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Master

Affiliation (Master)

  • Faculty of Medicine　Pathological Science　Pathology

Affiliation (Master)

  • Faculty of Medicine　Pathological Science　Pathology

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Profile and Settings

Profile and Settings

  • Name (Japanese)

    Miyatake

  • Name (Kana)

    Yukiko

  • Name

    201301086924145652

Alternate Names

Achievement

Research Interests

  • 膵がん   がん三次元培養   産学連携   創薬支援技術   がん免疫   マイクロ腫瘍   ナノバイオサイエンス   

Research Areas

  • Life sciences / Tumor biology
  • Nanotechnology/Materials / Nanobioscience
  • Life sciences / Pathobiochemistry
  • Life sciences / Experimental pathology
  • Life sciences / Immunology

Research Experience

  • 2010/07 - Today Department of Integrative Pathology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University Assistant Professor
  • 2022/11 - 2023/11 苫小牧看護専門学校 非常勤講師
  • 2010/08 - 2021/09 王子総合病院附属看護専門学校 非常勤講師
  • 2007/09 - 2010/06 Centre for Research in Infectious Diseases, UCD, Dublin Postdoctoral fellow
  • 2007/04 - 2007/08 ヒューマンサイエンス振興財団 リサーチレジデント
  • 2005/04 - 2007/03 Hokkaido University Graduate School of Medicine
  • 1997/04 - 1999/03 市立札幌病院 耳鼻咽喉科 非常勤職員
  • 1994/04 - 1996/03 北海道大学医学部耳鼻咽喉科 実験補助員

Education

  • 2001/04 - 2005/03  北海道大学大学院
  • 1999/04 - 2001/03  北海道大学大学院 地球環境科学研究科
  • 1995/10 - 1997/10  The Open University of Japan
  • 1991/04 - 1994/03  Hokkaido University
  • 1988/04 - 1991/03  北海道札幌南高等学校

Awards

  • 2022/02 JST SCOREに係る北海道大学等スタートアップ育成プラットフォーム推進会議 北海道・大学等発スタートアップ育成プラットフォームに係るHSFC Demo Day 奨励賞（３位）
     Cancer-on-a-chipデバイスによる 新しいがん創薬の世界へ 
    受賞者: 繁富 香織 (宮武 由甲子)
  • 2021/10 第7回北海道大学部局横断シンポジウム研究助成採択 金賞
     
    受賞者: 高野勇太;宮武由甲子;山田勇磨;繁富(栗林)香織
  • 2020/10 第6回 北大・部局横断シンポジウム ベストプレゼン賞
     
    受賞者: 高野勇太;宮武由甲子;山田勇磨;繁富(栗林)香織
  • 2019/10 国際ソロプチミスト旭川クラブ賞
     
    受賞者: 宮武由甲子
  • 2019/07 第12回 資生堂 女性研究者サイエンスグラント
     
    受賞者: 宮武由甲子
  • 2019/04 Scientific Reports Top 100 2018
     in Cell and Molecular Biology (1-25) 
    受賞者: Yukiko Miyatake
  • 2007/03 高桑榮松奨励賞
     
    受賞者: 宮武由甲子
  • 2005/12 第1回 北大医学部 第一病理同門会研究奨励賞 Young Scientist of the Year 2005
     
    受賞者: 宮武 由甲子

Published Papers

  • Hanjun Zhao, Rina Naganawa, Yuma Yamada, Yasuko Osakada, Mamoru Fujitsuka, Hideyuki Mitomo, Yukiko Miyatake, Hideyoshi Harashima, Vasudevanpillai Biju, Yuta Takano
    Journal of Photochemistry and Photobiology A: Chemistry 115397 - 115397 1010-6030 2023/12/12
  • Excitation-Wavelength-dependent Functionalities of Temporally controlled Sensing and Generation of Singlet Oxygen by a Photoexcited State Engineered Rhodamine 6G-anthracene Conjugate.
    Hanjun Zhao, Yuta Takano, Devika Sasikumar, Yukiko Miyatake, Vasudevanpillai Biju
    Chemistry - A European Journal 2022/10 [Refereed][Not invited]
  • Yukiko Miyatake, Kaori Kuribayashi-Shigetomi, Yusuke Ohta, Shunji Ikeshita, Agus Subagyo, Kazuhisa Sueoka, Akira Kakugo, Maho Amano, Toshiyuki Takahashi, Takaharu Okajima, Masanori Kasahara
    Scientific Reports 8, Article number: 14054 2045-2322 2018/09/19 [Refereed][Not invited]
  • Yukiko Miyatake, Yusuke Ohta, Shunji Ikeshita, Masanori Kasahara
    Oncotarget 9 (52) 29845 - 29856 1949-2553 2018/07/06 [Refereed][Not invited]
  • Rania Hassan Mohamed, Yoichi Sutoh, Yasushi Itoh, Noriyuki Otsuka, Yukiko Miyatake, Kazumasa Ogasawara, Masanori Kasahara
    PLOS ONE 10 (4) 1932-6203 2015/04 [Refereed][Not invited]
     
    Dendritic epidermal T cells, which express an invariant V.5V delta 1 T-cell receptor and account for 95% of all resident T cells in the mouse epidermis, play a critical role in skin immune surveillance. These gamma delta T cells are generated by positive selection in the fetal thymus, after which they migrate to the skin. The development of dendritic epidermal T cells is critically dependent on the Skint1 gene expressed specifically in keratinocytes and thymic epithelial cells, suggesting an indispensable role for Skint1 in the selection machinery for specific intraepithelial lymphocytes. Phylogenetically, rodents have functional SKINT1 molecules, but humans and chimpanzees have a SKINT1-like (SKINT1L) gene with multiple inactivating mutations. In the present study, we analyzed SKINT1L sequences in representative primate species and found that all hominoid species have a common inactivating mutation, but that Old World monkeys such as olive baboons, green monkeys, cynomolgus macaques and rhesus macaques have apparently functional SKINT1L sequences, indicating that SKINT1L was inactivated in a common ancestor of hominoids. Interestingly, the epidermis of cynomolgus macaques contained a population of dendritic-shaped gamma delta T cells expressing a semi-invariant V.10/V delta 1 T-cell receptor. However, this population of macaque T cells differed from rodent dendritic epidermal T cells in that their V.10/V delta 1 T-cell receptors displayed junctional diversity and expression of V.10 was not epidermis-specific. Therefore, macaques do not appear to have rodent-type dendritic epidermal T cells despite having apparently functional SKINT1L. Comprehensive bioinformatics analysis indicates that SKINT1L emerged in an ancestor of placental mammals but was inactivated or lost multiple times in mammalian evolution and that Skint1 arose by gene duplication in a rodent lineage, suggesting that authentic dendritic epidermal T cells are presumably unique to rodents.
  • Yukiko Miyatake, Noreen Sheehy, Shunji Ikeshita, William W. Hall, Masanori Kasahara
    CANCER LETTERS 357 (1) 355 - 363 0304-3835 2015/02 [Refereed][Not invited]
     
    Adult T-cell leukemia/lymphoma (ATL) is an intractable T-cell malignancy accompanied by massive invasion of lymphoma cells into various tissues. We demonstrate here that ATL cells cultured on a layer of epithelial-like feeder cells form anchorage-dependent multicellular aggregates (Ad-MCAs) and that a fraction of MCA-forming ATL cells acquire CD44 high cancer stem cell-like phenotypes. ATL cells forming Ad-MCAs displayed extracellular microvesicles with enhanced expression of CD44v9 at cell synapses, augmented expression of multidrug resistance protein 1, and increased NF-kappa B activity. Blockade of the NF kappa B pathway dramatically reduced Ad-MCA formation by ATL cells and the emergence of CD44 high ATL cells, but left a considerable number of ATL cells adhering to the feeder layer. Disruption of vimentin cytoskeleton by treatment with withaferin A, a natural steroidal lactone, suppressed not only the adhesion of ATL cells to the feeder layer but also subsequent Ad-MCA formation by ATL cells, suggesting the involvement of vimentin in anchoring ATL cells to the feeder layer. Ad-MCA formation by ATL cells on a layer of epithelial-like feeder cells may mimic critical events that occur in metastatic colonization. (c) 2014 Elsevier Ireland Ltd. All rights reserved.
  • Shizuka Kiuchi, Shunji Ikeshita, Yukiko Miyatake, Masanori Kasahara
    EXPERIMENTAL AND MOLECULAR PATHOLOGY 98 (1) 41 - 46 0014-4800 2015/02 [Refereed][Not invited]
     
    Pancreatic cancer is one of the most lethal cancers with high metastatic potential and strong chemoresistance. Its intractable natures are attributed to high robustness in tumor cells for their survival. We demonstrate here that pancreatic cancer cells (PCCs) with an epithelial phenotype upregulate cell surface expression of CD44 variant 9 (CD44v9), an important cancer stem cell marker, during the mitotic phases of the cell cycle. Of five human CD44(+) PCC lines examined, three cell lines, PCI-24, PCI-43 and PCI-55, expressed E-cadherin and CD44 variants, suggesting that they have an epithelial phenotype. By contrast PANC-1 and MIA PaCa-2 cells expressed vimentin and ZEB1, suggesting that they have a mesenchymal phenotype. PCCs with an epithelial phenotype upregulated cell surface expression of CD44v9 in prophase, metaphase, anaphase and telophase and downregulated CD44v9 expression in late-telophase, cytokinesis and interphase. Sorted CD44v9-negative PCI-55 cells resumed CD44v9 expression when they re-entered the mitotic stage. Interestingly, CD44v9(bright) mitotic cells expressed multidrug resistance protein 1 (MDR1) intracellularly. Upregulated expression of CD44v9 and MDR1 might contribute to the intractable nature of PCCs with high proliferative activity. (C) 2014 Elsevier Inc. All rights reserved.
  • Yukiko Miyatake, Masanori Kasahara
    Inflammation and Immunity in Cancer 75 - 84 2015/01/01 [Refereed][Not invited]
     
    Adult T cell leukemia/lymphoma (ATL) is a highly invasive and intractable T cell malignancy caused by human T cell leukemia virus-1 infection. Leukemia/lymphoma cells that have invaded the tissues exhibit a propensity for strong resistance to chemotherapy, presenting a major obstacle to the treatment of ATL patients. Therefore, understanding how tissue-infiltrating leukemia/lymphoma cells acquire intractable features is important for developing effective treatments for ATL patients. We have recently found that, when co-cultured with epithelial-like feeder cells, ATL cells form anchorage-dependent multicellular aggregates and that a fraction of aggregate-forming ATL cells acquire quiescent CD44 high cancer stem cell-like phenotypes. This observation suggests that the intractability of tissue infiltrating ATL cells may be partly accounted for by the acquisition of cancer stem cell-like properties.
  • Shunji Ikeshita, Yukiko Miyatake, Noriyuki Otsuka, Masanori Kasahara
    EXPERIMENTAL AND MOLECULAR PATHOLOGY 97 (1) 171 - 175 0014-4800 2014/08 [Refereed][Not invited]
     
    Infiltrating macrophages accumulate in fatty streak lesions and transform into foam cells, leading to the formation of atherosclerotic plaques. Inflammatory mechanisms underlying the plaque formation mediated by NKG2D-positive lymphocytes such as CD8(+) T cells, natural killer cells and natural killer T cells have been extensively investigated. Yet, the involvement of the NKG2D system itself remains poorly understood. Recent work in mouse models has shown that blockade of an NKG2D receptor ligand interaction reduces plaque formation and suppresses inflammation in aortae. In this study, we conducted immunohistochemical analysis of NKG2D ligand expression in autopsy-derived aortic specimens. Foam cells expressing NKG2D ligands MICA/B were found in advanced atherosclerotic lesions accompanied by a large necrotic core or hemorrhage. Human monocyte-derived macrophages treated in vitro with acetylated low-density lipoproteins enhanced expression of MICA/B and scavenger receptor A, thus accounting for NKG2D ligand expression in foam cells infiltrating atherosclerotic plaques. Our results suggest that, as in mice, the NKG2D system might be involved in the development of atherosclerosis in humans. (C) 2014 Elsevier Inc. All rights reserved.
  • Y. Aoki, N. Otsuka, N. Yamamoto, T. Miyazaki, Y. Miyatake, M. Kasahara
    Journal of Reproductive Immunology 106 19 - 19 2014
  • Yukiko Miyatake, Andre L. A. Oliveira, Mohamed Ali Jarboui, Shuichi Ota, Utano Tomaru, Takanori Teshima, William W. Hall, Masanori Kasahara
    AMERICAN JOURNAL OF PATHOLOGY 182 (5) 1832 - 1842 0002-9440 2013/05 [Refereed][Not invited]
     
    Adult T-cell leukemia/lymphoma (ATL) is a highly invasive and intractable T-cell malignancy caused by human T-cell leukemia virus-1 infection. We demonstrate herein that normal tissue-derived epithelial cells (NECs) exert protective effects on the survival of leukemic cells, which may partially account for high resistance to antileukemic therapies in patients with ATL. Viral gene-silenced, ATL-derived cell Lines (ATL cells) dramatically escaped from histone deacetylase inhibitor-induced apoptosis by direct co-culture with NECs. Adhesions to NECs suppressed p21(Cip1) expression and increased a proportion of resting G0/G1 phase cells in trichostatin A (TSA)-treated ATL cells. ATL cells adhering to NECs down-regulated CD25 expression and enhanced vimentin expression, suggesting that most ATL cells acquired a quiescent state by cell-cell interactions with NECs. ATL cells adhering to NECs displayed highly elevated expression of the cancer stem cell marker CD44. Blockade of CD44 signaling diminished the NEC-conferred resistance of ATL cells to TSA-induced apoptosis. Co-culture with NECs also suppressed the expression of NKG2D Ligands on TSA-treated ATL cells, resulting in decreased natural killer cell-mediated cytotoxicity. Combined evidence suggests that interactions with normal epithelial cells augment the resistance of ATL cells to TSA-induced apoptosis and facilitate immune evasion by ATL cells.
  • Utano Tomaru, Satomi Takahashi, Akihiro Ishizu, Yukiko Miyatake, Aya Gohda, Sayuri Suzuki, Ayako Ono, Jiro Ohara, Tomohisa Baba, Shigeo Murata, Keiji Tanaka, Masanori Kasahara
    AMERICAN JOURNAL OF PATHOLOGY 180 (3) 963 - 972 0002-9440 2012/03 [Refereed][Not invited]
     
    The proteasome is a multicatalytic enzyme complex responsible for the degradation of both normal and damaged proteins. An age-related decline in proteasomal activity has been implicated in various age-related pathologies. The relevance of decreased proteasomal activity to aging and age-related diseases remains unclear, however, because suitable animal models are not available. In the present study, we established a transgenic (Tg) mouse model with decreased proteasomal chymotrypsin-like activity. Tg mice exhibited a shortened life span and developed age-related phenotypes. In Tg mice, polyubiquitinated and oxidized proteins accumulated, and the expression levels of cellular proteins such as Bcl-xL and RNase L were altered. When Tg mice were fed a high-fat diet, they developed more pronounced obesity and hepatic steatosis than did wild-type mice. Consistent with its role in lipid droplet formation, the expression of adipose differentiation-related protein (ADRP) was elevated in the livers of Tg mice. Of note, obesity and hepatic steatosis induced by a high-fat diet were more pronounced in aged than in young wild-type mice, and aged wild-type mice had elevated levels of ADRP, suggesting that the metabolic abnormalities present in Tg mice mimic those in aged mice. Our results proteasomal chymotrypsin-like activity affects longevity and aggravates age-related metabolic disorders, such as obesity and hepatic steatosis. (Am J Pathol(2012, 180:963-972; DOI. 10.1016/j.ajpath.2011.11.012)
  • Yukiko Miyatake, Utano Tomaru, André L A Oliveira, Noreen Sheehy, Takashi Yoshiki, Masanori Kasahara, William W Hall
    Retrovirology 8 (Suppl 1) 2011
  • Akihiro Ishizu, Asami Abe, Yukiko Miyatake, Tomohisa Baba, Chihiro Iinuma, Utano Tomaru, Takashi Yoshiki
    MODERN RHEUMATOLOGY 20 (2) 134 - 138 1439-7595 2010/04 [Refereed][Not invited]
     
    Overproduction of interleukin (IL)-6 from synovial cells is critically involved in the pathogenesis of rheumatoid arthritis (RA). Cyclic adenosine monophosphate (AMP) response element-binding protein (CREB), a leucine zipper transcription factor, is expressed at a high level in synovial cells of patients with RA. Although CREB transactivates IL-6 expression in vascular smooth muscle cells, the relation between CREB expression and IL-6 production from arthritic synovial cells remains unclear. In this study, to determine whether CREB is implicated in IL-6 production from arthritic synovial cells, a dominant negative molecule of activation transcription factor 1 (ATF-1) was transfected into synovial cells obtained from arthritic joints of env-pX rats. These transgenic rats carrying the env-pX gene of human T-cell leukemia virus type-1 develop destructive arthritis with high titers of serum rheumatoid factor and are thus regarded as a suitable model of RA. The dominant negative ATF-1 (ATF-1DN) constitutes a heterodimer with CREB and inhibits CREB function, as CREB/ATF-1DN heterodimers no longer bind to the target sequence of CREB. We showed that transfection of ATF-1DN significantly reduced IL-6 production from arthritic synovial cells. These findings suggest that CREB is implicated in IL-6 production from synovial cells and plays an important role in RA pathogenesis.
  • Utano Tomaru, Akihiro Ishizu, Shigeo Murata, Yukiko Miyatake, Sayuri Suzuki, Satomi Takahashi, Taku Kazamaki, Jiro Ohara, Tomohisa Baba, Sari Iwasaki, Kazunori Fugo, Noriyuki Otsuka, Keiji Tanaka, Masanori Kasahara
    BLOOD 113 (21) 5186 - 5191 0006-4971 2009/05 [Refereed][Not invited]
     
    The ubiquitin-proteasome pathway, which degrades intracellular proteins, is involved in numerous cellular processes, including the supply of immunocompetent peptides to the antigen presenting machinery. Proteolysis by proteasomes is conducted by three beta subunits, beta 1, beta 2, and beta 5, of the 20S proteasome. Recently, a novel beta subunit expressed exclusively in cortical thymic epithelial cells was discovered in mice. This subunit, designated beta 5t, is a component of the thymoproteasome, a specialized type of proteasomes implicated in thymic positive selection. In this study, we show that, like its mouse counterpart, human beta 5t is expressed exclusively in the thymic cortex. Human beta 5t was expressed in approximately 80% of cortical thymic epithelial cells and some cortical dendritic cells. Human beta 5t was incorporated into proteasomes with two other catalytically active beta subunits beta 1i and beta 2i, forming 20S proteasomes with subunit compositions characteristic of thymoproteasomes. The present study demonstrates, for the first time, the existence of thymoproteasomes in the human thymic cortex, indicating that thymoproteasome function is likely conserved between humans and mice. (Blood. 2009; 113: 5186-5191)
  • Akio Takada, Shigeru Yoshida, Mizuho Kajikawa, Yukiko Miyatake, Utano Tomaru, Masaharu Sakai, Hitoshi Chiba, Katsumi Maenaka, Daisuke Kohda, Kazunori Fugo, Masanori Kasahara
    JOURNAL OF IMMUNOLOGY 180 (3) 1678 - 1685 0022-1767 2008/02 [Refereed][Not invited]
     
    H60, originally described as a dominant minor histocompatibility Ag, is an MHC class I-like molecule that serves as a ligand for the NKG2D receptor. In the present study, we identified two novel mouse chromosome 10-encoded NKG2D ligands structurally resembling H60. These ligands, which we named H60b and H60c, encode MHC class I-like molecules with two extracellular domains. Whereas H60b has a transmembrane region, H60c is a GPI-anchored protein. Recombinant soluble H60b and H60c proteins bound to NKG2D with affinities typical of cell-cell recognition receptors (K(d) = 310 nM for H60b and K(d) = 8.7 mu M for H60c). Furthermore, expression of H60b or H60c rendered Ba/F3 cells susceptible to lysis by NK cells, thereby establishing H60b and H60c as functional ligands for NKG2D. H60b and H60c transcripts were detected only at low levels in tissues of healthy adult mice. Whereas H60b transcripts were detectable in various tissues, H60c transcripts were detected mainly in the skin. Infection of mouse embryonic fibroblasts with murine cytomegalovirus induced expression of H60b, but not H60c or the previously known H60 gene, indicating that transcriptional activation of the three types of H60 genes is differentially regulated. The present study adds two new members to the current list of NKG2D ligands.
  • N. Otsuka, Y. Miyatake, A. Ishizu, S. Tanaka, Y. Yamamoto, H. Ikeda, T. Yoshiki
    AIDS RESEARCH AND HUMAN RETROVIRUSES 22 (11) 1148 - 1151 0889-2229 2006/11 [Refereed][Not invited]
     
    To investigate the biological roles of human endogenous retrovirus-R (HERV-R) in vivo, we established transgenic rats carrying the full sequence of the viral genome with control of its own long terminal repeat promoter. The Env protein was expressed on the surface of the epidermis of fetal HERV-R transgenic rats on day 10 of gestation. The epidermal Env expression disappeared by day 18 of gestation. After day 18 of gestation, the Env protein was detected in the prickle layer of the esophageal epithelium of transgenic rats. Interestingly, it was not detected in the basal layer of the epithelium, and the expression in the granular layer was weaker than in the prickle layer. These findings suggest that expression of HERV-R is linked not only to the development but also to the differentiation of squamous cells. Next, we examined alterations in the expression of the HERV-R env gene in cultured human squamous cells after exposure to all-trans retinoic acids ( ATRA). The env expression was increased by ATRA in a dose-dependent manner, while the expression of transglutaminase 1 (TGM1), a terminal marker for squamous differentiation, was decreased. TGM1 is expressed in the granular layer of the squamous epithelium, and ATRA suppresses the differentiation of cultured squamous cells. Thus, these in vitro data also suggest that HERV-R expression is regulated by a mechanism closely related to the differentiation of squamous cells. This study is the first to demonstrate the association of HERV-R expression and differentiation of squamous cells.
  • Y Miyatake, H Ikeda, A Ishizu, T Baba, T Ichihashi, A Suzuki, U Tomaru, M Kasahara, T Yoshiki
    AMERICAN JOURNAL OF PATHOLOGY 169 (1) 189 - 199 0002-9440 2006/07 [Refereed][Not invited]
     
    Human T-cell leukemia virus type I (HTLV-1) is the causative agent of not only adult T-cell leukemia but also HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Among die rat strains infected with HTLV-1, chronic progressive myelopathy, named HAM rat disease, occurs exclusively in WKAH rats. In the present study, we found that HTLV-1 infection induces interferon (IFN)-gamma production in the spinal cords of HAM-resistant strains but not in those of WKAH rats. Neurons were the major cells that produced IFN-gamma in HTLV-1-infected, HAM-resistant strains. Administration of IFN-gamma suppressed expression of pX, the gene critically involved in the onset of HAM rat disease, in an HTLV-1-immortalized rat T-cell line, indicating that IFN-gamma protects against the development of HAM rat disease. The inability of WKAH spinal cord neurons to produce IFN-gamma after infection appeared to stem from defects in signaling through the interleukin (IL)-12 receptor. Specifically, WKAH-derived spinal cord cells were unable to up-regulate the IL-12 receptor beta 2 gene in response to IL-12 stimulation. We suggest that the failure of spinal cord neurons to produce IFN-gamma through the IL-12 pathway is involved in the development of HAM rat disease.
  • Muneharu Tsuji, Hitoshi Ikeda, Akihiro Ishizu, Yukiko Miyatake, Hiroko Hayase, Takashi Yoshiki
    PATHOBIOLOGY 73 (6) 304 - 309 1015-2008 2006 [Refereed][Not invited]
     
    Objective: High-dose steroid hormones cause necrosis of the femoral head. Since steroid hormones function as blood coagulants, we hypothesized that ischemic hypoxia induced by steroid hormones is critical for apoptosis which occurs before necrosis of osteocytes. Methods: We performed an analysis of gene expression in the process of leading osteocytes to apoptosis, using a mouse cell line. Cultured osteocytes were loaded with hypoxic stress with or without exposure to steroid hormones, and the gene expression under these conditions was investigated using a cDNA array and real-time quantitative RT-PCR. Results: The proapoptotic p53 gene was downregulated under a hypoxic (1% O-2) condition without exposure to steroid hormones. On the other hand, the expression of antiapoptotic Bcl-2 gene was increased by exposure to high-dose steroid hormones under a normoxic condition (20% O-2). Interestingly, both proapoptotic (p53 and Bax) and antiapoptotic (Bcl-2 and MDM2) genes were downregulated in osteocytes treated with high-dose steroid hormones in the hypoxic environment. Conclusions: These findings suggest that osteocytes exposed to high-dose steroid hormones appear to be more sensitive to apoptosis in the hypoxic environment than those without exposure to steroid hormones. This concept helps to understand the pathogenesis of idiopathic necrosis of the bone. Copyright (c) 2006 S. Karger AG, Basel.
  • H Hayase, A Ishizu, H Ikeda, Y Miyatake, T Baba, M Higuchi, A Abe, U Tomaru, T Yoshiki
    INTERNATIONAL IMMUNOLOGY 17 (6) 677 - 684 0953-8178 2005/06 [Refereed][Not invited]
     
    Transgenic rats expressing the env-pX gene of human T cell leukemia virus type-I under the control of the viral long terminal repeat promoter (env-pX rats) developed systemic autoimmune diseases. Prior to disease manifestation, the immunosuppressive function of CD25(+)CD4(+) T (T-reg) cells was impaired in these rats. Since T cell differentiation appeared to be disordered in env-pX rats, we assumed that the impairment of T-reg cells might be caused by an abortive differentiation in the thymus. However, reciprocal bone marrow transfers between env-pX and wild-type rats revealed that direct effects of the transgene unrelated to the thymus framework induced the abnormality of T-reg cells. To identify molecular changes, comparative analyses were done between env-pX and wild-type T-reg cells. Expression of the Foxp3 gene and cell-surface markers supported a naive phenotype for env-pX T-reg cells. Array analyses of gene expression showed some interesting profiles, e.g. up-regulation of genes associated with the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways in env-pX T-reg cells. Additionally, expression of the suppressor of cytokine signaling (SOCS) family genes, which inhibit the JAK/STAT signals, was extremely low in env-pX T-reg cells. These findings suggest that the transgene may mediate the down-regulation of the SOCS family genes and that subsequent excess signals through the JAK/STAT pathways may result in the loss of function of env-pX T-reg cells. We suggest that investigation of the pathology of T-reg cells in our autoimmune-prone rat model may aid in understanding the roles of T-reg cells in human autoimmune diseases.
  • T Baba, A Ishizu, H Ikeda, Y Miyatake, T Tsuji, A Suzuki, U Tomaru, T Yoshiki
    EUROPEAN JOURNAL OF IMMUNOLOGY 35 (6) 1731 - 1740 0014-2980 2005/06 [Refereed][Not invited]
     
    We earlier reported that the human T cell leukemia virus type-1 pX gene transduced into rat thymic epithelial cells had an impact on biology of the cells. We report here that FW-pX rats born by mating of F344 transgenic rats expressing the pX gene without tissue specificity with nontransgenic Wistar rats developed disorders, including atrophy of the thymus, lymphocytopenia, and inflammatory cell infiltration into multiple organs, similar to events in chronic graft-vs.-host disease (GVHD). Vanishment of thymic epithelial cells especially in the cortex and marked depletion of CD4 CD8 double-positive thymocytes were evident in the neonatal thymus in these rats. The relative abundance of CD8 compared to CD4 T cells may be related to dominant infiltration of CD8 T cells into the affected organs. Additionally, adoptive transfer of FW-pX splenocytes could induce lymphocytic infiltration into sublethally irradiated wild-type syngeneic recipients. Analysis of the expression level of the Foxp3 gene in peripheral blood mononuclear cells revealed that the numbers of immunoregulatory T cells were less in FW-pX rats than in wild-type rats. The collective evidence suggested that the FW-pX rats spontaneously developed chronic GVHD-like autoimmune diseases, following abortive differentiation of T cells in the thymus in early days of the newborn. This rat model may shed light on the pathogenesis of chronic GVHD and also other systemic autoimmune diseases, the etiology of which is unknown.
  • Y Miyatake, H Ikeda, R Michimata, S Koizumi, A Ishizu, N Nishimura, T Yoshiki
    EXPERIMENTAL AND MOLECULAR PATHOLOGY 77 (3) 222 - 230 0014-4800 2004/12 [Refereed][Not invited]
     
    The aim of this study is to determine if warm ischemia after surgical extirpation impacts gene expression in tissue samples which will be used for cDNA array analysis. We investigated effects of warm ischemia on gene expression in lung, liver, kidney, and spleen of rats, chronologically, using an original cDNA array, real-time quantitative RT-PCR and inummohistochemistry. Although no visible alteration was found in RNA quality, cDNA array showed that expression of many genes was modulated by warm ischemia within 60 min in these tissues, 19.1% of the tested genes in lung, 11.0% in liver, 5.1% in kidney, and 16.2% in spleen. Quantitative RT-PCR revealed that warm ischemia significantly induced up-regulation of immediate early genes, c-fos, Egr-1, and c-jun, in lung, but not in liver. These findings suggest that genes may show tissue-dependent differential transcriptional response against warm ischemia. Tissue samples obtained from patients during surgery cannot completely escape effects of ischemia. In case of examination by cDNA array analysis, biologists should keep in mind that tissue samples come equipped with particular footprints. (C) 2004 Elsevier Inc. All rights reserved.
  • A Abe, A Ishizu, H Ikeda, H Hayase, T Tsuji, Y Miyatake, M Tsuji, K Fugo, T Sugaya, M Higuchi, T Matsuno, T Yoshiki
    INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY 85 (4) 191 - 200 0959-9673 2004/08 [Refereed][Not invited]
     
    Transgenic rats carrying the env-pX gene of human T-cell leukaemia virus type-I (env-pX rats) were immunized with type II collagen (CII), and chronological alterations of arthritis were compared with findings of collagen-induced arthritis (CIA) in wildtype Wistar-King-Aptekman-Hokudai (WKAH) rats. Arthritis induced by CII in env-pX rats was more severe and persisted longer than CIA in WKAH rats. To determine whether the phenomenon is caused mainly by the transgene-carrying lymphocytes or articular tissues, we immunized lethally irradiated env-pX and WKAH rats with reciprocal bone marrow cell (BMC) transplantation. A severe but transient arthritis was induced by CII in WKAH rats reconstituted by env-pX BMC (w/tB/CII rats). On the other hand, in env-pX rats reconstituted by WKAH BMC, arthritis persisted longer than in w/tB/CII rats, although the degree was less at an early phase after CII immunization. These findings suggest that articular tissues rather than the BMCs carrying the env-pX transgene play a role in the prolongation of arthritis in env-pX rats, although BMCs carrying the transgene are associated with the severity of arthritis. When inflammatory cytokines in synovial cells isolated from env-pX rats before they developed arthritis were examined, interleukin-6 (IL-6) was detected at a higher level than in synovial cells from WKAH rats, thus suggesting the critical role of IL-6 in env-pX arthritis.

Books etc

  • 日本臨牀増刊号 「リンパ腫学」 正常上皮系細胞との相互作用によるATLL細胞への癌幹細胞特性の誘導
    宮武由甲子 (Contributor)
    日本臨牀社 2015
  • Inflammation and Immunity in Cancer; Anchorage-dependent multicellular aggregate formation induces CD44 high cancer stem cell-like phenotypes in adult T-cell leukemia/lymphoma cells.
    Yukiko Miyatake, Masanori Kasahara (Contributor)
    Springer 2015

Presentations

  • 宮武 由甲子, 太田 悠介, 繁富 (栗林) 香織, 得能 寿子, 大 紘太郎, 長谷川 明莉, 岩崎 沙理, 田中 敏, 篠塚 啓, 谷口 浩二
    第112回 日本病理学会総会  2023/04
  • 高野 勇太, 宮武 由甲子, 山田 勇麿, 繁富(栗林)香織
    第８回北大・部局横断シンポジウム 新領域創成に向けた若手連携の推進  2022/10
  • 宮武 由甲子, 繁富 香織, 得能 寿子, 大 紘太郎, 篠塚 啓, 谷口 浩二
    第102回 北海道医学大会 腫瘍系分科会 第124回北海道癌談話会例会  2022/10
  • 膵がん細胞集団の捕食機構を利用した高性能ミトコンドリア標的型光がん治療薬の開発  [Not invited]
    高野 勇太, 宮武 由甲子, 山田 勇磨, 繁富 香織
    第7回 北大・部局横断シンポジウム～新領域創成に向けた若手連携の形成～  2021/10
  • Behavior of Tumors with Differences in Malignancy using Micro/Nano Pattern Substrates  [Not invited]
    繁富 香織、宮武 由甲子
    日本機械学会 2021年度年次大会  2021/09  千葉大学
  • マイクロ・ナノ融合パターン基板を用いた微小癌自己組織の構築  [Not invited]
    宮武 由甲子, 繁富(栗林)香織, 太田 悠介
    第 33 回代用臓器・再生医学研究会総会/ 日本バイオマテリアル学会北海道ブロック第 5 回研究会  2021/02
  • New micro-patterned 3D cell culture platform reveals unknown cancer behavior  [Invited]
    Yukiko MIyatake
    The 21st RIES-HOKUDAI International Symposium  2020/12
  • 高野 勇太, 宮武 由甲子, 山田 勇磨, 繁富(栗林)香織
    第6回 北大・部局横断シンポジウム  2020/10
  • 膵管腺癌におけるマイクロ組織レベルの治療抵抗性ダイナミクス  [Not invited]
    太田 悠介, 宮武 由甲子, 繁富 香織, 天野 麻穂, 高橋 利幸, 岡嶋 孝治, 笠原 正典
    第100回 北海道医学大会 腫瘍系分科会（第122回北海道癌談話会例会）  2020/10
  • 宮武 由甲子
    がん教育と健康増進コズモフロンティアセミナー 札幌市立開成中等教育学校  2020/10
  • Chemoresistance dynamics at the microtissue-level in pancreatic ductal adenocarcinoma  [Not invited]
    太田 悠介, 宮武 由甲子, 笠原 正典
    第７９回日本癌学会学術総会  2020/10
  • Visualising the dynamics of live pancreatic microtumours in immune evasion using novel micro-platform  [Invited]
    Yukiko Miyatake
    資生堂サイエンスグラント第12回研究報告会  2020/09
  • 太田 悠介、宮武 由甲子、繁富 香織、大塚 紀幸、田中 敏、笠原 正典
    第１０９回日本病理学会総会  2020/07
  • マイクロ組織レベルのがん研究を可能にする３D細胞組織培養チップの開発  [Invited]
    宮武 由甲子
    札幌医科大学セミナー  2020/02
  • 自己組織化微小癌を誘導できるマイクロ・ナノ基板の開発  [Not invited]
    宮武 由甲子, 繁富(栗林)香織, 太田 悠介, 岡嶋 孝治, 笠原 正典
    第３回がん三次元培養研究会  2019/11
  • 革新的３次元培養デバイスを利用した高性能ミトコンドリア標的型光がん治療薬の開発  [Not invited]
    高野 勇太, 宮武, 由甲子, 山田, 勇麿, 繁富 香織
    第５回北海道大学部局横断シンポジウム  2019/11
  • 初めて見えた！ 生きている悪性新生物の動き～マイクロ・ナノ基板の発明までの道のり～  [Invited]
    宮武 由甲子
    国際ソロプチミスト旭川１０月例会  2019/10
  • 膵癌自己組織化を誘導する新規マイクロ・ナノ基板の開発  [Not invited]
    太田 悠介, 宮武 由甲子, 繁富 香織, 天野 麻穂, 高橋 利幸, 岡嶋 孝治, 笠原 正典
    第99回 北海道医学大会 腫瘍系分科会（第120回北海道癌談話会例会）  2019/10
  • EMTは膵微小癌における組織レベルの挙動に影響する  [Not invited]
    宮武 由甲子, 太田 悠介, 繁富 香織, 天野 麻穂, 高橋 利幸, 岡嶋 孝治, 笠原 正典
    第99回 北海道医学大会 腫瘍系分科会 (第120回北海道癌談話会例会)  2019/10
  • New micro-cell culture platform "micro/nanoplate" induces self-organization of microtumor in PDACs  [Not invited]
    Yusuke Ohta, Yukiko Miyatake, Masanori Kasahara
    The 78th Annual Meeting of the Japanese Cancer Association  2019/09
  • 癌腫瘍組織のダイナミクス観察のためのマイクロ・ナノパターン基板  [Not invited]
    繁富 香織, 宮武 由甲子, 太田 悠介, アグス スバギョ, 末岡 和久, 笠原 正典, 岡嶋 孝治
    第８０回 応用物理学会秋季学術講演会  2019/09
  • マイクロパターン基板上に形成する微小腫瘍のcell-in-cell構造の観察  [Not invited]
    伊藤 一馬, 繁富(栗林) 香織, 宮武 由甲子, アグス スバギョ, 末岡 和久, 岡嶋 孝治
    第８０回 応用物理学会秋季学術講演会  2019/09
  • マイクロナノ基板を用いた癌微小癌自己組織を構築  [Not invited]
    繁富 香織, 太田 悠介, 宮武 由甲子
    2019年度 日本機械学会年次大会  2019/09
  • New micro-cell culture platform "micro/nanoplate" induces self-organization of microtumor in PDACs  [Not invited]
    Yusuke Ohta, Yukiko Miyatake, Kaori Kuribayashi-Shigetomi, Shunji Ikeshita, Agus Subagyo, Kazuhisa Sueoka, Akira Kakugo, Maho Amano, Toshiyuki Takahashi, Takaharu Okajima, Masanori Kasahara
    The 38th Sapporo International Cancer Symposium  2019/07
  • 宮武由甲子
    アカデミックフォーラム  2019/07  東京ビッグサイト  インターフェックス Week 2019
  • New micro -platform “micro/nanoplate” induces self-organization of microtumor in PDACs  [Not invited]
    太田悠介, 宮武由甲子, 池下隼司, 笠原正典
    第108回日本病理学会総会  2019/05
  • 宮武由甲子
    バイオ関連研究シーズ公開会 in 北海道  2019/03  札幌  経済産業省北海道経済産業局
    Download
  • マイクロ・ナノ基板を用いた膵癌腫瘍組織のダイナミクスの可視化  [Not invited]
    太田悠介, 宮武由甲子, 繁富(栗林)香織, 池下隼司, アグス・スバギョ, 末岡和久, 角五 彰, 天野麻穂, 高橋利幸, 岡嶋孝治, 笠原正典
    第４回北海道大学部局横断シンポジウム  2019/01
  • マイクロナノバイオデバイスによる膵癌オルガノイドのダイナミクス解析  [Not invited]
    宮武由甲子, 繁富(栗林)香織
    化学とマイクロ・ナノシステム学会主催 第38 回研究会  2018/11
    Download
  • 膵管腺癌細胞の細胞集団化における遺伝子プロファイルの臨床的関連性の検討  [Not invited]
    太田悠介, 宮武由甲子, 池下隼司, 笠原正典
    第98回北海道医学大会（第51回北海道病理談話会）  2018/10
  • Alteration of gene profiles in anchorage-dependent multicellular aggregates formed by PDAC cells  [Not invited]
    Yusuke Ohta, Yukiko Miyatake, Masanori Kasahara
    The 77th Annual Meeting of the Japanese Cancer Association  2018/09
  • 膵管腺癌細胞における足場依存性多細胞凝集塊（Ad-MCA）形成による難治性形質の誘導  [Not invited]
    太田悠介, 宮武由甲子, 池下隼司, 笠原正典
    第107回日本病理学会総会  2018/06
  • マイクロナノバイオデバイスによって惹起されるがん細胞の自己組織化  [Invited]
    宮武由甲子
    NanoBio第11回若手ネットワーキングシンポジウム  2018/06
  • マイクロナノデバイスによって惹起される微小癌のダイナミクス  [Invited]
    宮武由甲子
    第７回 蛍光イメージング・ミニシンポジウム  2018/06
  • 足場依存性の多細胞凝集塊形成とがん幹細胞特性の獲得  [Invited]
    宮武由甲子
    第5回 細胞凝集研究会  2017/11
  • マイクロナノ基板上に細胞内浸潤によって自己組織化される生きている微小癌のダイナミクス  [Not invited]
    宮武由甲子
    科学技術振興機構(JST) ライフサイエンス系新技術説明会  2017/11
    Download
  • 上皮系フェノタイプを持つ膵癌細胞では細胞分裂時にCD44v9とMDR1の発現が亢進する．  [Not invited]
    池下隼司, 宮武由甲子, 笠原正典
    第74回日本癌学会学術総会  2015/10
  • 膵管腺細胞は細胞分裂時にCD44v9とMDR1の発現を亢進させる．  [Not invited]
    池下隼司, 木内静香, 宮武由甲子, 笠原正典
    第112回北海道癌談話会例会（腫瘍系分科会）  2015/09
  • 上皮系フェノタイプを持った膵癌細胞では細胞分裂時にCD44v9とMDR1の発現が亢進する．  [Not invited]
    池下隼司, 宮武由甲子, 木内静香, 朴鐘建, 大塚紀幸, 笠原正典
    第104回日本病理学会総会  2015/04
  • 膵がん細胞は血管内皮細胞との細胞接触を介してがん幹細胞マーカーを発現する．  [Not invited]
    朴鐘建, 宮武由甲子, 池下隼司, 大塚紀幸, 笠原正典
    第104回日本病理学会総会  2015/04
  • 上皮系ニッチにおいて多細胞凝集塊(MCA)を形成した膵癌細胞は治療抵抗性を獲得する．  [Not invited]
    池下隼司, 宮武由甲子, 朴鐘建, 大塚紀幸, 笠原正典
    第104回日本病理学会総会  2015/04
  • 成人T細胞白血病細胞は多細胞凝集塊の形成によってCD44highがん幹細胞様細胞が出現する．  [Not invited]
    宮武由甲子, Noreen Sheefy, 池下隼司, William W.Hall, 笠原正典
    第104回日本病理学会総会  2015/04
  • CD44 high cancer stem cell-like ATL cells are expanded by anchorage-dependent multicellular aggregate formation through NF-κB signaling．  [Not invited]
    Yukiko Miyatake, Noreen Sheefy,William W.Hall, Masanori Kasahara
    第43回日本免疫学会総会・学術集会  2014/12
  • 成人T細胞白血病細胞の足場依存性multicellular aggregate（MCA）formationによるがん幹細胞様細胞の拡大  [Not invited]
    宮武由甲子, Sheefy Noreen, 池下隼司, Hall William W, 笠原正典
    第47回北海道病理談話会（病理分科会）  2014/10
  • 血管内皮細胞との直接共培養は膵がん細胞にPSF1とCD44variant9の発現を誘導する.  [Not invited]
    朴鐘建, 宮武由甲子, 笠原正典
    第73回日本癌学会学術総会  2014/09
  • 成人T細胞白血病/リンパ腫細胞は足場依存性多細胞凝集塊形成によってCD44強陽性がん幹細胞様特性を獲得する.  [Not invited]
    宮武由甲子, Noreen Sheefy,William W.Hall, 笠原正典
    第73回日本癌学会学術総会  2014/09
  • SKINT1様遺伝子は類人猿では不活性化されているが旧世界猿では機能を保持している.  [Not invited]
    Rania Hassan Mohamed, 須藤洋一, 伊藤靖, 大塚紀幸, 宮武由甲子, 小笠原一誠, 笠原正典
    第23回日本組織適合性学会大会  2014/09
  • 上皮系ニッチに多細胞凝集塊（MCA）を形成した膵癌細胞は治療抗体性を獲得する.  [Not invited]
    池下隼司, 宮武由甲子, 朴鐘建, 大塚紀幸, 笠原正典
    第110回北海道病理談話会例会（腫瘍系分科会）  2014/09
  • ATL細胞はNF-ｋBシグナル経路を介した足場依存性のmulticellular aggregate（MCA）formationによってがん幹細胞様特性を獲得する.  [Not invited]
    宮武由甲子, Noreen Sheefy, 池下隼司, William W. Hall, 笠原正典
    第1回日本HTLV-1学会学術集会  2014/08
  • 成人T細胞白血病／リンパ腫（ATL）細胞は足場依存性multicellular aggregate（MCA）形成によってがん幹細胞様特性を獲得する．  [Not invited]
    宮武由甲子, Noreen Sheefy,William W.Hall, 笠原正典
    第79回日本インターフェロン・サイトカイン学会 学術集会  2014/06
  • 成人T細胞白血病／リンパ腫（ATL）細胞は正常上皮細胞との相互作用によってがん幹細胞化が誘導される．  [Not invited]
    宮武由甲子, Sheefy Noreen. Hall, W.William, 笠原正典
    第103回日本病理学会総会  2014/04
  • 上皮細胞存在下でコロニーを形成した膵癌細胞ではCD44バリアントの発現パターンが変化する．  [Not invited]
    池下隼司, 宮武由甲子, 朴鐘建, 大塚紀幸, 笠原正典
    第103回日本病理学会総会  2014/04
  • 血管内皮細胞との直接共培養は膵癌細胞にがん幹細胞様性質を誘導する．  [Not invited]
    朴鐘建, 宮武由甲子, 池下隼司, 大塚紀幸, 笠原正典
    第103回日本病理学会総会  2014/04
  • Anchorage-dependent multicellular aggregate formation induces a quiescent CD44v8-10 high stem-like phenotype in pancreatic cancer cells  [Not invited]
    Kasahara M, Miyatake Y
    The 4th International Symposium on Carcinogenic Spiral Infection, Immunity, and Cancer  2014/02
  • Normal epithelial cells protect the survival of adult T-cell leukemia/lymphoma cells．  [Not invited]
    Miyatake, Y, Hall, W. W, Kasahara, M
    第42回日本免疫学会学術集会  2013/12
  • Inactivation of Skint1 in hominoids but not in Old World monkeys.  [Not invited]
    Rania Hassan-Mohamed, Sutho Y, Itoh Y, Otsuka N, Miytake Y, Ogasawara K, Kasahara M
    第42回日本免疫学会学術集会  2013/12
  • 膵臓癌とその周囲微小環境における細胞間相互作用の検討．  [Not invited]
    池下隼司, 宮武由甲子, 大塚紀幸, 笠原正典
    第46回北海道病理談話会（病理分科会）  2013/10
  • 成人T細胞白血病細胞の生存における上皮細胞の保護的役割．  [Not invited]
    宮武由甲子, 笠原正典
    第72回日本癌学会学術総会  2013/10
  • 正常上皮細胞は成人T細胞白血病/リンパ腫（ATLL）細胞の生存を保護する  [Not invited]
    宮武由甲子, Hall William W, 笠原正典
    第108回北海道癌談話会例会  2013/09
  • Epithelial cells protect survival of adult T-cell leukemia/lymphoma cells．  [Not invited]
    Miyatake, Y, André L.A. Oliveira, Mohamed Ali Jarboui, Ota, S, Tomaru, U, Teshima, T, William W. Hall, Kasahara, M
    16th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV 2013  2013/06
  • 胎盤形成期におけるNKG2D リガンド発現意義の検討．  [Not invited]
    大塚紀幸, 山本菜見子, 須藤洋一, 宮武由甲子, 笠原正典
    第102回日本病理学会総会  2013/06
  • アテローム性動脈硬化症とヒトNKG2D リガンドMICA/B との関わりについての検討．  [Not invited]
    池下隼司, 宮武由甲子, 大塚紀幸, 外丸詩野, 笠原正典
    第102回日本病理学会総会  2013/06
  • ワークショップ「造血器腫瘍病理学の新展開」成人T 細胞白血病/ リンパ腫（ATLL）の病態における正常上皮細胞の役割．  [Not invited]
    宮武由甲子, Andre L.A.O, Ali, J.M, 太田秀一, 外丸詩野, 豊嶋崇徳, W. W. Hall, 笠原正典
    第102回日本病理学会総会  2013/06
  • Contact with epithelial cells induces cancer stem cell-like properties in adult T-cell leukemia/lymphoma cells．  [Not invited]
    Miyatake, Y, Tomaru, U, Hall, W. W, Kasahara, M
    第41回日本免疫学会学術集会  2012/12
  • Involvement of an NKG2D ligand H60c in epidermal dendritic T cell-mediated wound repair．  [Not invited]
    Mohamed, R. H, Yoshida, S, Miyatake, Y, Otsuka, N, Kasahara, M
    第41回日本免疫学会学術集会  2012/12
  • 上皮細胞は接着している成人T細胞白血病細胞を細胞静止状態にして保護する．  [Not invited]
    宮武由甲子, 外丸詩野, 笠原正典
    第71回日本癌学会学術総会  2012/09
  • 成人T細胞白血病における上皮細胞の潜在的役割．  [Not invited]
    宮武由甲子, L.A. Oliveira Andre, Sheehy Noreen, 大塚紀幸, 外丸詩野, Hall William W, 笠原正典
    第92回北海道医学大会  2012/09
  • 成人T細胞白血病（ATL）の病態における上皮細胞の役割の検討．  [Not invited]
    宮武由甲子, 外丸詩野, Noreen Sheehy, 石津明洋, William W. Hall, 笠原正典
    第101回日本病理学会総会  2012/04
  • Insights into cell-cell interactions between adult T-cell leukemia cells and endothelial cells.  [Not invited]
    Miyatake, Y, Tomaru, U, Oliveira, L.A, Sheehy, N, Hall, W.W, Kasahara, M
    The XXV Symposium of the International Association for Comparative Research on Leukemia and Related Diseases.  2011/09
  • プロテアソーム機能に着目した老化、脂質代謝異常の病態解明  [Not invited]
    外丸詩野, 高橋里美, 宮武由甲子, 小野綾子, 小原次郎, 紺野沙織, 村田茂穂, 田中啓二, 石津明洋, 笠原正典
    第44回北海道病理談話会  2011/09
  • プロテアソームの機能異常による病理作用：脂質代謝や脂肪肝との関連性について  [Not invited]
    高橋里美, 外丸詩野, 合田文, 小野綾子, 小原次郎, 宮武由甲子, 村田茂穂, 田中啓二, 石津明洋, 笠原正典
    第100回日本病理学会  2011/04
  • プロテアソームの機能異常による病理作用  [Not invited]
    高橋里美, 外丸詩野, 小野綾子, 合田文, 鈴木小百合, 宮武由甲子, 小原次郎, 村田茂穂, 田中啓二, 石津明洋, 笠原正典
    第43回北海道病理談話会  2010/10
  • Skewed T cell development in mice with ectopic expression of thymoproteasome.  [Not invited]
    Tomaru, U, Suzuki, S, Ishizu, A, Takahashi, S, Ohara, J, Miyatake, Y, Murata, S, Tanaka, K, Kasahara, M
    14th International Congress of Immunology  2010/08
  • 胸腺プロテアソームの異所性発現によるT 細胞分化の異常  [Not invited]
    鈴木小百合, 外丸詩野, 高橋里美, 小原次郎, 風巻拓, 小野綾子, 宮武由甲子, 村田茂穂, 田中啓二, 石津明洋, 笠原正典
    第99回日本病理学会総会  2010/04

Association Memberships

  • The American Society for Investigative Pathology (ASIP)   日本癌学会   日本免疫学会   日本病理学会   

Research Projects

  • 文部科学省 科学研究費補助金 基盤研究(C)
    Date (from‐to) : 2022/04 -2025/03 
    Author : (代表)宮武 由甲子、(分担)谷口 浩二
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)
    Date (from‐to) : 2021/04 -2025/03 
    Author : (代表)高野 勇太、(分担)宮武 由甲子, 平田 恵理, 山田 勇磨, 繁富 香織
  • 細胞培養器材に関する技術
    北海道大学 産学連携推進機構 特許ライセンス加速度資金
    Date (from‐to) : 2022/09 -2023/03 
    Author : (代表) 宮武 由甲子、(分担)繁富 香織
  • 膵臓がん細胞集団の捕食機構を解明・利用したトロイの木馬型がん治療薬の開発
    日本学術振興会：科学研究費助成事業
    Date (from‐to) : 2021/07 -2023/03 
    Author : (代表)高野 勇太、(連携研究者)宮武 由甲子
  • 細胞培養器材に関する技術
    北海道大学 産学連携推進機構 特許ライセンス加速度資金：
    Date (from‐to) : 2021/09 -2022/08 
    Author : (代表)宮武 由甲子、(分担)繁富 香織
  • 膵がん細胞集団の捕食機構を利用した高性能ミトコンドリア標的型光がん治療薬の開発
    第7回北海道大学部局横断シンポジウム研究助成 金賞：
    Date (from‐to) : 2021/10 -2022/03 
    Author : (代表)高野勇太, (分担)宮武由甲子, 山田勇磨, 繁富(栗林)香織
  • Cancer-on-chipデバイスによる 癌腫瘍組織と創薬開発応用に向けて
    科学技術振興機構（JST）：SCORE大学推進型（拠点都市環境整備型）起業活動支援プログラム
    Date (from‐to) : 2021/07 -2022/03 
    Author : (代表)繁富香織、(分担)宮武由甲子
  • 科博技術振興機構（JST)：研究成果最適展開支援プログラム 令和元年度 A-STEP実証研究タイプ
    Date (from‐to) : 2019/11 -2021/03 
    Author : (代表)宮武由甲子、(分担)繁富 香織
  • 文部科学省：科学研究費補助金 基盤研究(C)
    Date (from‐to) : 2018/04 -2021/03 
    Author : (代表)宮武由甲子
  • マイクロナノバイオデバイスを用いた癌腫瘍組織の免疫回避のダイナミクス
    株式会社 資生堂：第１２回 資生堂 女性研究者サイエンスグラント
    Date (from‐to) : 2019/07 -2020/06 
    Author : (代表)宮武由甲子
  • 北海道大学：第1回若手共同研究助成公募
    Date (from‐to) : 2019/11 -2020/03 
    Author : (代表)高野勇太, (分担)宮武由甲子, 山田勇麿, 繁富香織
  • 科学技術振興機構（JST）：A-STEP機能検証フェーズ 試験研究タイプ
    Date (from‐to) : 2018/09 -2019/08 
    Author : (代表)繁富香織、(分担)宮武由甲子
  • 科学技術振興機構（JST）：地域産学バリュープログラム
    Date (from‐to) : 2017/10 -2018/09 
    Author : (代表)宮武由甲子
  • 文部科学省：科学研究費補助金(基盤研究(C))
    Date (from‐to) : 2014 -2017 
    Author : 宮武 由甲子
  • “静かな癌幹細胞”の発生因子探索におけるグライコミクスの有用性検証
    科学技術振興機構（JST）：第1回マッチングプランナープログラム探索試験
    Date (from‐to) : 2015/10 -2016/09 
    Author : (代表)宮武由甲子
  • 膵癌細胞における癌細胞集合体の細胞間相互作用への影響
    文部科学省：物質・材料研究機構ナノテクノロジープラットフォームセンター試行的利用TypeA
    Date (from‐to) : 2015/10 -2016/03 
    Author : (代表)宮武由甲子
  • がん幹細胞様特性誘導システムを用いた低分子化合物スクリーニング
    AMED 北海道臨床開発機構：橋渡し事業シーズA
    Date (from‐to) : 2015/04 -2016/03 
    Author : (代表)宮武由甲子
  • 膵癌の転移・再発を抑制するための新規分子標的薬候補因子の探索
    公益信託小野がん研究助成基金：小野がん研究助成金
    Date (from‐to) : 2015/04 -2016/03 
    Author : 宮武由甲子
  • 足場依存性多細胞凝集塊によるがん幹細胞様細胞の出現に関与するケモカイン分子の同定
    金沢大学：金沢大学がん進展制御研究所共同研究課題
    Date (from‐to) : 2015/04 -2016/03 
    Author : (代表)宮武由甲子
  • がん幹細胞様特性誘導システムを用いた分子標的薬候補分子の同定
    HOPPERs事業：北海道大学実証研究推進助成事業
    Date (from‐to) : 2014/04 -2015/03 
    Author : (代表)宮武由甲子
  • 文部科学省：科学研究費補助金
    Date (from‐to) : 2011 -2013 
    Author : 宮武 由甲子

Industrial Property Rights

Social Contribution

  • Date (from-to) : 2021/10/13-2021/10/17
    Role : Appearance
    Sponser, Organizer, Publisher  : 札幌市
    Event, Program, Title : NoMaps Conference 2021
    NoMaps Conference 2021 世の中を変えるためのあの手この手 ～大学発研究開発型スタートアップの挑戦～ カンファレンス 知る・学ぶ スタートアップ・起業支援 共創・連携 日時 2021年10月15日（金）18:00～19:00 会場 YouTube 大学等から生まれる叡知を起点に、新しい産業構造の構築をめざす道内大学・高専のネットワーク「HSFC（エイチフォース）」。文科省・JSTのSCORE事業を活用し、スタートアップが生まれる環境をつくっています。今回のカンファレンスは、HSFCのファンド採択案件から、「工学」と「病理学」の異なるジャンルのコラボにフォーカス！専門的な研究の中に、実は世の中をいい方向に変えていく大きなヒントやビジネスの種が詰まっています。ＭＣ＆産学協働マネージャーの解説とともに、プロジェクトの意義やゴールも紹介。新設インキュベーション拠点ＨＸから配信。
  • コズモフロンティアセミナー「がんを知る」
    Date (from-to) : 2020/10/14
    Role : Lecturer
    Sponser, Organizer, Publisher  : 公益財団法人札幌がんセミナー 市立札幌開成中等教育学校
  • Date (from-to) : 2018/09/25
    Role : Informant
    Sponser, Organizer, Publisher  : 北海道大学
    プレスリリース
  • Date (from-to) : 2018/09/19
    Role : Demonstrator Youtube マイクロナノ基板を用いたライブイメージング動画です。

Media Coverage

  • Date : 2020/07/07
    Writer: Other than myself
    Publisher, broadcasting station: 朝日新聞 朝刊 道内版
    Program, newspaper magazine: 朝日新聞社
    Paper 北海道大学の研究者が、がん細胞が集まり腫瘍（しゅよう）組織に成長する様子を立体的に観察できるガラスプレートを開発した。プレートに作った小さな凹凸が細胞を刺激し、成長するのだという。できあがった腫瘍が、ナメクジのように動く姿も確認できた。将来的にはがんなどの新薬開発にも応用できる可能性があるといい、プレートの製品化を目指している。
  • Date : 2020/06/28
    Writer: Other than myself
    Publisher, broadcasting station: 朝日新聞デジタル
    Program, newspaper magazine: 朝日新聞社
    Internet
  • 社会貢献で表彰
    Date : 2019/11/15
    Publisher, broadcasting station: 北海道新聞
    Paper
  • 父を奪ったがん…諦めず研究―北大・宮武さん 資生堂が助成金―
    Date : 2019/07/06
    Publisher, broadcasting station: 北海道新聞
    Paper
  • 体外で増殖するがんを再現 北海道大学助教 宮武由甲子
    Date : 2019/01/25
    Program, newspaper magazine: 日本経済新聞 かがくアゴラ
    Paper がん細胞が動き回りながら成長する様子を体外で再現する技術を、北海道大学の宮武由甲子助教が開発した。病原体など外敵から身を守る免疫細胞の攻撃をがん細胞が回避する仕組みの解明のほか、新たな抗がん剤の開発などに役立つと期待されている。
  • Micro/nanoplate news list
    Date : 2018/11/20
    Publisher, broadcasting station: ネットニュース記事（１～３３）
    Internet 1）2018年10月2日 Asian Scientist Magazine（シンガポール） 「Microtumor Self-Organization, Demystified」 ２）2018年9月26日 Science and Technology Research News (米国） 「New Micro-Platform Reveals Cancer Cells’ Natural Behavior」 ３）2018年9月26日 patient worthy（米国） 「This New Tech Allows Scientists to Observe The Natural Behavior of Pancreatic Cancer Cells」 ４）2018年9月25日 Medgadget（米国） 「Micro-Patterned Cell Culture Platform Reveals Unknown Cancer Behavior」 ５）2018年9月25日 The Tech News（米国） 「Micro-Patterned Cell Culture Platform Reveals Unknown Cancer Behavior」 ６）2018年9月23日 LAB WORLDWIDE（ドイツ） 「Natural Behavior of Cancer Cells Revealed」 ７）2018年9月22日 European Pharmaceutical Review（英国） 「New micro-platform improves understanding of cancer cells」 ８）2018年9月20日 ScienceDaily（米国） 「New micro-platform reveals cancer cells’ natural behavior」 ９）2018年9月20日 Medicine news line（米国） 「Novel micro-platform reveals never-before-seen behaviors of cancer cells」 １０）2018年9月20日 Technology Networks（英国） 「Observing Cancer Cell Behavior」 １１）2018年9月20日 Health Medicine Network（英国） 「New micro-platform reveals cancer cells’ natural behavior」 １２）2018年9月20日 Genetic Engineering ＆ Biotechnology News（GEN)（米国） 「Pancreatic Cancer Therapies May Be Improved through Novel Live-Tumor Imaging Method」 １３）2018年9月20日 GEN Clinical Omics（米国） 「New Live-Tumor Imaging Method Could Speed Pancreatic Cancer Therapy Development」 １４）2018年9月20日 ecancernews (英国） 「New Micro-Platform Reveals Cancer Cells’ Natural Behavior」 １５）2018年9月20日 MEDICA Magazine（ドイツ） 「New Micro-Platform Reveals Cancer Cells’ Natural Behavior」 １６）2018年9月20日 Hercules Therapeutics （香港） 「新的微平台揭示了癌细胞的自然行为」 １７）2018年9月19日 SCIENMAG (英国） 「New Micro-Platform Reveals Cancer Cells’ Natural Behavior」 １８）2018年9月19日 Electronic Component News （ECN)（米国） 「New Micro-Platform Reveals Cancer Cells’ Natural Behavior」 １９）2018年9月19日 Biocompare（米国） 「Novel Tumor-Imaging Technique Developed」 ２０）2018年9月19日 Tunis Daily News (チュニジア) 「Study: New micro-platform reveals cancer cells’ natural behavior」 ２１）2018年9月19日 The Medical News(豪州） 「Novel micro-platform reveals never-before-seen behaviors of cancer cells」 ２２）2018年9月19日 ResearchSEA(英国） 「New micro-platform reveals cancer cells’ natural behavior」 ２３）2018年9月19日 Alpha Galileo（英国） 「New micro-platform reveals cancer cells’ natural behavior」 ２４）2018年9月19日 Udaipur Kiran（インド） 「New micro-platform reveals cancer cells’ natural」 behavior」 ２５）2018年9月19日 Medical Xpress（英国） 「New micro-platform reveals cancer cells’ natural」 behavior」 ２６）2018年9月19日 EurekAlert!（米国） 「New micro-platform reveals cancer cells’ natural behavior」 ２７）2018年9月19日 Bright Surf（英国） 「New micro-platform reveals cancer cells’ natural behavior」 ２８）2018年10月22日 每日頭條（中国） 「距離人類戰勝癌症又進了一步-癌細胞增殖人體外視頻攝製成功」 読売新聞記事（2018年10月17日）の内容
  • Date : 2018/10/18
    Writer: Other than myself
    Publisher, broadcasting station: YAHOO JAPANニュース IT 科学
    Program, newspaper magazine: ヨミドクター
    Internet
  • Date : 2018/10/17
    Publisher, broadcasting station: YOMIURI ONLINE ヨミドクター
    Internet
  • Date : 2018/10/17
    Writer: Other than myself
    Publisher, broadcasting station: YOMIURI ONLINE
    Internet
  • Date : 2018/10/17
    Writer: Other than myself
    Publisher, broadcasting station: 読売新聞 夕刊 全国版
    Program, newspaper magazine: 読売新聞社
    Paper
  • Date : 2018/10/12
    Writer: Other than myself
    Program, newspaper magazine: 北海道医療新聞
    Paper
  • Date : 2018/10/04
    Writer: Other than myself
    Program, newspaper magazine: 日刊工業新聞
    Paper
  • Date : 2018/10/04
    Writer: Other than myself
    Publisher, broadcasting station: 日刊工業新聞電子版
    Program, newspaper magazine: 日刊工業新聞
    Internet
  • Date : 2018/09/19
    Publisher, broadcasting station: Hokkaido University
    Hokkaido University Internet Research Press Release
  • Publisher, broadcasting station: 科学技術振興機構（JST）
    Program, newspaper magazine: JST NEWS 2018年4月号
    Pr

Others

  • 2021/01 Nikon APPLICATION NOTE
    Visualizing the dynamics of pancreatic cancer cells self- organized on the micro/nanoplate
  • 2021/01 ニコン アプリケーションノート
    マイクロナノ基板上に自己組織化する膵がん細胞の動態を可視化
  • 2018/11 マイクロ・ナノ基板開発に関する国内報道まとめ
  • 2018/09 マイクロ・ナノ基板の海外ウェブ報道まとめ

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