the genomes of consecutive developmental stages found no DNA demethylation that was related to zygotic gene activation. Additionally, 5hmC was hardly detected by mass spectrometry in the developmental samples, suggesting a lack of demethylation mediated by ten eleven translocation (TET) methylcytosine dioxygenase in C. intestinalis. We conclude that DNA methylation is not involved in regulating DNA replication-dependent transcriptional activation. (C) 2016 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.ygeno.2016.10.001

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  13. Identical sets of methylated and nonmethylated genes in Ciona intestinalis sperm and muscle cells Reviewed

    Miho M. Suzuki, Akiko Yoshinari, Madoka Obara, Shohei Takuno, Shuji Shigenobu, Yasunori Sasakura, Alastair R.W. Kerr, Shaun Webb, Adrian Bird, Atsuo Nakayama

    Epigenetics and Chromatin   Vol. 6 ( 1 ) page: 38   2013

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    Background: The discovery of gene body methylation, which refers to DNA methylation within gene coding region, suggests an as yet unknown role of DNA methylation at actively transcribed genes. In invertebrates, gene bodies are the primary targets of DNA methylation, and only a subset of expressed genes is modified. Results: Here we investigate the tissue variability of both the global levels and distribution of 5-methylcytosine (5mC) in the sea squirt Ciona intestinalis. We find that global 5mC content of early developmental embryos is high, but is strikingly reduced in body wall tissues. We chose sperm and adult muscle cells, with high and reduced levels of global 5mC respectively, for genome-wide analysis of 5mC targets. By means of CXXC-affinity purification followed by deep sequencing (CAP-seq), and genome-wide bisulfite sequencing (BS-seq), we designated body-methylated and unmethylated genes in each tissue. Surprisingly, body-methylated and unmethylated gene groups are identical in the sperm and muscle cells. Our analysis of microarray expression data shows that gene body methylation is associated with broad expression throughout development. Moreover, transgenic analysis reveals contrasting gene body methylation at an identical gene-promoter combination when integrated at different genomic sites. Conclusions: We conclude that gene body methylation is not a direct regulator of tissue specific gene expression in C. intestinalis. Our findings reveal constant targeting of gene body methylation irrespective of cell type, and they emphasize a correlation between gene body methylation and ubiquitously expressed genes. Our transgenic experiments suggest that the promoter does not determine the methylation status of the associated gene body. © 2013Suzuki et al.
    licensee BioMed Central Ltd.

    DOI: 10.1186/1756-8935-6-38

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  14. Maternal factor-mediated epigenetic gene silencing in the ascidian Ciona intestinalis Reviewed

    Yasunori Sasakura, Miho M. Suzuki, Akiko Hozumi, Kazuo Inaba, Nori Satoh

    MOLECULAR GENETICS AND GENOMICS   Vol. 283 ( 1 ) page: 99 - 110   2010.1

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    Epigenetic regulation of genes plays a critical role in achieving proper gene expression during development, and it has been reported that epigenetic modifications are associated with transposon silencing in many organisms. Here, we report a type of epigenetic gene silencing, maternal gfp/gene silencing (MGS), in the basal chordate Ciona intestinalis. A transgenic line of Ciona, Tg[MiT-Fr3dTPOG] 45 (abbreviated as Tg45), which was created with the Minos transposon, has a tandemly arrayed insertion of gfp in the promoter region of Ci-CesA. Progeny of Tg45 showed a reduced level of GFP expression when eggs of Tg45 were fertilized with sperm of other gfp transgenic lines. Although the genotype is the same, animals developed from Tg45 sperm and the eggs of other transgenic lines did not exhibit this phenomenon, suggesting the involvement of a maternal cytoplasmic factor that influences GFP expression. The silencing starts during oogenesis and continues after fertilization without any tissue specificity. We found that post-transcriptional degradation of the gfp mRNA is involved in MGS.

    DOI: 10.1007/s00438-009-0500-4

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  15. DNA methylation landscapes: provocative insights from epigenomics Reviewed

    Miho M. Suzuki, Adrian Bird

    NATURE REVIEWS GENETICS   Vol. 9 ( 6 ) page: 465 - 476   2008.6

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    The genomes of many animals, plants and fungi are tagged by methylation of DNA cytosine. To understand the biological significance of this epigenetic mark it is essential to know where in the genome it is located. New techniques are making it easier to map DNA methylation patterns on a large scale and the results have already provided surprises. In particular, the conventional view that DNA methylation functions predominantly to irreversibly silence transcription is being challenged. Not only is promoter methylation often highly dynamic during development, but many organisms also seem to target DNA methylation specifically to the bodies of active genes.

    DOI: 10.1038/nrg2341

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  16. CpG methylation is targeted to transcription units in an invertebrate genome Reviewed

    Miho M. Suzuki, Alastair R. W. Kerr, Dina De Sousa, Adrian Bird

    GENOME RESEARCH   Vol. 17 ( 5 ) page: 625 - 631   2007.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT  

    DNA is methylated at the dinucleotide CpG in genomes of a wide range of plants and animals. Among animals, variable patterns of genomic CpG methylation have been described, ranging from undetectable levels (e.g., in Caenorhabditis elegans) to high levels of global methylation in the vertebrates. The most frequent pattern in invertebrate animals, however, is mosaic methylation, comprising domains of methylated DNA interspersed with unmethylated domains. To understand the origin of mosaic DNA methylation patterns, we examined the distribution of DNA methylation in the Ciona intestinalis genome. Bisulfite sequencing and computational analysis revealed methylated domains with sharp boundaries that strongly colocalize with similar to 60% of transcription units. By contrast, promoters, intergenic DNA, and transposons are not preferentially targeted by DNA methylation. Methylated transcription units include evolutionarily conserved genes, whereas the most highly expressed genes preferentially belong to the unmethylated fraction. The results lend support to the hypothesis that CpG methylation functions to suppress spurious transcriptional initiation within infrequently transcribed genes.

    DOI: 10.1101/gr.6163007

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  17. Transposable element in fish

    Koga A, Suzuki M, Inagaki H, Bessho Y, Hori H

    NATURE   Vol. 383 ( 6595 ) page: 30 - 30   1996.9

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Books 2

  1. 動物の事典

    末光 隆志( Role: Joint author ,  第3章 動物遺伝子の発現)

    朝倉書店  2020.11  ( ISBN:4254171668

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    Language:Japanese Book type:Dictionary, encyclopedia

  2. 遺伝子発現制御機構―クロマチン,転写制御,エピジェネティクス―

    鈴木美穂, 有吉眞理子( Role: Contributor ,  第六章 DNAのメチル化)

    東京化学同人  2017.3 

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MISC 4

  1. ヒストンメチル化制御阻害剤

    鈴木美穂 近藤豊

    遺伝子医学MOOK 36号「エピゲノムで新たな解明 が進む『先天性疾患』」     2021.4

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  2. Operating principle of EZH2 inhibitor and current development situation

      Vol. 266 ( 11 ) page: 834 - 839   2018.9

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    Language:Japanese  

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  3. 長鎖非コード RNA をターゲットにした膠芽腫の治療.

    鈴木美穂, 勝島啓佑, 近藤豊

    Medical Science Digest   Vol. 44   page: 238 - 40   2018.5

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  4. DNA methylation in bodies of transcribed genes and pre-mRNA processing

    Miho M. Suzuki

    GENES & GENETIC SYSTEMS   Vol. 88 ( 6 ) page: 337 - 337   2013.12

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    Language:English   Publishing type:Research paper, summary (international conference)   Publisher:GENETICS SOC JAPAN  

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Presentations 21

  1. The role of lncRNA TUG1 and RNA helicases in regulation of DNA replication stress Invited

    Miho Suzuki, Keiko Shinjo, Tatsunori Nishimura, Yutaka Kondo

    第83回日本癌学会学術総会  2024.9.19 

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    Event date: 2024.9

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  2. 高次脳構造形成における長鎖非翻訳RNAの役割 Invited

    鈴木 美穂, 渡辺新也, 新城 恵子, 西村建徳, 近藤 豊

    第17回日本エピジェネティクス研究会  2024.6.14 

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    Event date: 2024.6

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  3. ノックアウトマウスで解明する、高次脳構造進化における長鎖非翻訳RNAの役割 Invited

    鈴木美穂, 渡辺新也, 近藤豊

    第154回関西実験動物研究会  2024.3.1 

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    Event date: 2024.3

    Presentation type:Oral presentation (invited, special)  

  4. がん細胞のDNA安定性を維持する長鎖非翻訳RNAと、それを標的とした核酸医薬の開発 Invited

    鈴木美穂

    第97回日本薬理学会年会  2023.12.14 

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    Event date: 2023.12

    Presentation type:Symposium, workshop panel (nominated)  

  5. Long noncoding RNA TUG1 resolves R-loop and maintains genome stability in cancer cells Invited

    2023.12.6 

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    Event date: 2023.12

    Presentation type:Symposium, workshop panel (nominated)  

  6. 複製ストレスを解消する長鎖非翻訳RNA Invited

    鈴木美穂

    患者由来がんモデル学会学術集会2023  2023.10.25 

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    Event date: 2023.10

    Presentation type:Symposium, workshop panel (nominated)  

  7. Regulation of genome instability by long non-coding RNA Invited

    2023.9.22 

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    Event date: 2023.9

    Presentation type:Symposium, workshop panel (nominated)  

  8. Function of long non-coding RNAs in R-loop resolution

    2023.6.19 

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    Event date: 2023.6

    Presentation type:Poster presentation  

  9. Maintenance of genome stability in cancer cells by long noncoding RNA Invited

    鈴木美穂, 飯島健太, 新城恵子, 近藤豊

    第81回日本癌学会学術総会  2022.10.29 

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    Event date: 2022.10 - 2022.11

    Presentation type:Oral presentation (invited, special)  

  10. R-loop調節における長鎖非翻訳RNATUG1の機能

    鈴木美穂, 飯島健太, 新城恵子, 近藤豊

    第15回日本エピジェネティクス研究会年会  2022.6.9 

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    Event date: 2022.6

    Presentation type:Poster presentation  

  11. 長鎖非翻訳RNAによるがん細胞特異的Rループ解消機構 Invited

    鈴木美穂

    先端モデル動物支援プラットフォーム成果発表会  2022.2.3 

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    Event date: 2022.2

    Presentation type:Oral presentation (invited, special)  

  12. Long noncoding RNA TUG1 regulates R-loop resolution and maintains cancer cell proliferation

    2021.12.3 

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    Event date: 2021.12

    Presentation type:Poster presentation  

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  13. Long noncoding RNA TUG1 regulates R-loop resolution and maintains cancer cell proliferation

    2021.9.30 

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    Event date: 2021.9 - 2021.10

    Presentation type:Oral presentation (general)  

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  14. 長鎖非翻訳RNA TUG1は核スペックル近傍で複製フォークを保護する Invited

    鈴木美穂

    第14回日本エピジェネティクス研究会年会  2021.3.31 

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    Event date: 2021.3

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:オンライン  

  15. Spatiotemporal regulation of long non-coding RNA to propagate Cancer Cells Invited

    2021.3.30 

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    Event date: 2021.3

    Presentation type:Symposium, workshop panel (nominated)  

  16. Spatiotemporal Regulation of Long non-coding RNA to propagate Cancer Cells Invited

    鈴木美穂, 近藤豊

    第126回日本解剖学会総会・全国学術集会  2021.3.30 

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    Event date: 2021.3

    Presentation type:Symposium, workshop panel (nominated)  

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  17. Spatiotemporal regulation of replication stress by TUG1 as a prerequisite for cancer cell proliferation Invited

    Miho Suzuki

    2020.12.3 

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    Event date: 2020.12

    Language:English   Presentation type:Symposium, workshop panel (nominated)  

  18. Spatiotemporal regulation of replication stress by TUG1 as a prerequisite for ca ncer cell proliferation Invited

    2020.12.3 

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    Event date: 2020.12

    Presentation type:Symposium, workshop panel (nominated)  

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  19. 長鎖非翻訳RNA TUG1による時空間的DNA複製ストレス制御 Invited

    鈴木美穂

    日本環境変異原学会第49回大会  2020.11.26 

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    Event date: 2020.11

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:沼津  

  20. The biological function of invertebrate DNA methylation in pre-mRNA processing Invited

    Suzuki MM

    第38回日本分子生物学会年会  2015.12.1 

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    Event date: 2015.12

    Language:English   Presentation type:Symposium, workshop panel (nominated)  

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  21. Genetic polymorphisms and DNA methylation patterns in the genome of Ciona intestinalis. International conference

    Suzuki MM

    Gordon Research Conference  2014 

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    Event date: 2014.5

    Language:English   Presentation type:Poster presentation  

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Research Project for Joint Research, Competitive Funding, etc. 1

  1. DDS技術を基盤とした革新的がん治療法の開発

    Grant number:21cm0106202h0006  2016.4 - 2022.3

    次世代がん医療創生研究事業 

    鈴木美穂

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    Authorship:Coinvestigator(s)  Grant type:Competitive

KAKENHI (Grants-in-Aid for Scientific Research) 9

  1. ミスマッチリペア機構欠損に依存しないマイクロサテライト不安定性誘導系の研究

    Grant number:23K06634  2023.4 - 2026.3

    科学研究費助成事業 基盤研究(C)   基盤研究(C)

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    Authorship:Principal investigator 

  2. がん細胞の複製ストレスを解消する新規lncRNAの機能解明

    Grant number:20K07570  2020.4 - 2023.3

    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)

    鈴木 美穂

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

    がん細胞に特徴的な高い複製ストレスは、ゲノム不安定性をもたらし、発がんの促進やがんの進展を加速させることがよく知られている。しかし、がん細胞が高い複製ストレスに晒されながらも、複製を完了させ細胞増殖していく機構は完全に解明されていない。本研究では、①がん細胞の複製ストレスの解消に関わる新規lncRNAの同定 ②lncRNAと相互作用するタンパク質の同定から、未知のがん細胞複製ストレス解消メカニズムを明らかにする。

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  3. the mechanism that eliminates transcription noise and maintains cell uniformity

    Grant number:17K07247  2017.4 - 2020.3

    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)

    Suzuki Miho

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    Authorship:Principal investigator 

    Grant amount:\4940000 ( Direct Cost: \3800000 、 Indirect Cost:\1140000 )

    To elucidate the mechanism that regulates the uniformity and variation of gene expression levels among individual cells, we focused on RNA molecules retained in the nucleus and analyzed them. We found that RNAs that require more time for pre-mRNA splicing are more likely to stay in the nucleus. In addition, we found that lncRNAs stocked in the nucleus, specifically in cancer cells, are involved in the regulation of DNA replication. This study shows that nuclear RNAs play an important role in the maintenance of cellular homeostasis.

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  4. DDS技術を基盤とした革新的がん治療法の開発

    2016 - 2021

    日本医療研究開発機構  次世代がん医療創生研究事業(P-CREATE) 

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    Authorship:Coinvestigator(s) 

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  5. 遺伝子転写領域のクロマチン構造とエピジェネティック制御の解明

    Grant number:14J40145  2014.4 - 2017.3

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    鈴木 美穂

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4940000 ( Direct Cost: \3800000 、 Indirect Cost:\1140000 )

    平成27年度に、カタユウレイボヤのDNAメチル化修飾をゲノムワイドに調べた。3つの発生ステージを比較した。平成28年度は、このデータに関して種々の解析を行い、論文として発表した(Genomics 2016)。主な結果は、カタユウレイボヤのDNAメチル化修飾は発生過程を通じて常に安定であること、遺伝子の発現変化とは無関係であること、また脱メチル化に関与する5hmシトシン修飾は検出されなかったこと、である。
    また、このデータから新たな発見が得られた。カタユウレイボヤ集団内にはDNAメチル化多型が存在する。DNAメチル化多型は、全ゲノム中約20アレルに見出された。これらのアレルのDNAメチル化状態は各個体によって異なる。また、DNAメチル化多型は環境ではなく、遺伝的に決定されていることが示唆された。今後は、DNAメチル化状態を決定する遺伝情報、ゲノム配列を同定する。

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  6. Phylogenetic analysis and rapid identification of spider mites based on RNA-sequencing data

    Grant number:25292033  2013.4 - 2017.3

    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)

    Gotoh Tetsuo

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Molecular information of spider mites is increasingly used to answer taxonomic and systematic questions. The COI gene and ITS2 region of nuclear ribosomal RNA have been used for phylogenetic reconstruction within the Tetranychidae, but these sequences have not consistently resolved genus-level phylogenetic relationships, because of low bootstrap values. So, we performed phylogenomics analysis for spider mites, derived from comparative RNA-Seq data for 88 strains of 87 species belonging to 15 genera. A phylogenetic tree using 652 orthologous protein-coding genes shared among taxa, was well-resolved and strongly supported for almost all nodes (67/70), allowing us to consider the phylogenetic relationships among genera of Tetranychidae. The topology presented here does not fully agree with the current taxonomic treatment, because the four genera were polyphyletic. These results indicate that the diagnostic morphological characters of the genera of Tetranychidae must be reconsidered.

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  7. Gene bodyメチル化の生物学的意義と分子機構の解明

    2009.10 - 2013.3

    JST  戦略的創造研究推進事業(さきがけ) 

    鈴木 美穂

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    Authorship:Principal investigator  Grant type:Competitive

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  8. Methylated DNA binding protein MBD2/3 and its interacting proteins in Ciona intestinalis

    Grant number:21810039  2009 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity start-up  Grant-in-Aid for Research Activity start-up

    SUZUKI Miho

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    Authorship:Principal investigator 

    Grant amount:\2756000 ( Direct Cost: \2120000 、 Indirect Cost:\636000 )

    MBD2/3is highly expressed in early developmental stages of Ciona intestinalis. A knock down experiment depleting MBD2/3 protein in embryos caused severe developmental defects. The result indicated an important role of DNA methylation and methylated DNA binding protein in regulation of gene expression. Genome-wide distribution of MBD2/3 was limited to methylated gene body region. MBD2/3 possibly regulates expression of those more than 100gene targets.

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  9. メダカ・トランスポゾンTo12による脊椎動物遺伝子改変系の構築

    Grant number:98J03521  1998 - 2000

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    鈴木 美穂

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Teaching Experience (On-campus) 12

  1. 病理病体学

    2023

  2. 遺伝と遺伝子

    2023

  3. 基礎セミナーA

    2023

  4. 病理病体学

    2022

  5. 遺伝と遺伝子

    2022

  6. 基礎セミナーA

    2022

  7. 基礎セミナーA

    2021

  8. 遺伝と遺伝子

    2021

  9. 病理病体学

    2021

  10. 遺伝と遺伝子

    2020

  11. 基礎セミナーA

    2020

  12. 病理病体学

    2020

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Media Coverage 1

  1. がん細胞の増殖助けるメカニズム解明・難治性の脳腫瘍の治療に突破口・名大などの研究グループ

    中日新聞  2023.8