Researcher Database

ODA Tsukasa
Institute for Molecular and Cellular Regulation
Assistant Professor
Last Updated :2025/05/29

Researcher Profile and Settings

Researcher

  • Name

    ODA Tsukasa

Profile and Settings

  • Name

    Oda, Tsukasa

Alternate Names

  • Tsukasa Oda

Foreign language

  • Use in presentation

    English
  • Use in publication

    English

Affiliation

  • Gunma University, Assistant Professor
  • Gunma University, Assistant Professor

Education

  • 1993, Hiroshima University, Graduate School, Division of Biophere Sciences
  • 1993, Hiroshima University
  • 1988, Hiroshima University, Faculty of General Science
  • 1988, Hiroshima University, School of Integrated Arts and Sciences, Integrated Arts and Sciences

Degree

  • 条件付必須項目の入力がありません
  • 条件付必須項目の入力がありません
  • 条件付必須項目の入力がありません, Hiroshima University

Association Memberships

  • The Japanese Association for Molecular Target Therapy of Cancer (JAMTTC)
  • Japanese Cancer Association
  • The Japanese Society of Hematology
  • The Molecular Biology Society of Japan

Research Experience

  • 1993, 1993, Harvard University
  • 1993, 1997
  • 1997, 2000
  • 2000, 2005, The University of Tokyo, The Institute of Medical Science
  • 2005, 9999

Research Activities

Research Areas

  • Life sciences, Tumor biology
  • Life Science, tumor immunology
  • Life sciences, Immunology

Research Interests

  • Notch signaling
  • tumor immunology
  • Notch signaling
  • Organoid

Research Themes

  • The regulation of DNA damage response pathway by molecular chaperone Hsp90, DNA damage, replication stress, molecular chaperone, heat shock protein, 2005, -, General Medical Chemistry, Molecular Biology, Grant-in-Aid for Scientific Research
  • Molecular mechanism of HSF1-depletion induced cellular senescence, Cellular senescence, HSF1, p53, DHRS2, Domestic Collaboration, 2011, -, Molecular Biology, Cell Biology, General Medical Chemistry, Grant-in-Aid for Scientific Research

Published Papers

  • IDO2 rs10109853 polymorphism affects the susceptibility to multiple myeloma., 12 Mar. 2021, Clinical and experimental medicine, Scientific journal
  • DNA-double strand breaks enhance the expression of major histocompatibility complex class II through the ATM-NF-κΒ-IRF1-CIITA pathway, Tsukasa Oda; Ruri Nakamura; Tetsuhiro Kasamatsu; Nanami Gotoh; Keiko Okuda; Takayuki Saitoh; Hiroshi Handa; Hirokazu Murakami; Takayuki Yamashita, 22 Feb. 2021, Cancer Gene Therapy, Scientific journal
  • DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment, Takayuki Saitoh; Tsukasa Oda, 28 Jan. 2021, Cancers, 13, 3, 504, 504, Scientific journal
  • Long Noncoding RNA PVT1 Is Regulated by Bromodomain Protein BRD4 in Multiple Myeloma and Is Associated with Disease Progression., Handa Hiroshi;Honma Kazuki;Oda Tsukasa;Kobayashi Nobuhiko;Kuroda Yuko;Kimura-Masuda Kei;Watanabe Saki;Ishihara Rei;Murakami Yuki;Masuda Yuta;Tahara Ken-Ichi;Takei Hisashi;Kasamatsu Tetsuhiro;Saitoh Takayuki;Murakami Hirokazu, 27 Sep. 2020, International journal of molecular sciences, 21, 19, Scientific journal
  • PARP1 V762A polymorphism affects the prognosis of myelodysplastic syndromes., Nanami Gotoh; Yusuke Minato; Takayuki Saitoh; Noriyuki Takahashi; Tetsuhiro Kasamatsu; Kana Souma; Tsukasa Oda; Takumi Hoshino; Toru Sakura; Takuma Ishizaki; Hiroaki Shimizu; Makiko Takizawa; Akihiko Yokohama; Norifumi Tsukamoto; Hiroshi Handa; Hirokazu Murakami, Jun. 2020, European journal of haematology, 104, 6, 526, 537, Scientific journal
  • Integrin α7 and Extracellular Matrix Laminin 211 Interaction Promotes Proliferation of Acute Myeloid Leukemia Cells and Is Associated with Granulocytic Sarcoma., Nobuhiko Kobayashi; Tsukasa Oda; Makiko Takizawa; Takuma Ishizaki; Norifumi Tsukamoto; Akihiko Yokohama; Hisashi Takei; Takayuki Saitoh; Hiroaki Shimizu; Kazuki Honma; Kei Kimura-Masuda; Yuko Kuroda; Rei Ishihara; Yuki Murakami; Hirokazu Murakami; Hiroshi Handa, 05 Feb. 2020, Cancers, 12, 2, Scientific journal
  • DNA損傷修復応答に関与するDNAポリメラーゼPOLQとPOLHの多発性骨髄腫における発現, ;;;;;;;;;;;;;;;;;;;;;;;;;, Aug. 2019, 69, 3, 296, Research society
  • 多発性骨髄腫におけるc-MAF、MAFB発現とp53, ;;;;;;;;;;;;;;;;;;;;;;;;;, Aug. 2019, 69, 3, 302, Research society
  • Association between OGG1 S326C CC genotype and elevated relapse risk in acute myeloid leukemia., Nanami Gotoh; Takayuki Saitoh; Noriyuki Takahashi; Tetsuhiro Kasamatsu; Yusuke Minato; Alkebsi Lobna; Tsukasa Oda; Takumi Hoshino; Toru Sakura; Hiroaki Shimizu; Makiko Takizawa; Hiroshi Handa; Akihiko Yokohama; Norifumi Tsukamoto; Hirokazu Murakami, Sep. 2018, International journal of hematology, 108, 3, 246, 253, Scientific journal
  • Long non-coding RNA NEAT1はHSF1によって制御され骨髄腫の進行に関与する(Long non-coding RNA NEAT1 is upregulated by HSF1 and associated with myeloma progression), ;;;;;;;;;;;;;;;;;;;, Sep. 2018, 59, 9, 1603, Research society
  • MYCは腫瘍抑制性TP53-micro RNA 34経路を遮断し骨髄腫の進行に関与する(MYC involves myeloma progression by abolishing tumor suppressive function of p53-miRNA 34 axis), ;;;;;;;;;;;;;;;;;;;;;, Sep. 2018, 59, 9, 1603, Research society
  • マトリックスメタロプロテーゼとその阻害因子は骨髄腫の進行と髄外形質細胞腫形成に関係する(MMP and TIMP is associated with multiple myeloma progression and extramedullary plasmacytoma), ;;;;;;;;;;;;;;;;;;, Sep. 2018, 59, 9, 1604, Research society
  • TNF-α-857C/T多型は骨髄異形成症候群の重症度に影響する(TNF-α-857C/T polymorphism affects the severity of myelodysplastic syndromes), ;;;;;;;;;;;;;;;, Sep. 2018, 59, 9, 1645, Research society
  • 多発性骨髄腫における新規治療標的としての塩基除去修復の役割(The role of base excision repair as a potential therapeutic target in multiple myeloma), ;;;;;;;;;;;;;;;;;;;;, Sep. 2018, 59, 9, 1669, Research society
  • MTH1 V83M多型VV型は骨髄異形成症候群の発症リスクとなる, ;;;;;;;;;;;;;;;;;;, Aug. 2018, 68, 3, 200, Research society
  • 多発性骨髄腫細胞株におけるmicroRNA-29、34 familyの発現制御機構, ;;;;;;;;;;;;;;;;;, Aug. 2018, 68, 3, 201, Research society
  • 多発性骨髄腫における髄外形質細胞腫とMatrix metalloproteinase(MMP)及びtissue inhibitor of metalloproteinases(TIMP)の発現, ;;;;;;;;;;;;;;;;;, Aug. 2018, 68, 3, 213, Research society
  • 多発性骨髄腫におけるlong non-cording RNA MALAT1とNEAT1およびNEAT1_2の発現, ;;;;;;;;;;;;;;;;;, Aug. 2018, 68, 3, 213, Research society
  • Polη, a Y-family translesion synthesis polymerase, promotes cellular tolerance of Myc-induced replication stress., Kiminori Kurashima; Takayuki Sekimoto; Tsukasa Oda; Tsuyoshi Kawabata; Fumio Hanaoka; Takayuki Yamashita, 25 Jun. 2018, Journal of cell science, 131, 12, UNSP jcs.212183
  • Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts, Tsukasa Oda; Takayuki Sekimoto; Kiminori Kurashima; Mitsuaki Fujimoto; Akira Nakai; Takayuki Yamashita, 01 May 2018, Journal of Cell Science, 131, 9, UNSP jcs210724, Scientific journal
  • Synthetic lethal interactions between Pol eta and MUS81-EME2 in cellular response to Myc-induced replication stress (RS), Kurashima, Kiminori;Sekimoto, Takayuki;Oda, Tsukasa;Hanaoka, Fumio;Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 230, 230, Research society
  • HSF1 depletion induces senescence through DHRS2-MDM2-p53 pathway in immortalized human diploid fibroblasts (iHDFs), Oda, Tsukasa;Sekimoto, Takayuki;Kurashima, Kiminori;Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 1005, 1005, Research society
  • 53BP1 is involved in the HSF1 depletion-induced senescence, Oda, Tsukasa;Sekimoto, Takashi;Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 461, 461, Research society
  • Matrix Metalloproteinase and Tissue Inhibitor of Metalloproteinases Is Associated with Multiple Myeloma Progression, Prognosis and Extramedullary Plasmacytoma, Ishihara, Rei;Murakami, Yuki;Homma, Kazuki;Watanabe, Saki;Oda, Tsukasa;Sunaga, Masanobu;Yamane, Eiko;Kobayashi, Nobuhiko;Osaki, Yohei;Ishizaki, Takuma;Shimizu, Hiroaki;Iriuchishima, Hirono;Koiso, Hiromi;Tsukamoto, Norifumi;Yokohama, Akihiko;Nanami, Gotoh;Ino, Rumi;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2018, BLOOD, 132, International conference proceedings
  • ゲノム安定性を脅かすDNA複製ストレスの実態 Y-familyポリメラーゼPolηはMus81/EME2ヌクレアーゼ複合体と協同してがん遺伝子c-Mycによるreplication stress(RS)を緩和する, ;;;;;;;;, Dec. 2017, 2017年度, [1PW03
  • MDM2阻害因子Dehydrogenase/reductase 2(DHRS2)の細胞老化における役割, ;;;;;;, Dec. 2017, 2017年度, [1P
  • DNA架橋剤メラファランは多発性骨髄腫細胞株において主要組織適合抗原クラスII(MHC II)の転写活性化因子CIITAの発現を促進する, ;;;;;;;;;, Dec. 2017, 2017年度, [2P
  • Myc誘導性複製ストレス応答においてPolηとMUS81-EME2の二重阻害は合成致死性を示す, ;;;;, Sep. 2017, 76回, P
  • HSF1抑制はDHRS2-MDM2-p53経路を介してヒト線維芽細胞に老化を誘導する, ;;;, Sep. 2017, 76回, P
  • Yファミリー損傷乗越えポリメラーゼPolηはc-MYC誘導性複製ストレスを軽減する, ;;;;, Oct. 2016, 75回, P
  • HSF1抑制はタンパク質毒性ストレス非依存的に細胞老化を誘導する, ;;;, Oct. 2016, 75回, P
  • Heat shock factor 1(HSF1)抑制はDNA損傷および蛋白変性ストレスと独立して細胞老化を誘導する, ;;;, Dec. 2015, 88回・38回, [3P0146]
  • Y-family損傷乗り越えDNAポリメラーゼ(Y-Pol)の一員PolηはMYCがん遺伝子の誘導する複製ストレスを軽減する, ;;;;;, Dec. 2015, 88回・38回, [2P0684]
  • Y-ファミリーDNAポリメラーゼの一つであるPolηはc-mycにより誘導されるDNA二本鎖切断の生成を抑制する, ;;;;, Oct. 2015, 74回, P
  • HSF1抑制は細胞依存的なメカニズムで老化を誘導する, ;;;, Oct. 2015, 74回, P
  • Both high-fidelity replicative and low-fidelity Y-family polymerases are involved in DNA rereplication., Takayuki Sekimoto; Tsukasa Oda; Kiminori Kurashima; Fumio Hanaoka; Takayuki Yamashita, Feb. 2015, Molecular and cellular biology, 35, 4, 699, 715
  • Y-family polymerases are involved in oncogene-induced aberrant replication, Sekimoto, Takayuki;Oda, Tsukasa;Kurashima, Kiminori;Hanaoka, Fumio;Yamashita, Takayuki, 2015, DNA REPAIR, 28, 144, 144
  • Regulation of the DNA-replication stress-response pathways by heat shock protein 90 (HSP90), ODA Tsukasa, Jul. 2012, 84, 7, 556, 562
  • Translesion DNA Synthesis and Hsp90, Takayuki Yamashita; Tsukasa Oda; Takayuki Sekimoto, 2012, Genes and Environment, 34, 2, 89, 93, Scientific journal
  • Molecular chaperone Hsp90 regulates REV1-mediated mutagenesis., Franklin Mayca Pozo; Tsukasa Oda; Takayuki Sekimoto; Yoshiki Murakumo; Chikahide Masutani; Fumio Hanaoka; Takayuki Yamashita, Aug. 2011, Molecular and cellular biology, 31, 16, 3396, 409, Scientific journal
  • The molecular chaperone Hsp90 regulates accumulation of DNA polymerase eta at replication stalling sites in UV-irradiated cells., Takayuki Sekimoto; Tsukasa Oda; Franklin Mayca Pozo; Yoshiki Murakumo; Chikahide Masutani; Fumio Hanaoka; Takayuki Yamashita, 15 Jan. 2010, Molecular cell, 37, 1, 79, 89, Scientific journal
  • Recent progress in understanding molecular pathogenesis of Fanconi anemia, YAMASHITA Takayuki, Jul. 2009, The Japanese journal of clinical hematology, 50, 7, 538, 546
  • Hsp90 and the Fanconi anemia pathway: A molecular link between protein quality control and the DNA damage response, Takayuki Yamashita; Tsukasa Oda; Takayuki Sekimoto, 15 Sep. 2007, Cell Cycle, 6, 18, 2232, 2235
  • Hsp90 regulates the Fanconi anemia DNA damage response pathway, Tsukasa Oda; Toshiya Hayano; Hidenobu Miyaso; Nobuhiro Takahashi; Takayuki Yamashita, Jun. 2007, BLOOD, 109, 11, 5016, 5026, Scientific journal
  • A requirement of FancL and FancD2 monoubiquitination in DNA repair, Sohsuke Seki; Mioko Ohzeki; Akiko Uchida; Seiki Hirano; Nobuko Matsushita; Hiroyuki Kitao; Tsukasa Oda; Takayuki Yamashita; Naoki Kashihara; Akio Tsubahara; Minoru Takata; Masamichi Ishiai, Mar. 2007, GENES TO CELLS, 12, 3, 299, 310, Scientific journal
  • Myeloid lineage-selective growth of revertant cells in Fanconi anaemia, S Hamanoue; H Yagasaki; T Tsuruta; T Oda; H Yabe; M Yabe; T Yamashita, Mar. 2006, BRITISH JOURNAL OF HAEMATOLOGY, 132, 5, 630, 636, Scientific journal
  • ABT1-associated protelin (ABTAP), a novel nuclear protein conserved from yeast to mammals, represses transcriptional activation by ABT1, T Oda; A Fukuda; H Hagiwara; Y Masuho; M Muramatsu; K Hisatake; T Yamashita, Nov. 2004, JOURNAL OF CELLULAR BIOCHEMISTRY, 93, 4, 788, 806, Scientific journal
  • Identification and characterization of novel mutations of the major Fanconi anemia gene FANCA in the Japanese population, H Yagasaki; S Hamanoue; T Oda; T Nakahata; S Asano; T Yamashita, 2004, HUMAN MUTATION, 24, 6, 481, 490, Scientific journal
  • Heterogeneous activation of the Fanconi anemia pathway by patient-derived FANCA mutants, D Adachi; T Oda; H Yagasaki; K Nakasato; K Nakasato; T Taniguchi; AD D'Andrea; S Asano; T Yamashita, Dec. 2002, HUMAN MOLECULAR GENETICS, 11, 25, 3125, 3134, Scientific journal
  • Two common founder mutations of the fanconi anemia group G gene FANCG/XRCC9 in the Japanese population., Tsukasa Oda, 01 May 2003, Human mutation, 21, 555, Scientific journal
  • A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA, H Yagasaki; D Adachi; T Oda; Garcia-Higuera, I; N Tetteh; AD D'Andrea; M Futaki; S Asano; T Yamashita, Dec. 2001, BLOOD, 98, 13, 3650, 3657, Scientific journal
  • HSH2: A novel SH2 domain-containing adapter protein involved in tyrosine kinase signaling in hematopoietic cells, Tsukasa Oda; Masa-aki Muramatsu; Takao Isogai; Yasuhiko Masuho; Shigetaka Asano; Takayuki Yamashita, 16 Nov. 2001, Biochemical and Biophysical Research Communications, 288, 5, 1078, 1086, Scientific journal
  • A novel TATA-binding protein-binding protein, ABT1, activates basal transcription and has a yeast homolog that is essential for growth, T Oda; K Kayukawa; H Hagiwara; HT Yudate; Y Masuho; Y Murakami; T Tamura; M Muramatsu, Feb. 2000, MOLECULAR AND CELLULAR BIOLOGY, 20, 4, 1407, 1418, Scientific journal
  • CRKL binding to BCR-ABL and BCR-ABL transformation, KS Kolibaba; A Bhat; C Heaney; T Oda; BJ Druker, Mar. 1999, LEUKEMIA & LYMPHOMA, 33, 1-2, 119, 126, Scientific journal
  • Interactions of p62(dok) with p210(bcr-abl) and Bcr-Abl-associated proteins, A Bhat; KJ Johnson; T Oda; AS Corbin; BJ Druker, Nov. 1998, JOURNAL OF BIOLOGICAL CHEMISTRY, 273, 48, 32360, 32368, Scientific journal
  • Survival by Mac-1-mediated adherence and anoikis in phorbol ester-treated HL-60 cells, H Nakamura; T Oda; K Hamada; T Hirano; N Shimizu; H Utiyama, Jun. 1998, JOURNAL OF BIOLOGICAL CHEMISTRY, 273, 25, 15345, 15351, Scientific journal
  • Involvement of Mac-1-mediated adherence and sphingosine 1-phosphate in survival of phorbol ester-treated U937 cells, K Hamada; H Nakamura; T Oda; T Hirano; N Shimizu; H Utiyama, Mar. 1998, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 244, 3, 745, 750, Scientific journal
  • Identification and characterization of two novel SH2 domain-containing proteins from a yeast two hybrid screen with the ABL tyrosine kinase, T Oda; J Kujovich; M Reis; B Newman; BJ Druker, Sep. 1997, ONCOGENE, 15, 11, 1255, 1262, Scientific journal
  • Interactions of CBL with BCR-ABL and CRKL in BCR-ABL-transformed myeloid cells, A Bhat; K Kolibaba; T Oda; S OhnoJones; C Heaney; BJ Druker, Jun. 1997, JOURNAL OF BIOLOGICAL CHEMISTRY, 272, 26, 16170, 16175, Scientific journal
  • Direct binding of CRKL to BCR-ABL is not required for BCR-ABL transformation, C Heaney; K Kolibaba; A Bhat; T Oda; S Ohno; S Fanning; BJ Druker, Jan. 1997, BLOOD, 89, 1, 297, 306, Scientific journal
  • THE SH2 DOMAIN OF ABL IS NOT REQUIRED FOR FACTOR-INDEPENDENT GROWTH INDUCED BY BCR-ABL IN A MURINE MYELOID CELL-LINE, T ODA; S TAMURA; T MATSUGUCHI; JD GRIFFIN; BJ DRUKER, Feb. 1995, LEUKEMIA, 9, 2, 295, 301, Scientific journal
  • LOSS OF AMPLIFIED C-MYC GENES IN THE SPONTANEOUSLY DIFFERENTIATED HL-60 CELLS, N SHIMIZU; H NAKAMURA; T KADOTA; K KITAJIMA; T ODA; T HIRANO; H UTIYAMA, Jul. 1994, CANCER RESEARCH, 54, 13, 3561, 3567, Scientific journal
  • INTERPLAY BETWEEN DIFFERENTIATION AND CELL-CYCLE ARREST AT G1 IN PHORBOL DIESTER-TREATED HUMAN MYELOCYTIC-LEUKEMIA CELLS, T ODA; K KITAJIMA; T HIRANO; N SHIMIZU; H UTIYAMA, Aug. 1993, INTERNATIONAL JOURNAL OF HEMATOLOGY, 58, 1-2, 125, 128
  • A GENE CODING FOR A ZINC FINGER PROTEIN IS INDUCED DURING 12-O-TETRADECANOYLPHORBOL-13-ACETATE-STIMULATED HL-60 CELL-DIFFERENTIATION, N SHIMIZU; M OHTA; C FUJIWARA; J SAGARA; N MOCHIZUKI; T ODA; H UTIYAMA, Feb. 1992, JOURNAL OF BIOCHEMISTRY, 111, 2, 272, 277, Scientific journal
  • DETERMINATION OF TRANSCRIPTIONAL ACTIVITIES OF TYPICAL GENE PROMOTERS IN HL-60 CELLS, K OGURO; K SAKAMOTO; K KITAJIMA; T ODA; T HIRANO; N SHIMIZU; H UTIYAMA, Jan. 1992, JOURNAL OF BIOCHEMISTRY, 111, 1, 103, 108, Scientific journal
  • EXPRESSION OF A NOVEL IMMEDIATE EARLY GENE DURING 12-O-TETRADECANOYLPHORBOL-13-ACETATE-INDUCED MACROPHAGIC DIFFERENTIATION OF HL-60 CELLS, N SHIMIZU; M OHTA; C FUJIWARA; J SAGARA; N MOCHIZUKI; T ODA; H UTIYAMA, Jul. 1991, JOURNAL OF BIOLOGICAL CHEMISTRY, 266, 19, 12157, 12161, Scientific journal
  • Association between OGG1 S326C CC genotype and elevated relapse risk in acute myeloid leukemia, Gotoh, Nanami;Saitoh, Takayuki;Takahashi, Noriyuki;Kasamatsu, Tetsuhiro;Minato, Yusuke;Lobna, Alkebsi;Oda, Tsukasa;Hoshino, Takumi;Sakura, Toru;Shimizu, Hiroaki;Takizawa, Makiko;Handa, Hiroshi;Yokohama, Akihiko;Tsukamoto, Norifumi;Murakami, Hirokazu, 2018, INTERNATIONAL JOURNAL OF HEMATOLOGY, 108, 3, 246, 253
  • Long Non-Coding A NEAT1 Is Upregulated By Heat Shock Factor 1 (HSF1) and Associated with Multiple Myeloma Progression, Watanabe, Saki;Oda, Tsukasa;Kuroda, Yuko;Homma, Kazuki;Murakami, Yuki;Ishihara, Rei;Yamane, Eiko;Sunaga, Masanobu;Kobayashi, Nobuhiko;Osaki, Yohei;Ishizaki, Takuma;Shimizu, Hiroaki;Koiso, Hiromi;Iriuchishima, Hirono;Takizawa, Makiko;Yokohama, Akihiko;Tsukamoto, Norifumi;Nanami, Gotoh;Ino, Rumi;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2018, BLOOD, 132
  • PARP1 V762A polymorphism affects the prognosis of myelodysplastic syndromes, Gotoh, Nanami;Minato, Yusuke;Saitoh, Takayuki;Takahashi, Noriyuki;Kasamatsu, Tetsuhiro;Souma, Kana;Oda, Tsukasa;Hoshino, Takumi;Sakura, Toru;Ishizaki, Takuma;Shimizu, Hiroaki;Takizawa, Makiko;Yokohama, Akihiko;Tsukamoto, Norifumi;Handa, Hiroshi;Murakami, Hirokazu, 2020, EUROPEAN JOURNAL OF HAEMATOLOGY, 104, 6, 526, 537
  • P53 Pathway Activation Mediated High c-MAF Expression Is Associated with Overall and Post-Progression Survival in Multiple Myeloma, Yamane, Eiko;Oda, Tsukasa;Sunaga, Masanobu;Murakami, Yuki;Ishihara, Rei;Asao, Yuta;Masuda, Yuta;Watanabe, Saki;Kobayashi, Nobuhiko;Takei, Hisashi;Osaki, Yohei;Nanami, Gotoh;Kasamatsu, Tetsuhiro;Shimizu, Hiroaki;Ishizaki, Takuma;Koiso, Hiromi;Takizawa, Makiko;Ogawa, Yoshiyuki;Yokohama, Akihiko;Tsukamoto, Norifumi;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2019, BLOOD, 134
  • DNA Polymerases Pol θ/Pol η Involved in Error-Prone DNA Repair Are Highly Expressed in Multiple Myeloma and Upregulated By DNA Damage, Sunaga, Masanobu;Oda, Tsukasa;Yamane, Eiko;Ishihara, Rei;Murakami, Yuki;Watanabe, Saki;Asao, Yuta;Masuda, Yuta;Takei, Hisashi;Kobayashi, Nobuhiko;Osaki, Yohei;Nanami, Gotoh;Kasamatsu, Tetsuhiro;Koiso, Hiromi;Takizawa, Makiko;Shimizu, Hiroaki;Ishizaki, Takuma;Ogawa, Yoshiyuki;Yokohama, Akihiko;Tsukamoto, Norifumi;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2019, BLOOD, 134
  • Long Noncoding RNA PVT1 Is Regulated by Bromodomain Protein BRD4 in Multiple Myeloma and Is Associated with Disease Progression, Handa, Hiroshi;Honma, Kazuki;Oda, Tsukasa;Kobayashi, Nobuhiko;Kuroda, Yuko;Kimura-Masuda, Kei;Watanabe, Saki;Ishihara, Rei;Murakami, Yuki;Masuda, Yuta;Tahara, Ken-ichi;Takei, Hisashi;Kasamatsu, Tetsuhiro;Saitoh, Takayuki;Murakami, Hirokazu, 2020, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21, 19
  • DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment, Saitoh, Takayuki;Oda, Tsukasa, 2021, CANCERS, 13, 3
  • DNA-double strand breaks enhance the expression of major histocompatibility complex class II through the ATM-NF-κΒ-IRF1-CIITA pathway, Oda, Tsukasa;Nakamura, Ruri;Kasamatsu, Tetsuhiro;Gotoh, Nanami;Okuda, Keiko;Saitoh, Takayuki;Handa, Hiroshi;Murakami, Hirokazu;Yamashita, Takayuki, 2022, CANCER GENE THERAPY, 29, 2, 225, 240
  • IDO2 rs10109853 polymorphism affects the susceptibility to multiple myeloma, Kasamatsu, Tetsuhiro;Hashimoto, Nao;Sakaya, Nao;Awata-Shiraiwa, Maaya;Ishihara, Rei;Murakami, Yuki;Masuda, Yuta;Gotoh, Nanami;Nagai, Kazue;Oda, Tsukasa;Yokohama, Akihiko;Saitoh, Takayuki;Handa, Hiroshi;Tsukamoto, Norifumi;Hayashi, Kunihiko;Murakami, Hirokazu, 2021, CLINICAL AND EXPERIMENTAL MEDICINE, 21, 2, 323, 329
  • MYC Causes Multiple Myeloma Progression via Attenuating TP53-Induced MicroRNA-34 Expression, Murakami, Yuki;Kimura-Masuda, Kei;Oda, Tsukasa;Matsumura, Ikuko;Masuda, Yuta;Ishihara, Rei;Watanabe, Saki;Kuroda, Yuko;Kasamatsu, Tetsuhiro;Gotoh, Nanami;Takei, Hisashi;Kobayashi, Nobuhiko;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2023, GENES, 14, 1
  • DNA damage-induced cellular senescence is regulated by 53BP1 accumulation in the nuclear foci and phase separation, Oda, Tsukasa;Gotoh, Nanami;Kasamatsu, Tetsuhiro;Handa, Hiroshi;Saitoh, Takayuki;Sasaki, Nobuo, 2023, CELL PROLIFERATION, 56, 6
  • Myeloma Microenvironmental TIMP1 Induces the Invasive Phenotype in Fibroblasts to Modulate Disease Progression, Ishihara, Rei;Oda, Tsukasa;Murakami, Yuki;Matsumura, Ikuko;Watanabe, Saki;Asao, Yuta;Masuda, Yuta;Gotoh, Nanami;Kasamatsu, Tetsuhiro;Takei, Hisashi;Kobayashi, Nobuhiko;Sasaki, Nobuo;Saitoh, Takayuki;Murakami, Hirokazu;Handa, Hiroshi, 2023, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 24, 3
  • Sub-lethal doses of chemotherapeutic agents induce senescence in T cells and upregulation of PD-1 expression, Kasamatsu, Tetsuhiro;Awata-Shiraiwa, Maaya;Ishihara, Rei;Murakami, Yuki;Masuda, Yuta;Gotoh, Nanami;Oda, Tsukasa;Yokohama, Akihiko;Matsumura, Ikuko;Handa, Hiroshi;Tsukamoto, Norifumi;Murakami, Hirokazu;Saitoh, Takayuki, 2023, CLINICAL AND EXPERIMENTAL MEDICINE
  • 多発性骨髄腫におけるmicroRNA-145の発現とその制御機構, ;;;;;;;;, Aug. 2021, 22, 学術集会, S165
  • 多発性骨髄腫の髄外進展におけるTIMP1の影響, ;;;;;;;;, Aug. 2021, 22, 学術集会, S165
  • 健常者T細胞における薬剤誘導性細胞老化の検討, ;;;;;;;;;, Aug. 2021, 22, 学術集会, S187
  • NFKB1-94ins/delATTGは急性骨髄性白血病のリスクと予後不良に関連する(NFKB1-94 ins/del ATTG is associated with the risk of AML and poor prognosis), ;;;;;;;;;;;;, Sep. 2021, 83回, PS
  • 健常者T細胞における薬剤誘導性細胞老化の検討(Melphalan and doxorubicin induce cellular senescence in T cells of healthy subjects), ;;;;;;;;;;;, Sep. 2021, 83回, PS
  • MYCは腫瘍抑制性TP53-microRNA-34経路を遮断し骨髄腫の進行に関与する(MYC involves multiple myeloma progression by attenuating tumor suppressive function of TP53-microRNA-34 axis), ;;;;;;;;;;;;;, May 2022, 12, 3, 153
  • Tissue inhibitor of metalloproteinase 1(TIMP1)は骨髄腫の進行と線維芽細胞の浸潤能に関与する(Tissue inhibitor of metalloproteinase 1(TIMP1) is associated with myeloma progression and fibroblast invasive capacity), ;;;;;;;;;;;;, May 2022, 12, 3, 157
  • 大腸上皮幹細胞ニッチであるDCS細胞の細胞系譜解析, ;;;;, Aug. 2022, 72, 3, 320
  • デフェロキサミンによるHIF-1安定化を介した多発性骨髄腫における遺伝子発現変動の解析, ;;;;;;;;;;;;;, Oct. 2023, 85回, 1177
  • DNA損傷誘導性細胞老化は液-液相分離で形成される53BP1核内フォーカスにより制御される(DNA damage-induced cellular senescence is regulated by 53BP1 accumulation in the nuclear foci and phase separation), ;;;;;, Sep. 2023, 82回, 964
  • Association between OGG1 S326C CC genotype and elevated relapse risk in acute myeloid leukemia., Gotoh Nanami;Saitoh Takayuki;Takahashi Noriyuki;Kasamatsu Tetsuhiro;Minato Yusuke;Lobna Alkebsi;Oda Tsukasa;Hoshino Takumi;Sakura Toru;Shimizu Hiroaki;Takizawa Makiko;Handa Hiroshi;Yokohama Akihiko;Tsukamoto Norifumi;Murakami Hirokazu, May 2018, International journal of hematology, 108, 3
  • PARP1 V762A polymorphism affects the prognosis of myelodysplastic syndromes., Gotoh Nanami;Minato Yusuke;Saitoh Takayuki;Takahashi Noriyuki;Kasamatsu Tetsuhiro;Souma Kana;Oda Tsukasa;Hoshino Takumi;Sakura Toru;Ishizaki Takuma;Shimizu Hiroaki;Takizawa Makiko;Yokohama Akihiko;Tsukamoto Norifumi;Handa Hiroshi;Murakami Hirokazu, Mar. 2020, European journal of haematology, 104, 6
  • DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment., Saitoh Takayuki;Oda Tsukasa, Jan. 2021, Cancers, 13, 3
  • Sub-lethal doses of chemotherapeutic agents induce senescence in T cells and upregulation of PD-1 expression., Kasamatsu Tetsuhiro;Awata-Shiraiwa Maaya;Ishihara Rei;Murakami Yuki;Masuda Yuta;Gotoh Nanami;Oda Tsukasa;Yokohama Akihiko;Matsumura Ikuko;Handa Hiroshi;Tsukamoto Norifumi;Murakami Hirokazu;Saitoh Takayuki, Mar. 2023, Clinical and experimental medicine, 23, 6
  • NFKB1-94ins/delATTGは急性骨髄性白血病のリスクと予後不良に関連する(NFKB1-94 ins/del ATTG is associated with the risk of AML and poor prognosis), ;;;;;;;;;;;;, Sep. 2021, 83回, PS
  • 健常者T細胞における薬剤誘導性細胞老化の検討(Melphalan and doxorubicin induce cellular senescence in T cells of healthy subjects), ;;;;;;;;;;;, Sep. 2021, 83回, PS
  • MYCは腫瘍抑制性TP53-microRNA-34経路を遮断し骨髄腫の進行に関与する(MYC involves multiple myeloma progression by attenuating tumor suppressive function of TP53-microRNA-34 axis), ;;;;;;;;;;;;;, May 2022, 12, 3, 153
  • Tissue inhibitor of metalloproteinase 1(TIMP1)は骨髄腫の進行と線維芽細胞の浸潤能に関与する(Tissue inhibitor of metalloproteinase 1(TIMP1) is associated with myeloma progression and fibroblast invasive capacity), ;;;;;;;;;;;;, May 2022, 12, 3, 157
  • HIF-1αの安定化剤を用いた模擬低酸素環境下における多発性骨髄腫細胞の遺伝子発現解析, ;;;;;;;;;;;;;, Aug. 2023, 73, 3, 254
  • 大腸上皮幹細胞ニッチであるDeep Crypt Secretory(DCS)細胞の細胞系譜解析, ;;;;, Aug. 2023, 73, 3, 254
  • ムチン層の制御に関与する腸内細菌の探索, ;;;;, Aug. 2023, 73, 3, 255
  • デフェロキサミンによるHIF-1安定化を介した多発性骨髄腫における遺伝子発現変動の解析, ;;;;;;;;;;;;;, Oct. 2022, 84回, 1177
  • DNA損傷誘導性細胞老化は液-液相分離で形成される53BP1核内フォーカスにより制御される(DNA damage-induced cellular senescence is regulated by 53BP1 accumulation in the nuclear foci and phase separation), ;;;;;, Sep. 2023, 82回, 964
  • APEX1 Polymorphisms Affect Acute Myeloid Leukemia Risk, and Its Expression Is Involved in Cell Proliferation and Differentiation, Nanami Gotoh; Tsukasa Oda; Yuya Kitamura; Natsuki Shiraishi; Runa Aoyagi; Ayane Omori; Kota Yanagisawa; Minami Iida; Yua Itoi; Hikaru Negishi; Ikuko Matsumura; Tetsuhiro Kasamatsu; Eiji Miyauchi; Nobuo Sasaki; Satoru Takada; Akihiko Yokohama; Hiroshi Handa; Hirokazu Murakami; Takayuki Saitoh, Apr. 2025, International Journal of Laboratory Hematology, Scientific journal
  • Role of Rac1 in p53-Related Proliferation and Drug Sensitivity in Multiple Myeloma, Ikuko Matsumura; Tsukasa Oda; Tetsuhiro Kasamatsu; Yuki Murakami; Rei Ishihara; Ayane Ohmori; Akira Matsumoto; Nanami Gotoh; Nobuhiko Kobayashi; Yuri Miyazawa; Yoshiyuki Ogawa; Akihiko Yokohama; Nobuo Sasaki; Takayuki Saitoh; Hiroshi Handa, 29 Jan. 2025, Cancers, Scientific journal
  • 大腸上皮幹細胞ニッチであるDeep Crypt Secretory(DCS)細胞の細胞系譜解析, 青柳 瑠南; 小田 司; 宮内 栄治; 齋藤 貴之; 佐々木 伸雄, Aug. 2023, 73, 3, 254, 255
  • HIF-1αの安定化剤を用いた模擬低酸素環境下における多発性骨髄腫細胞の遺伝子発現解析, 白石 菜月; 後藤 七海; 小田 司; 笠松 哲光; 青柳 瑠南; 大森 綺音; 柳澤 宏太; 糸井 悠晏; 飯田 南美; 根岸 光; 佐々木 伸雄; 横濱 章彦; 半田 寛; 齋藤 貴之, Aug. 2023, 73, 3, 254, 254
  • Sub-lethal doses of chemotherapeutic agents induce senescence in T cells and upregulation of PD-1 expression., Tetsuhiro Kasamatsu; Maaya Awata-Shiraiwa; Rei Ishihara; Yuki Murakami; Yuta Masuda; Nanami Gotoh; Tsukasa Oda; Akihiko Yokohama; Ikuko Matsumura; Hiroshi Handa; Norifumi Tsukamoto; Hirokazu Murakami; Takayuki Saitoh, 13 Mar. 2023, Clinical and experimental medicine, 23, 6, 2695, 2703, Scientific journal
  • Myeloma Microenvironmental TIMP1 Induces the Invasive Phenotype in Fibroblasts to Modulate Disease Progression., Rei Ishihara; Tsukasa Oda; Yuki Murakami; Ikuko Matsumura; Saki Watanabe; Yuta Asao; Yuta Masuda; Nanami Gotoh; Tetsuhiro Kasamatsu; Hisashi Takei; Nobuhiko Kobayashi; Nobuo Sasaki; Takayuki Saitoh; Hirokazu Murakami; Hiroshi Handa, 22 Jan. 2023, International journal of molecular sciences, 24, 3, Scientific journal
  • DNA damage-induced cellular senescence is regulated by 53BP1 accumulation in the nuclear foci and phase separation., Tsukasa Oda; Nanami Gotoh; Tetsuhiro Kasamatsu; Hiroshi Handa; Takayuki Saitoh; Nobuo Sasaki, 15 Jan. 2023, Cell proliferation, 56, 6, e13398, Scientific journal
  • MYC Causes Multiple Myeloma Progression via Attenuating TP53-Induced MicroRNA-34 Expression., Yuki Murakami; Kei Kimura-Masuda; Tsukasa Oda; Ikuko Matsumura; Yuta Masuda; Rei Ishihara; Saki Watanabe; Yuko Kuroda; Tetsuhiro Kasamatsu; Nanami Gotoh; Hisashi Takei; Nobuhiko Kobayashi; Takayuki Saitoh; Hirokazu Murakami; Hiroshi Handa, 29 Dec. 2022, Genes, 14, 1, Scientific journal
  • デフェロキサミンによるHIF-1安定化を介した多発性骨髄腫における遺伝子発現変動の解析, 白石 菜月; 後藤 七海; 小田 司; 笠松 哲光; 青柳 瑠南; 大森 綺音; 柳澤 宏太; 糸井 悠晏; 飯田 南美; 根岸 光; 佐々木 伸雄; 横濱 章彦; 半田 寛; 齋藤 貴之, Oct. 2022, 日本血液学会学術集会, 84回, 1177, 1177
  • 大腸上皮幹細胞ニッチであるDCS細胞の細胞系譜解析, 青柳 瑠南; 小田 司; 宮内 英治; 齋藤 貴之; 佐々木 伸雄, Aug. 2022, 72, 3, 320, 320
  • MYCは腫瘍抑制性TP53-microRNA-34経路を遮断し骨髄腫の進行に関与する(MYC involves multiple myeloma progression by attenuating tumor suppressive function of TP53-microRNA-34 axis), 村上 有希; 木村 恵[増田]; 小田 司; 増田 裕太; 石原 領; 渡辺 早貴; 黒田 裕子; 笠松 哲光; 後藤 七海; 武井 寿史; 小林 宣彦; 齊藤 貴之; 村上 博和; 半田 寛, May 2022, International Journal of Myeloma, 12, 3, 153, 153
  • Tissue inhibitor of metalloproteinase 1(TIMP1)は骨髄腫の進行と線維芽細胞の浸潤能に関与する(Tissue inhibitor of metalloproteinase 1(TIMP1) is associated with myeloma progression and fibroblast invasive capacity), 石原 領; 小田 司; 村上 有希; 松村 郁子; 渡辺 早貴; 浅尾 優太; 後藤 七海; 笠松 哲光; 武井 寿史; 小林 宣彦; 齋藤 貴之; 村上 博和; 半田 寛, May 2022, International Journal of Myeloma, 12, 3, 157, 157
  • NFKB1-94ins/delATTGは急性骨髄性白血病のリスクと予後不良に関連する(NFKB1-94 ins/del ATTG is associated with the risk of AML and poor prognosis), 佐藤 理水; 後藤 七海; 笠松 哲光; 小田 司; 大川 貴史; 石原 領; 白岩 真彩; 村上 有希; 高田 覚; 塚本 憲史; 横濱 章彦; 半田 寛; 齋藤 貴之, Sep. 2021, 日本血液学会学術集会, 83回, PS, 3
  • 健常者T細胞における薬剤誘導性細胞老化の検討(Melphalan and doxorubicin induce cellular senescence in T cells of healthy subjects), 笠松 哲光; 白岩 真彩; 小田 司; 大川 貴史; 佐藤 理水; 石原 領; 村上 有希; 後藤 七海; 横濱 章彦; 半田 寛; 村上 博和; 齋藤 貴之, Sep. 2021, 日本血液学会学術集会, 83回, PS, 4
  • NFKB1-94 ins/del ATTG is associated with the risk of AML and poor prognosis(和訳中), 佐藤 理水; 後藤 七海; 笠松 哲光; 小田 司; 大川 貴史; 石原 領; 白岩 真彩; 村上 有希; 高田 覚; 塚本 憲史; 横濱 章彦; 半田 寛; 齋藤 貴之, Sep. 2021, 日本血液学会学術集会, 83回, PS, 3
  • Melphalan and doxorubicin induce cellular senescence in T cells of healthy subjects(和訳中), 笠松 哲光; 白岩 真彩; 小田 司; 大川 貴史; 佐藤 理水; 石原 領; 村上 有希; 後藤 七海; 横濱 章彦; 半田 寛; 村上 博和; 齋藤 貴之, Sep. 2021, 日本血液学会学術集会, 83回, PS, 4
  • 多発性骨髄腫におけるmicroRNA-145の発現とその制御機構, 村上 有希; 小田 司; 石原 領; 浅尾 優太; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2021, 22, 学術集会, S165, S165
  • 多発性骨髄腫の髄外進展におけるTIMP1の影響, 石原 領; 小田 司; 村上 有希; 浅尾 優太; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2021, 22, 学術集会, S165, S165
  • 健常者T細胞における薬剤誘導性細胞老化の検討, 笠松 哲光; 白岩 真彩; 小田 司; 石原 領; 村上 有希; 佐藤 理水; 後藤 七海; 半田 寛; 村上 博和; 齋藤 貴之, Aug. 2021, 22, 学術集会, S187, S187
  • 多発性骨髄腫におけるmicroRNA-145の発現とその制御機構, 村上 有希; 小田 司; 石原 領; 浅尾 優太; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2021, 22, 学術集会, S165, S165
  • 多発性骨髄腫の髄外進展におけるTIMP1の影響, 石原 領; 小田 司; 村上 有希; 浅尾 優太; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2021, 22, 学術集会, S165, S165
  • 健常者T細胞における薬剤誘導性細胞老化の検討, 笠松 哲光; 白岩 真彩; 小田 司; 石原 領; 村上 有希; 佐藤 理水; 後藤 七海; 半田 寛; 村上 博和; 齋藤 貴之, Aug. 2021, 22, 学術集会, S187, S187
  • Long Noncoding RNA PVT1 Is Regulated by Bromodomain Protein BRD4 in Multiple Myeloma and Is Associated with Disease Progression., Hiroshi Handa; Kazuki Honma; Tsukasa Oda; Nobuhiko Kobayashi; Yuko Kuroda; Kei Kimura-Masuda; Saki Watanabe; Rei Ishihara; Yuki Murakami; Yuta Masuda; Ken-Ichi Tahara; Hisashi Takei; Tetsuhiro Kasamatsu; Takayuki Saitoh; Hirokazu Murakami, 27 Sep. 2020, International journal of molecular sciences, 21, 19, Scientific journal
  • DNA損傷修復応答に関与するDNAポリメラーゼPOLQとPOLHの多発性骨髄腫における発現, 須永 征伸; 小田 司; 山根 瑛子; 石原 領; 村上 有希; 浅尾 優太; 武井 寿史; 小林 宜彦; 大崎 洋平; 松本 守生; 後藤 七海; 笠松 哲光; 清水 啓明; 石埼 卓馬; 小磯 博美; 滝沢 牧子; 入内島 裕乃; 関上 智美; 横濱 章彦; 塚本 憲史; 増田 裕太; 栗田 真彩; 相馬 佳奈; 橋本 菜央; 齋藤 貴之; 半田 寛, Aug. 2019, 69, 3, 296, 297
  • 多発性骨髄腫におけるc-MAF、MAFB発現とp53, 山根 瑛子; 小田 司; 須永 征伸; 村上 有希; 石原 領; 浅尾 優太; 武井 寿史; 小林 宜彦; 大崎 洋平; 松本 守生; 後藤 七海; 笠松 哲光; 清水 啓明; 石埼 卓馬; 小磯 博美; 滝沢 牧子; 入内島 裕乃; 関上 智美; 横濱 章彦; 塚本 憲史; 増田 裕太; 粟田 真彩; 相馬 佳奈; 橋本 菜央; 齋藤 貴之; 半田 寛, Aug. 2019, 69, 3, 302, 303
  • Long non-coding RNA NEAT1はHSF1によって制御され骨髄腫の進行に関与する(Long non-coding RNA NEAT1 is upregulated by HSF1 and associated with myeloma progression), 渡辺 早貴; 小田 司; 黒田 裕子; 村上 有希; 石原 領; 須永 征伸; 山根 瑛子; 小林 宣彦; 大崎 洋平; 石埼 卓馬; 清水 啓明; 小磯 博美; 入内島 裕乃; 後藤 七海; 笠松 哲光; 横濱 章彦; 齋藤 貴之; 村上 博和; 塚本 憲史; 半田 寛, Sep. 2018, 臨床血液, 59, 9, 1603, 1603
  • MYCは腫瘍抑制性TP53-micro RNA 34経路を遮断し骨髄腫の進行に関与する(MYC involves myeloma progression by abolishing tumor suppressive function of p53-miRNA 34 axis), 村上 有希; 増田 恵; 小田 司; 増田 裕太; 服部 光; 石原 領; 本間 和貴; 渡辺 早貴; 黒田 裕子; 小林 宣彦; 齋藤 貴之; 入内島 裕乃; 小磯 博美; 石埼 卓馬; 清水 啓明; 大崎 洋平; 横濱 章彦; 塚本 憲史; 後藤 七海; 笠松 哲光; 村上 博和; 半田 寛, Sep. 2018, 臨床血液, 59, 9, 1603, 1603
  • マトリックスメタロプロテーゼとその阻害因子は骨髄腫の進行と髄外形質細胞腫形成に関係する(MMP and TIMP is associated with multiple myeloma progression and extramedullary plasmacytoma), 石原 領; 村上 有希; 渡辺 早貴; 小田 司; 須永 征伸; 山根 瑛子; 小林 宣彦; 大崎 洋平; 石埼 卓馬; 清水 啓明; 小磯 博美; 入内島 裕乃; 後藤 七海; 笠松 哲光; 横濱 章彦; 齋藤 貴之; 村上 博和; 塚本 憲史; 半田 寛, Sep. 2018, 臨床血液, 59, 9, 1604, 1604
  • TNF-α-857C/T多型は骨髄異形成症候群の重症度に影響する(TNF-α-857C/T polymorphism affects the severity of myelodysplastic syndromes), 相馬 佳奈; 齋藤 貴之; 後藤 七海; 北村 裕也; 高橋 範行; 須永 征伸; 山根 瑛子; 小田 司; 笠松 哲光; 清水 啓明; 滝沢 牧子; 佐倉 徹; 横濱 章彦; 塚本 憲史; 半田 寛; 村上 博和, Sep. 2018, 臨床血液, 59, 9, 1645, 1645
  • 多発性骨髄腫における新規治療標的としての塩基除去修復の役割(The role of base excision repair as a potential therapeutic target in multiple myeloma), 後藤 七海; 齋藤 貴之; 井野 瑠美; 高橋 範行; 小田 司; 粟田 真彩; 石原 領; 大圃 真純; 金井 敬海; 村田 圭祐; 村上 有希; 渡辺 早貴; 笠松 哲光; 清水 啓明; 滝沢 牧子; 松本 守生; 澤村 守夫; 横濱 章彦; 塚本 憲史; 半田 寛; 村上 博和, Sep. 2018, 臨床血液, 59, 9, 1669, 1669
  • MTH1 V83M多型VV型は骨髄異形成症候群の発症リスクとなる, 倉持 真留美; 齋藤 貴之; 坂元 亜衣; 塩田 みのり; 後藤 七海; 相馬 佳奈; 須永 征伸; 山根 瑛子; 粟田 真彩; 石原 領; 大圃 真純; 金井 敬海; 村上 有希; 村田 圭祐; 渡辺 早貴; 小田 司; 笠松 哲光; 半田 寛; 村上 博和, Aug. 2018, 68, 3, 200, 201
  • 多発性骨髄腫細胞株におけるmicroRNA-29、34 familyの発現制御機構, 村上 有希; 小田 司; 石原 領; 渡辺 早貴; 増田 裕太; 須永 征伸; 山根 瑛子; 小林 宣彦; 武井 寿史; 田原 研一; 大崎 洋平; 石埼 卓馬; 清水 啓明; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2018, 68, 3, 201, 201
  • 多発性骨髄腫における髄外形質細胞腫とMatrix metalloproteinase(MMP)及びtissue inhibitor of metalloproteinases(TIMP)の発現, 石原 領; 小田 司; 渡辺 早貴; 村上 有希; 増田 裕太; 須永 征伸; 山根 瑛子; 小林 宣彦; 武井 寿史; 田原 研一; 大崎 洋平; 石埼 卓馬; 清水 啓明; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2018, 68, 3, 213, 213
  • 多発性骨髄腫におけるlong non-cording RNA MALAT1とNEAT1およびNEAT1_2の発現, 渡辺 早貴; 小田 司; 石原 領; 村上 有希; 増田 裕太; 須永 征伸; 山根 瑛子; 小林 宣彦; 武井 寿史; 田原 研一; 大崎 洋平; 石埼 卓馬; 清水 啓明; 後藤 七海; 笠松 哲光; 齋藤 貴之; 村上 博和; 半田 寛, Aug. 2018, 68, 3, 213, 213
  • Matrix Metalloproteinase and Tissue Inhibitor of Metalloproteinases Is Associated with Multiple Myeloma Progression, Prognosis and Extramedullary Plasmacytoma, Ishihara, Rei; Murakami, Yuki; Homma, Kazuki; Watanabe, Saki; Oda, Tsukasa; Sunaga, Masanobu; Yamane, Eiko; Kobayashi, Nobuhiko; Osaki, Yohei; Ishizaki, Takuma; Shimizu, Hiroaki; Iriuchishima, Hirono; Koiso, Hiromi; Tsukamoto, Norifumi; Yokohama, Akihiko; Nanami, Gotoh; Ino, Rumi; Saitoh, Takayuki; Murakami, Hirokazu; Handa, Hiroshi, 2018, BLOOD, 132, International conference proceedings
  • 53BP1 is involved in the HSF1 depletion-induced senescence, Oda, Tsukasa; Sekimoto, Takashi; Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 461, 461, Research society
  • HSF1 depletion induces senescence through DHRS2-MDM2-p53 pathway in immortalized human diploid fibroblasts (iHDFs), Oda, Tsukasa; Sekimoto, Takayuki; Kurashima, Kiminori; Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 1005, 1005, Research society
  • Synthetic lethal interactions between Pol eta and MUS81-EME2 in cellular response to Myc-induced replication stress (RS), Kurashima, Kiminori; Sekimoto, Takayuki; Oda, Tsukasa; Hanaoka, Fumio; Yamashita, Takayuki, 2018, CANCER SCIENCE, 109, 230, 230, Research society
  • DNA架橋剤メラファランは多発性骨髄腫細胞株において主要組織適合抗原クラスII(MHC II)の転写活性化因子CIITAの発現を促進する, 中村 瑠里; 小田 司; 関本 隆志; 松田 美弥子; 大圃 真純; 半田 寛; 笠松 哲光; 齋藤 貴之; 村上 博和; 山下 孝之, Dec. 2017, 2017年度, [2P
  • MDM2阻害因子Dehydrogenase/reductase 2(DHRS2)の細胞老化における役割, 小田 司; 関本 隆志; 倉島 公憲; 中村 瑠里; 松田 美弥子; 大圃 真純; 山下 孝之, Dec. 2017, 2017年度, [1P
  • ゲノム安定性を脅かすDNA複製ストレスの実態 Y-familyポリメラーゼPolηはMus81/EME2ヌクレアーゼ複合体と協同してがん遺伝子c-Mycによるreplication stress(RS)を緩和する, 関本 隆志; 倉島 公憲; 小田 司; 川端 剛; 松田 美弥子; 中村 瑠里; 大圃 真純; 花岡 文雄; 山下 孝之, Dec. 2017, 2017年度, [1PW03
  • HSF1抑制はDHRS2-MDM2-p53経路を介してヒト線維芽細胞に老化を誘導する, 小田 司; 関本 隆志; 倉島 公憲; 山下 孝之, Sep. 2017, 76回, P
  • Myc誘導性複製ストレス応答においてPolηとMUS81-EME2の二重阻害は合成致死性を示す, 倉島 公憲; 関本 隆志; 小田 司; 花岡 文雄; 山下 孝之, Sep. 2017, 76回, P
  • HSF1抑制はタンパク質毒性ストレス非依存的に細胞老化を誘導する, 小田 司; 関本 隆志; 倉島 公憲; 山下 孝之, Oct. 2016, 75回, P
  • Yファミリー損傷乗越えポリメラーゼPolηはc-MYC誘導性複製ストレスを軽減する, 倉島 公憲; 関本 隆志; 小田 司; 花岡 文雄; 山下 孝之, Oct. 2016, 75回, P
  • Y-family損傷乗り越えDNAポリメラーゼ(Y-Pol)の一員PolηはMYCがん遺伝子の誘導する複製ストレスを軽減する, 倉島 公憲; 関本 隆志; 小田 司; 川端 剛; 花岡 文雄; 山下 孝之, Dec. 2015, 88回・38回, [2P0684]
  • Heat shock factor 1(HSF1)抑制はDNA損傷および蛋白変性ストレスと独立して細胞老化を誘導する, 小田 司; 関本 隆志; 倉島 公憲; 山下 孝之, Dec. 2015, 88回・38回, [3P0146]
  • HSF1抑制は細胞依存的なメカニズムで老化を誘導する, 小田 司; 関本 隆志; 倉島 公憲; 山下 孝之, Oct. 2015, 74回, P
  • Y-ファミリーDNAポリメラーゼの一つであるPolηはc-mycにより誘導されるDNA二本鎖切断の生成を抑制する, 倉島 公憲; 関本 隆志; 小田 司; 花岡 文雄; 山下 孝之, Oct. 2015, 74回, P
  • Coexistence of phosphotyrosine-dependent and -independent interactions between Cbl and Bcr-Abl., Isabelle Gaston; Kara J Johnson; Tsukasa Oda; Arun Bhat; Margaret Reis; Wallace Langdon; Lei Shen; Michael W Deininger; Brian J Druker, Jan. 2004, Experimental hematology, 32, 1, 113, 21, Scientific journal
  • 赤血球造血と鉄代謝研究の分子生物学的展開Fanconi貧血の分子病態 : 遺伝子から表現型へ, 山下 孝之; 小田 司; 谷ケ崎 博; 足立 大樹; 二木 真琴; D'ANDREA Alan D.; 浅野 茂隆, 30 May 2001, 42, 5, 385, 389
  • Crkl is the major tyrosine-phosphorylated protein in neutrophils from patients with chronic myelogenous leukemia., Tsukasa Oda, 01 Sep. 1994, The Journal of biological chemistry, Scientific journal

MISC

  • Different activation of the Fanconi anemia (FA) pathway by patient-derived FANCA mutants., D Adachi; T Oda; H Yagasaki; K Nakasato; T Taniguchi; AD D'Andrea; S Asano; T Yamashita, Nov. 2001, BLOOD, 98, 11, 215A, 215A, Summary international conference
  • DNA損傷修復応答に関与するDNAポリメラーゼPOLQとPOLHの多発性骨髄腫における発現, 須永 征伸; 小田 司; 山根 瑛子; 石原 領; 村上 有希; 浅尾 優太; 武井 寿史; 小林 宜彦; 大崎 洋平; 松本 守生; 後藤 七海; 笠松 哲光; 清水 啓明; 石埼 卓馬; 小磯 博美; 滝沢 牧子; 入内島 裕乃; 関上 智美; 横濱 章彦; 塚本 憲史; 増田 裕太; 栗田 真彩; 相馬 佳奈; 橋本 菜央; 齋藤 貴之; 半田 寛, Aug. 2019, 69, 3, 296, 297
  • 多発性骨髄腫におけるc-MAF、MAFB発現とp53, 山根 瑛子; 小田 司; 須永 征伸; 村上 有希; 石原 領; 浅尾 優太; 武井 寿史; 小林 宜彦; 大崎 洋平; 松本 守生; 後藤 七海; 笠松 哲光; 清水 啓明; 石埼 卓馬; 小磯 博美; 滝沢 牧子; 入内島 裕乃; 関上 智美; 横濱 章彦; 塚本 憲史; 増田 裕太; 粟田 真彩; 相馬 佳奈; 橋本 菜央; 齋藤 貴之; 半田 寛, Aug. 2019, 69, 3, 302, 303
  • Fanconi anemia: genotoxic stress and senescence of hematopoietic stem cells, 山下孝之; 小田司; 関本隆志, 2008, Japanese journal of clinical medicine, 66, 3, 477, 482
  • Fanconi貧血の分子病態―最近の進歩, 山下孝之; 小田司; 関本隆志, 2009, 50, 7, 538, 546
  • 我が国のFanconi貧血(FA)患者における遺伝子変異の解析, 谷ヶ崎 博; 足立 大樹; 小田 司; 中畑 龍俊; 浅野 茂隆; 山下 孝之, Aug. 2002, 臨床血液, 43, 8, 87, 87
  • 体細胞モザイクを示したFanconi貧血(FA)患者におけるFANCA復帰変異, 谷ヶ崎 博; 浜之上 聡; 望月 慎史; 鶴田 敏久; 足立 大樹; 小田 司; 中畑 龍俊; 浅野 茂隆; 山下 孝之, Aug. 2003, 日本小児血液学会雑誌, 17, 4, 228, 228
  • CRKL IS THE MAJOR TYROSINE-PHOSPHORYLATED PROTEIN IN NEUTROPHILS FROM PATIENTS WITH CHRONIC MYELOGENOUS LEUKEMIA, C HEANEY; T ODA; HAGOPIAN, JR; K OKUDA; JD GRIFFIN; BJ DRUKER, Nov. 1994, BLOOD, 84, 10, A381, A381, Summary international conference
  • Y-family polymerases are involved in oncogene-induced aberrant replication, Takayuki Sekimoto; Tsukasa Oda; Kiminori Kurashima; Fumio Hanaoka; Takayuki Yamashita, Apr. 2015, DNA REPAIR, 28, 144, 144, Summary international conference
  • 紫外線照射DNAの損傷乗り越え複製においてDNAポリメラーゼイータとイオタが果たす生理的役割(Physiological roles of DNA polymerases η and ι in translesion synthesis past UV-induced DNA damage), 櫻井 靖高; 横井 雅幸; 塚本 徹哉; 小田 司; 魏 民; 山下 孝之; 鰐渕 英機; 立松 正衛; 村雲 芳樹; 花岡 文雄, Sep. 2014, 日本癌学会総会記事, 73回, P, 3076
  • Regulation of the DNA-replication stress-response pathways by heat shock protein 90 (HSP90), Tsukasa Oda, 2012, Seikagaku, 84, 7, 556, 562, Book review
  • A novel SH2 domain-containing protein, HSH2, may link tyrosine kinase signaling to CDC42-regulated kinase ACK1 in hematopoietic cells., T Oda; M Muramatsu; T Isogai; Y Masuho; S Asano; T Yamashita, Nov. 2000, BLOOD, 96, 11, 78A, 78A, Summary international conference
  • Role of RAS-related C3 botulinus toxin substrate 1(Rac1) in multiple myeloma progression and relationship with p53, MATSUMURA Ikuko; 小田司; 笠松哲光; 村上有希; 石原領; 大森綺音; 後藤七海; 小林宣彦; 宮澤悠里; 小川孔幸; 横濱章彦; 佐々木伸雄; 齋藤貴之; 半田寛, 2024, International Journal of Myeloma (Web), 14, 3
  • 多発性骨髄腫におけるRho-GTPaseファミリーRac1の役割の解明と標的にした治療法の検討, 松村郁子; 小田司; 笠松哲光; 大森綺音; 村上有希; 石原領; 松本彬; 後藤七海; 小林宣彦; 宮澤悠里; 小川孔幸; 横濱章彦; 佐々木伸雄; 齋藤貴之; 半田寛, 2024, 71st
  • Long Non-Coding A NEAT1 Is Upregulated By Heat Shock Factor 1 (HSF1) and Associated with Multiple Myeloma Progression, Saki Watanabe; Tsukasa Oda; Yuko Kuroda; Kazuki Homma; Yuki Murakami; Rei Ishihara; Eiko Yamane; Masanobu Sunaga; Nobuhiko Kobayashi; Yohei Osaki; Takuma Ishizaki; Hiroaki Shimizu; Hiromi Koiso; Hirono Iriuchishima; Makiko Takizawa; Akihiko Yokohama; Norifumi Tsukamoto; Gotoh Nanami; Rumi Ino; Takayuki Saitoh; Hirokazu Murakami; Hiroshi Handa, Nov. 2018, BLOOD, 132, Summary international conference
  • The Mechanism of Phorbol Ester-Induced Differentiation of Human Myelocytic Leukemia Cells, ODA Tsukasa, 31 Dec. 1993, Memoirs of the Faculty of Integrated Arts and Sciences, Hiroshima University. IV, Science reports : studies of fundamental and environmental sciences, 19, 189, 191

Books etc

  • 分子シャペロンHSP90による複製ストレス応答機構の制御, 2012
  • 腸オルガノイド, Joint work, 2021
  • 熱ショック転写因子HSF1の抑制による細胞老化の誘導機構, 2012
  • 鉄代謝・骨髄機能不全 Fanconi貧血の分子病態 最近の進歩(解説), 2009
  • 【貧血 最新の基礎と臨床】 基礎編 貧血の分子病態 各論 Fanconi貧血 ゲノム損傷ストレスと造血幹細胞の老化(解説/特集), 2008
  • 鉄代謝・骨髄機能不全 Fanconi貧血の分子病態 最近の進歩(会議録), 2008
  • 分子シャペロンHsp90はUV照射を受けた細胞においてDNAポリメラーゼeta(Polη)の複製フォーカスへの動員を促進する, 2007
  • Heat shock protein(Hsp)90阻害剤はファンコニ貧血(FA)経路を抑制して腫瘍細胞のDNA架橋剤への感受性を増強する(会議録), 2006

Presentations

  • DNA Polymerases Pol θ/Pol η Involved in Error-Prone DNA Repair Are Highly Expressed in Multiple Myeloma and Upregulated By DNA Damage,, 須永征伸, 第61回 アメリカ血液学会, 09 Dec. 2019, English
  • P53 Pathway Activation Mediated High c-MAF Expression Is Associated with Overall and Post-Progression Survival in Multiple Myeloma, 山根瑛子, 第61回 アメリカ血液学会, 09 Dec. 2019, English
  • 多発性骨髄腫におけるc-MAF、MAFB発現とp53, 山根 瑛子; 小田 司; 須永 征伸; 村上 有希; 石原 領; 浅尾 優太; 武井 寿史; 小林 宜彦; 大崎 洋平; 松本 守生; 後藤 七海; 笠松 哲光; 清水 啓明; 石埼 卓馬; 小磯 博美; 滝沢 牧子; 入内島 裕乃; 関上 智美; 横濱 章彦; 塚本 憲史; 増田 裕太; 粟田 真彩; 相馬 佳奈; 橋本 菜央; 齋藤 貴之; 半田 寛, 第66回北関東医学会総会, 28 Sep. 2019, Japanese
  • Long non-coding RNA PVT1 and MYC are co-regulated by bromodomain protein BRD4 in multiple myeloma and associated with disease progression, The American Society of Hematology, 2017
  • Apurinic/apyrimidinic endonuclease 1 is involved in the pathogenesis of acute myeloid leukemia, The 79th Annual Meeting of the Japanese Society of Hematology, 2017
  • DNA架橋剤メルファランは多発性骨髄腫細胞株において主要組織適合抗原クラスII (MHC II)の転写活性化因子CIITAの発現を促進する, 第40回日本分子生物学会年会, 2017
  • MDM2阻害因子Dehydrogenase/reductase 2 (DHRS2)の細胞老化における役割, 第40回日本分子生物学会年会, 2017
  • Y-familyポリメラーゼPolηはMus81/EME2ヌクレアーゼ複合体と協同してがん遺伝子c-Mycによるreplication stress (RS)を緩和する, 第40回日本分子生物学会年会, 2017
  • Synthetic lethal interactions between Polη and MUS81-EME2 in cellular response to Myc-induced replication stress (RS), 76 th Annual Meeting of the Japanese Cancer Association, 2017
  • HSF1 depletion induces senescence through DHRS2-MDM2-p53 pathway in immortalized human diploid fibroblasts (iHDFs), 76 th Annual Meeting of the Japanese Cancer Association, 2017
  • Long non-coding RNA PVT1 and MYC are co-regulated by bromodomain protein BRD4 in multiple myeloma and associated with disease progression, The American Society of Hematology, 2017
  • Apurinic/apyrimidinic endonuclease 1 is involved in the pathogenesis of acute myeloid leukemia, The 79th Annual Meeting of the Japanese Society of Hematology, 2017
  • Synthetic lethal interactions between Polη and MUS81-EME2 in cellular response to Myc-induced replication stress (RS), 76 th Annual Meeting of the Japanese Cancer Association, 2017
  • HSF1 depletion induces senescence through DHRS2-MDM2-p53 pathway in immortalized human diploid fibroblasts (iHDFs), 76 th Annual Meeting of the Japanese Cancer Association, 2017
  • Y-familyポリメラーゼPolηとエンドヌクレアーゼMus81-Eme2複合体は段階的に協調してc-MYCがん遺伝子誘導性複製ストレスを抑制する, 第39回日本分子生物学会年会, 2016
  • Polη, a Y-family translesion synthesis (TLS) polymerase, mitigates c-Myc induced replication stress., 75th Annual Meeting of the Japanese Cancer Association, 2016
  • 熱ショック応答転写因子Heat shock factor 1 (HSF1)の発現抑制による細胞老化はMDM2阻害蛋白質Dehydrogenase/reductase 2 (DHRS2)に制御されている可能性がある, 第39回日本分子生物学会年会, 2016
  • HSF1 depletion induces cellular senescence independently of proteotoxic stress in immortalized human diploid fibroblasts (iHDFs)., 75th Annual Meeting of the Japanese Cancer Association, 2016
  • Polη, a Y-family translesion synthesis (TLS) polymerase, mitigates c-Myc induced replication stress., 75th Annual Meeting of the Japanese Cancer Association, 2016
  • HSF1 depletion induces cellular senescence independently of proteotoxic stress in immortalized human diploid fibroblasts (iHDFs)., 75th Annual Meeting of the Japanese Cancer Association, 2016
  • Acute inhibition of heat shock factor 1 (HSF1) induces cellular senescence through cell type-dependent mechanisms, 2015
  • Y-family DNAポリメラーゼはc-mycがん遺伝子の誘導する複製ストレスを軽減する, 2015
  • Heat shock factor 1 (HSF1) 抑制による老化誘導機構は細胞種により異なり、またHSPs非依存的である, 2015
  • Pol-eta a member of Y-family DNA polymerases prevents generation of DNA double strand breaks induced by c-myc expression, 2015
  • Acute inhibition of heat shock factor 1 (HSF1) induces cellular senescence through cell type-dependent mechanisms, 2015
  • Pol-eta a member of Y-family DNA polymerases prevents generation of DNA double strand breaks induced by c-myc expression, 2015
  • Y-family polymerases are involved in oncogene-induced aberrant replication., 2014
  • Inhibition of heat shock factor 1 (HSF1) selectively activates cellular senescence program, 2014
  • DNA polymerase-eta promotes DNA rereplication. International symposium on xeroderma pigmentosum and related disorders, 2014
  • Y-family polymerases are involved in oncogene-induced aberrant replication., 2014
  • Inhibition of heat shock factor 1 (HSF1) selectively activates cellular senescence program, 2014
  • DNA polymerase-eta promotes DNA rereplication. International symposium on xeroderma pigmentosum and related disorders, 2014
  • Polymerase-etaは発がん遺伝子が誘導するDNA再複製に関与する, 2013
  • DHRS2: a potential mediator of cellular senescence induced by depletion of heat shock factor 1 (HSF1), 2013
  • DHRS2 は熱ショック転写因子HSF1抑制で誘導される細胞老化に関与する可能性がある, 2013
  • Y-family DNAポリメラーゼは、発がんシグナルが誘導するDNA再複製に関与する, 2013
  • Polymerase-etaは発がん遺伝子が誘導するDNA再複製に関与する, 2013
  • DHRS2: a potential mediator of cellular senescence induced by depletion of heat shock factor 1 (HSF1), 2013
  • Y-family DNAポリメラーゼは、発がんシグナルが誘導するDNA再複製に関与する, 2013
  • ポリメラーゼηは発がんシグナルが誘導するDNA再複製とDNA損傷応答に関与する, 第71回日本癌学会学術総会, 2012
  • Y-family DNAポリメラーゼは、発がんシグナルが誘導するDNA再複製に関与する, 第35回日本分子生物学会年会, 2012
  • 熱ショック応答転写因子Heat shock factor 1 (HSF1)の抑制による細胞老化の誘導機構: DHRS2とp300/CBPの関与, 第35回日本分子生物学会年かい, 2012
  • Y-family DNAポリメラーゼによる損傷乗り越えDNA合成は、cyclin E過剰発現によるDNA複製ストレス応答に関与する, 第34回日本分子生物学会年会, 2011
  • 熱ショック応答転写因子Heat shock factor 1 (HSF1)の発現抑制はp53-p21経路を介した細胞老化を誘導する, 第34回日本分子生物学会年会, 2011
  • 分子シャペロンHsp90はREV1による突然変異の誘発を制御する, 第70回日本癌学会学術総会, 2011
  • 熱ショック転写因子HSF1の急性欠乏は複数の腫瘍抑制経路を介して細胞老化プログラムを活性化する, 第70回日本癌学会学術総会, 2011
  • 熱ショック転写因子HSF1の急性欠乏は腫瘍抑制性の細胞プログラムを活性化する, 第69回日本癌学会総会, 2010
  • 分子シャペロンHsp90はY-family DNAポリメラーゼREV1のDNA損傷による核内フォーカス形成を促進する, 第32回日本分子生物学会年会, 2009
  • 熱ショック応答転写因子Heat shock facter1(HSF1)の 発現制御はhTERT不死化ヒト細胞においてp53-p21を介する細胞老化を引き起こす, 第32回日本分子生物学会年会, 2009
  • 分子シャペロンHsp90によるDNA損傷応答経路の制御, 第4回麒麟塾, 2008
  • 分子シャペロンHSP90はPolymerase-η (Pol-η)の複製フォーカスへの集積と損傷乗越えDNA合成(TLS)を促進する, 第31回日本分子生物学会年会, 2008
  • 分子シャペロンHsp90によるFA/BRCA経路の制御, 千葉県がんセンター研究局集談会, 2007
  • 分子シャペロンHsp90はTranslesion DNA Synthesis (TLS)に関与するDNA polymerase-eta (Pol-h)のReplication focus (RF)への動員に必要である, 日本分子生物学会, 2007
  • 分子シャペロンHsp90はUV照射を受けた細胞においてDNAポリメラーゼeta(Pol h)の複製フォーカスへの動員を促進する, 日本癌学会学術総会, 2007
  • Heat shock protein (Hsp90)阻害剤はファンコニ貧血(FA)経路を抑制して腫瘍細胞のDNA架橋剤への感受性を増強する, 日本癌学会学術総会, 2006
  • Hsp90/Hsp70/CHIPシャペロン・ユビキチンリガーゼ系によるFanconi貧血(FA)分子経路の制御, 日本血液学会・日本臨床血液学会回総会, 2005
  • シャペロン複合体Hsc70/Hsp90によるFanconi貧血(FA)分子経路の制御, 日本血液学会・日本臨床血液学会回総会, 2004

Awards

  • 2002

Research Projects

  • 2018, Principal investigator, Competitive research funding
  • 2010, Principal investigator, Competitive research funding
  • 2010, 2011, Principal investigator, Competitive research funding
  • 2007, Principal investigator, Competitive research funding
  • Apr. 2015, Mar. 2018, Principal investigator, Competitive research funding
  • 01 Apr. 2022, 31 Mar. 2025, 22K07412
  • Mechanism of drug resistance by microRNA-DNA repair in multiple myeloma, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Gunma University, 01 Apr. 2021, 31 Mar. 2024, 21K07312
  • The role of Y-family polymerase in aberrant DNA replication and genomic instability, Yamashita Takayuki; ODA Tsukasa; SEKIMOTO Takayuki, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Gunma University, 01 Apr. 2015, 31 Mar. 2018, Growth of neoplastic cells relies on their tolerance to oncogene-induced replication stress (RS). Translesion synthesis (TLS) plays a critical role in cellular tolerance to various types of RS by employing specialized polymerases. Here, we report that Polη, a Y-family TLS polymerase, promotes cellular tolerance to Myc-induced RS. Polη was recruited to Myc-induced RS sites, and Polη depletion enhanced the Myc-induced slowing and stalling of replication forks and the subsequent generation of double-strand breaks (DSBs). In the absence of Polη, Myc-induced DSB formation depended on MUS81-EME2 (the S-phase specific endonuclease complex), and concomitant depletion of MUS81-EME2 and Polη enhanced RS and cell death in a synergistic manner. Collectively, these results indicate that Polη alleviates the Myc-induced RS, and highlight the possibility of synthetic sick or lethal interaction between Polη and MUS81-EME2 in cells experiencing Myc-induced RS., 15K06826
  • Analysis of oncogene-induced replication stress response patyways, Sekimoto Takayuki; YAMASHITA Takayuki; ODA Tsukasa, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Gunma University, 01 Apr. 2015, 31 Mar. 2018, Growth of cancer cells relies on their tolerance of oncogene-induced replication stress (RS). Translesion synthesis (TLS) plays an essential role in cellular tolerance of various types of RS. However, limited information is available about the role of TLS polymerases in oncogene-induced RS. Polη, a Y-family TLS polymerase, promotes cellular tolerance of Myc-induced RS. Polη was recruited to Myc-induced RS sites, and Polη depletion enhanced the Myc-induced stalling of replication forks and the subsequent generation of double-strand breaks (DSBs). In the absence of Polη, Myc-induced DSB formation depended on MUS81-EME2, and concomitant depletion of MUS81-EME2 and Polη enhanced RS and cell death in a synergistic manner. Collectively, these results indicate that Polη facilitates fork progression during Myc-induced RS. Additionally, the present study highlights the possibility of a synthetic lethal interaction between Polη and MUS81-EME2 in cells experiencing Myc-induced RS., 15K06825
  • Apr. 2011, Mar. 2013, Competitive research funding
  • Apr. 2010, Mar. 2012, Principal investigator, Competitive research funding
  • Molecular mechanism of HSF1-depletion induced cellular senescence, Grant-in-Aid for Scientific Research, 2011, Competitive research funding
  • Apr. 2008, Mar. 2010, Competitive research funding
  • Apr. 2007, Mar. 2008, Principal investigator, Competitive research funding
  • Molecular pathogenesis of Fanconi anemia, YAMASHITA Takayuki; ODA Tsukasa, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Gunma University, 2004, 2005, Fanconi anemia (FA) is a genetically heterogeneous inherited disorder characterized by bone marrow failure and congenital anomalies. Although an increasing number of reports suggest that reverse mosaicism noted in peripheral blood lymphocytes (PBL) is associated with mild hematopoietic failure in FA, direct examination of myeloid cells have been done in few cases. We found a patient with prolonged mild pancytopenia in whom proliferation of revertant cells was detected in mature myeloid cells but not in PBL. While this patient had inherited heterozygous mutations, 2546delC and 3720-3724del, in the major Fanconi anemia gene FANCA, lymphoblastoid cells from the patient had 2546C>T instead of 2546delC, resulting in expression of a functional missense protein. Since the identical reversion was detected in polymorphonuclear granulocytes and mononuclear phagocytes, sustained hematopoiesis in the patient is attributed to selective growth advantage of revertant myeloid cells. It is noteworthy that such a myeloid lineage-selective mosaicism is overlooked in routine examination of PBL. Recognition of this status will expand the role of reverse mosaicism in the pathophysiology of FA. Bone marrow failure in FA often shows progression to myelodysplastic syndrome (MDS) and leukemia, which may be attributed to mutations of oncogenes and tumor suppressor genes based on DNA repair deficiency. However, specific mutations of these genes have not been identified in FA leukemic cells. We hypothesized that epigenetic abnormalities may be associated with the pathophysiology of FA. To address this question, we analyzed promoter methylation of five tumor suppressor genes, p15, p16. DAP kinase, RAR-β, E-cadherin. The results showed that 8 of 11 patients (72.7%) had hypermethylation in one or more of these genes. The methylation abnormalities were observed more frequently in patients with MDS than in those without MDS. These results suggest that epigenetic abnormalities might be involbed in leukmogensis in FA., 16590928
  • The regulation of DNA damage response pathway by molecular chaperone Hsp90, Grant-in-Aid for Scientific Research, 2005, Competitive research funding
  • 2004, 2004, 16021213
  • Apr. 2002, Mar. 2003, Principal investigator, Competitive research funding
  • Apr. 2001, Mar. 2003, Principal investigator, Competitive research funding
  • 2003, 2003, 15023215
  • Study of molecular pathogenesis of Fanconi anemia, YAMASHITA Takayuki; ODA Tsukasa, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), The University of Tokyo, 2002, 2003, Fanconi anemia is an autosomal recessive disorder of hematopoiesis with at least 11 genetically different groups, characterized by cellular hypersensitivity to DNA cross-linkers and chromosome instability. To date, 8 genes have been identified. A multiprotein complex including these gene products, FANCAICJE/F/G/L is required for activation of FANCD2 into a monoubiquitinated form. This active form affects genomic instability in collaboration with BRCA1 and BRCA2IFANCD1. In this project, we studied functions of FANCA mutants with amino acid substitution in its N-terminal region including nuclear localization signal and FANCG-binding sites. Our results indicate that formation of a stable complex including FANCAICIE/FIGIL is not essential for FANCD2 activation. It seems that nuclear import of FANCA/L complex palys a central role in this pathway, and that FANCG negatively regulates nuclear import of FANCA. Furthermore, we identified Hsc7O as a FANCA-binding protein. A dominant-negative form of Hsc7O and 17-AAG, a specific inhibitor of Hsp9O, inhibited nuclear localization of FANCA, suggesting that a chaperone complex including Hsc7O is required for nuclear import of FANCA. We identified FANCA mutations in 27 Japanese FA patients and found novel molecular mechanisms of generation of large deletions in this gene. We found that long-term remission of bone marrow failurewas associated with myeloid lineage-selective expansion of cells with reversion in a patient. This case suggests the clinical usefulness of gene therapy., 14570963
  • 2002, 2002, 14026012


Copyright © MEDIA FUSION Co.,Ltd. All rights reserved.