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紺谷 桂一 コンタニ ケイイチ

所属
医学部
医学科
職名准教授
Last Updated :2020/09/17

研究者基本情報

学歴

  • 1975年03月 - 現在, 石川県立金沢二水高等学校卒業

学位

  • 医学博士

所属学協会

  • 日本免疫学会
  • 日本癌学会
  • 日本乳癌学会
  • 日本胸部外科学会
  • 日本外科学会

経歴

  •  - 現在, 香川大学医学部呼吸器・乳腺内分泌外科

研究活動情報

研究分野

  • ライフサイエンス / 呼吸器外科学
  • ライフサイエンス / 心臓血管外科学
  • ライフサイエンス / 外科学一般、小児外科学

研究キーワード

    腫瘍学, 腫瘍免疫学, 内分泌外科, 乳腺外科, oncology, tumor immunology, endocrine surgery, breast surgery

論文

  • [Efficacy of TS-1 as a Late-Line Treatment for Metastatic Breast Cancer]., Murazawa C, Kontani K, Hashimoto S, Hashimoto N, Norimura S, Ohtani M, Date M, Yokomise H, Gan to kagaku ryoho. Cancer & chemotherapy, Gan to kagaku ryoho. Cancer & chemotherapy, 46, (9) 1461 - 1463,   2019年09月, [査読有り]
  • [Utility of Prophylactic Administration of Pegfilgrastim in Breast Cancer Chemotherapy]., Norimura S, Kontani K, Morishita A, Kubo T, Murazawa C, Hashimoto S, Hashimoto N, Kenzaki K, Miura K, Yokomise H, Gan to kagaku ryoho. Cancer & chemotherapy, Gan to kagaku ryoho. Cancer & chemotherapy, 45, (12) 1729 - 1732,   2018年12月, [査読有り]
  • Candidate biomarkers predictive of anthracycline and taxane efficacy against breast cancer, Shoko Norimura, Keiichi Kontani, Takako Kubo, Shin-Ichiro Hashimoto, Chisa Murazawa, Koichiro Kenzaki, Dage Liu, Masafumi Tamaki, Fuminori Aki, Kazumasa Miura, Kiyoshi Yoshizawa, Akira Tangoku, Hiroyasu Yokomise, Journal of Cancer Research and Therapeutics, Journal of Cancer Research and Therapeutics, 14, (2) 409 - 415,   2018年01月01日, [査読有り]
  • Hypertension and Proteinuria as Predictive Factors of Effects of Bevacizumab on Advanced Breast Cancer in Japan., Hiroaki Tanaka, Koichi Takahashi, Kazunori Yamaguchi, Keiichi Kontani, Takahiro Motoki, Masato Asakura, Shinji Kosaka, Hiroyasu Yokomise, Hitoshi Houchi, Biological & pharmaceutical bulletin, Biological & pharmaceutical bulletin, 41, (4) 644 - 648,   2018年, [査読有り]
  • Predictive biomarkers and effectiveness of MUC1-targeted dendritic-cell-based vaccine in patients with refractory non-small cell lung cancer, Koji Teramoto, Yoshitomo Ozaki, Jun Hanaoka, Satoru Sawai, Noriaki Tezuka, Shozo Fujino, Yataro Daigo, Keiichi Kontani, THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY, THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY, 9, (3) 147 - 157,   2017年03月, [査読有り]
  • Indication of metronomic chemotherapy for metastatic breast cancer: Clinical outcomes and responsive subtypes., Kontani K, Hashimoto SI, Murazawa C, Norimura S, Tanaka H, Ohtani M, Fujiwara-Honjo N, Date M, Teramoto K, Houchi H, Yokomise H, Molecular and clinical oncology, Molecular and clinical oncology, 4, (6) 947 - 953,   2016年06月, [査読有り]
  • Factors responsible for long-term survival in metastatic breast cancer, Keiichi Kontani, Shin-ichiro Hashimoto, Chisa Murazawa, Shoko Norimura, Hiroaki Tanaka, Masahiro Ohtani, Naomi Fujiwara-Honjo, Manabu Date, Koji Teramoto, Hitoshi Houchi, Hiroyasu Yokomise, WORLD JOURNAL OF SURGICAL ONCOLOGY, WORLD JOURNAL OF SURGICAL ONCOLOGY, 12,   2014年11月, [査読有り]
  • Simultaneous activation of T helper function can augment the potency of dendritic cell-based cancer immunotherapy, Koji Teramoto, Yasuhiko Ohshio, Takuya Fujita, Jun Hanaoka, Keiichi Kontani, JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, 139, (5) 861 - 870,   2013年05月, [査読有り]
  • Ectopic mediastinal parathyroid adenoma: A cause of acute pancreatitis, Hitomi Imachi, Koji Murao, Keiichi Kontani, Hiroyasu Yokomise, Yumi Miyai, Yuka Yamamoto, Yoshio Kushida, Reiji Haba, Toshihiko Ishida, Endocrine, Endocrine, 36, (2) 194 - 197,   2009年10月, [査読有り]
  • Galectin-9, a novel prognostic factor with antimetastatic potential in breast cancer., Yamauchi A, Kontani K, Kihara M, Nishi N, Yokomise H, Hirashima M, The breast journal, The breast journal, 12, (5 Suppl 2) S196 - 200,   2006年09月, [査読有り]
  • Wnt5a expression is associated with the tumor proliferation and the stromal vascular endothelial growth factor - An expression in non-small-cell lung cancer, CL Huang, D Liu, J Nakano, S Ishikawa, K Kontani, H Yokomise, M Ueno, JOURNAL OF CLINICAL ONCOLOGY, JOURNAL OF CLINICAL ONCOLOGY, 23, (34) 8765 - 8773,   2005年12月, [査読有り]
  • Galectin-9 induces maturation of human monocyte-derived dendritic cells., Dai SY, Nakagawa R, Itoh A, Murakami H, Kashio Y, Abe H, Katoh S, Kontani K, Kihara M, Zhang SL, Hata T, Nakamura T, Yamauchi A, Hirashima M, Journal of immunology (Baltimore, Md. : 1950), Journal of immunology (Baltimore, Md. : 1950), 175, (5) 2974 - 2981,   2005年09月, [査読有り]
  • Recovery of parathyroid function after total thyroidectomy: Long-term follow-up study, M Kihara, A Miyauchi, K Kontani, A Yamauchi, H Yokomise, ANZ JOURNAL OF SURGERY, ANZ JOURNAL OF SURGERY, 75, (7) 532 - 536,   2005年07月, [査読有り]
  • Expression of thioredoxin in patients with Graves' disease, M Kihara, K Kontani, A Yamauchi, A Miyauchi, H Nakamura, J Yodoi, H Yokomise, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 15, (5) 795 - 799,   2005年05月, [査読有り]
  • [Two cases of advanced breast cancer responding to oral chemoendocrine therapy with 5'-deoxy-5-fluorouridine, medroxyprogesterone acetate and cyclophosphamide (DMpC)]., Kihara M, Kontani K, Yamauchi A, Yokomise H, Gan to kagaku ryoho. Cancer & chemotherapy, Gan to kagaku ryoho. Cancer & chemotherapy, 32, (5) 683 - 686,   2005年05月, [査読有り]
  • Galectin89 Induces Maturation of Human Monocyte-derived Dendritic Cells, Akira Yamauchi, Shu-Yan Dai, Ryusuke Nakagawa, Yumiko Kashio, Hiroko Abe, Shigeki Katoh, Keiichi Kontani, Mitsuomi Hirashima, Japanese Journal of Clinical Immunology, Japanese Journal of Clinical Immunology, 28, (6) 381 - 388,   2005年, [査読有り]
  • Involvement of 90K/Mac-2 binding protein in cancer metastases by increased cellular adhesiveness in lung cancer, Y Ozaki, K Kontani, K Teramoto, T Fujita, N Tezuka, S Sawai, T Maeda, H Watanabe, S Fujino, T Asai, Ohkubo, I, ONCOLOGY REPORTS, ONCOLOGY REPORTS, 12, (5) 1071 - 1077,   2004年11月, [査読有り]
  • Identification by proteomic analysis of calreticulin as a marker for bladder cancer and evaluation of the diagnostic accuracy of its detection in urine, S Kageyama, T Isono, H Iwaki, Y Wakabayashi, Y Okada, K Kotani, K Yoshimura, A Terai, Y Arai, T Yoshiki, CLINICAL CHEMISTRY, CLINICAL CHEMISTRY, 50, (5) 857 - 866,   2004年05月, [査読有り]
  • Identification of antigenic epitopes recognized by Mac-2 binding protein-specific cytotoxic T lymphocytes for use in cancer immunotherapy, Y Ozaki, K Kontani, K Teramoto, T Fujita, N Tezuka, S Sawai, H Watanabe, S Fujino, T Asai, Ohkubo, I, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 317, (4) 1089 - 1095,   2004年05月, [査読有り]
  • RB1CC1 suppresses cell cycle progression through RB1 expression in human neoplastic cells, K Kontani, T Chano, Y Ozaki, N Tezuka, S Sawai, S Fujino, Y Saeki, H Okabe, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 12, (5) 767 - 769,   2003年11月, [査読有り]
  • Deoxyribonucleic acid (DNA) encoding a pan-major histocompatibility complex class II peptide analogue augmented antigen-specific cellular immunity and suppressive effects on tumor growth elicited by DNA vaccine immunotherapy, K Teramoto, K Kontani, Y Ozaki, S Sawai, N Tezuka, T Nagata, S Fujino, Y Itoh, O Taguchi, Y Koide, T Asai, Ohkubo, I, K Ogasawara, CANCER RESEARCH, CANCER RESEARCH, 63, (22) 7920 - 7925,   2003年11月, [査読有り]
  • Dendritic cell vaccine immunotherapy of cancer targeting MUC1 mucin, K Kontani, O Taguchi, Y Ozaki, J Hanaoka, S Sawai, S Inoue, H Abe, K Hanasawa, S Fujino, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 12, (4) 493 - 502,   2003年10月, [査読有り]
  • Expression and immunogenicity of a tumor-associated antigen, 90K/Mac-2 binding protein, in lung carcinoma - The possibility of its clinical use as a tumor marker anal a target antigen in cancer immunotherapy, Y Ozaki, K Kontani, J Hanaoka, T Chano, K Teramoto, N Tezuka, S Sawai, S Fujino, T Yoshiki, H Okabe, Ohkubo, I, CANCER, CANCER, 95, (9) 1954 - 1962,   2002年11月, [査読有り]
  • Novel vaccination protocol consisting of injecting MUC1 DNA and nonprimed dendritic cells at the same region greatly enhanced MUC1-specific antitumor immunity in a murine model, K Kontani, O Taguchi, Y Ozaki, J Hanaoka, N Tezuka, S Sawai, S Inoue, S Fujino, T Maeda, Y Itoh, K Ogasawara, H Sato, Ohkubo, I, T Kudo, CANCER GENE THERAPY, CANCER GENE THERAPY, 9, (4) 330 - 337,   2002年04月, [査読有り]
  • Identification of RB1CC1, a novel human gene that can induce RB1 in various human cells, T Chano, S Ikegawa, K Kontani, H Okabe, N Baldini, Y Saeki, ONCOGENE, ONCOGENE, 21, (8) 1295 - 1298,   2002年02月, [査読有り]
  • Truncating mutations of RB1CC1 in human breast cancer, Tokuhiro Chano, Keiichi Kontani, Koji Teramoto, Hidetoshi Okabe, Shiro Ikegawa, Nature Genetics, Nature Genetics, 31, (3) 285 - 288,   2002年, [査読有り]
  • Mediastinal cavernous hemangioma in a child: Report of a case, J Hanaoka, S Inoue, S Fujino, K Kontani, S Sawai, N Tezuka, Y Ozaki, K Teramoto, H Kashima, SURGERY TODAY, SURGERY TODAY, 32, (11) 985 - 988,   2002年, [査読有り]

Misc

  • Inhibition of transforming growth factor-β release from tumor cells reduces their motility associated with epithelial-mesenchymal transition, Yasuhiko Ohshio, Koji Teramoto, Masayuki Hashimoto, Shoji Kitamura, Jun Hanaoka, Keiichi Kontani, Oncology Reports, 30, (2), 1000 - 1006,   2013年08月, [査読有り]
    The high level of transforming growth factor-β (TGF-β) in tumor tissue, which is primarily released from tumor cells, helps maintain their metastatic nature and exacerbates the creation of a pro-tumor microenvironment. Although the strategy of targeting TGF-β in cancer therapy has shown promise, its effects remain limited. In the present study, we focused on tumor cells as sources of TGF-β release, and hypothesized that inhibition of their TGF-β release could suppress their epithelial-mesenchymal transition (EMT)-associated metastatic nature and inactivate the induction of suppressor immune cells. To investigate this hypothesis, LLC1 cells, a mouse lung cancer cell line, were cultured with the TGF-β release inhibitor tranilast and the motility of LLC1 cells was examined. Furthermore, to examine whether inhibition of TGF-β release influences the induction of regulatory T (Treg) cells, spleen cells from normal mice were cultured in medium in which LLC1 cells had been cultured with tranilast. The results showed that tranilast inhibited the release of TGF-β1 from LLC1 cells without affecting their proliferation. Inhibition of TGF-β1 release suppressed the invasive activity of LLC1 cells, but enhanced their activity to adhere. mRNA levels of Slug and Twist were decreased in LLC1 cells, whereas levels of E-cadherin were recovered. Treg cells were less frequently induced by medium in which LLC1 cells had been cultured with tranilast. Taken together, inhibition of TGF-β1 release dampens the metastatic nature of LLC1 cells through the downregulation of EMT and possesses the possibility to improve antitumor immune responses through suppression of Treg cell induction. These findings provide a new rationale for development of TGF-β-targeted molecular immunotherapy against cancer.
  • Behavior of Bone Marrow-Derived Cells Following in Vivo Transplantation Differentiation into Stromal Cells with Roles in Organ Maintenance, Osamu Taguchi, Kunio Tsujimura, Keiichi Kontani, Yosuke Harada, Sachiyo Nomura, Hiroshi Ikeda, Akimichi Morita, Hideshi Sugiura, Norio Hayashi, Yasushi Yatabe, Masao Seto, Masae Tatematsu, Toshitada Takahashi, Atsuki Fukushima, AMERICAN JOURNAL OF PATHOLOGY, 182, (4), 1255 - 1262,   2013年04月, [査読有り]
    After injection of green fluorescent protein positive (GFP(+)) bone marrow (BM) cells into lethally irradiated wild-type mice, the organs of the recipient mice [BM transplantation (BMT) mice] were regenerated; however, irradiation of the cecum or spleen (only) blocked their regeneration with loss of injected BM cells. These results suggest that the donor cells first enter the BM and then migrate to the peripheral organs. The maintenance of epithelial structure and function is controlled by interactions between stromal cells and the epithelia; the organ is stable only if the stroma is functioning normally. In BMT mice, intestinal GFP(+) stromal cells were regenerated fairly rapidly although GFP(+) cells were observed only rarely in the intestinal epithelium even if it passes several weeks or months post BMT, indicating that BM-derived stromal cells play a pivotal role in epithelial renewal and are crucial for maintaining organ structure and function. BM-derived cells in the periphery possess a special key to return to the BM and then to migrate to various organs to become resident cells.
  • Metronomic chemotherapy for metastatic breast cancer to prolong time to treatment failure to 12 months or more, 紺谷桂一, 横見瀬裕保, Mol. Clin. Oncol., 1, (2), 225-230,   2013年03月, [査読有り]
  • 術前乳腺MRIにより予定術式が変更された乳癌症例の検討:画像と病理診断が一致した5症例, 紺谷桂一, 法村 尚子, 乳癌の臨床, 26, (1), 67-73,   2011年, [査読有り]
  • Menin, a product of the MENI gene, binds to estrogen receptor to enhance its activity in breast cancer cells: possibility of a novel predictive factor for tamoxifen resistance, Hitomi Imachi, Koji Murao, Hiroaki Dobashi, Mohammad M. Bhuyan, Xueyuan Cao, Keiichi Kontani, Shoko Niki, Chisa Murazawa, Hiroo Nakajima, Norio Kohno, Hiroko Yamashita, Hirotaka Iwase, Shin-ichi Hayashi, Toshihiko Ishida, Akira Yamauchi, BREAST CANCER RESEARCH AND TREATMENT, 122, (2), 395 - 407,   2010年07月, [査読有り]
    Multiple coactivator and corepressor complexes play an important role in endocrine processes and breast cancer; in particular, estrogen and estrogen receptor-alpha (ER alpha) promote the proliferation of breast cancer cells. Menin is a tumor suppressor encoded by Men1 that is mutated in the human-inherited tumor syndrome multiple endocrine neoplasia type 1 (MEN1); it also serves as a critical link in the recruitment of nuclear receptor-mediated transcription. Here, we show that menin expressed in breast cancer cell line MCF-7 is colocalized with ER alpha and functions as a direct coactivator of ER-mediated transcription in breast cancer cells. In MCF-7 cells, coexpression of menin and estrogen-response element-luciferase induced the activity of the latter in a hormone-dependent manner. Cells knocked down for ER alpha exhibited impaired ERE-luciferase activity induced by menin. Mammalian two-hybrid assay and GST pull-down assays indicated that menin could interact with the AF-2 domain of ER alpha. These results indicate that menin is a direct activator of ER alpha function. Tamoxifen inhibited the binding of menin to AF-2 in mammalian two-hybrid assay, but in menin-overexpressing clones, tamoxifen suppressed ERE-luciferase activity only to the levels of nontreated wild-type MCF-7. In a clinical study with 65 ER-positive breast cancer samples-all of which had been treated with tamoxifen for 2-5 years as adjuvant therapies-menin-positive tumors had a worse outcome than menin-negative ones. These indicated that menin can function as a transcriptional regulator of ER alpha and is a possible predictive factor for tamoxifen resistance.
  • Study of the measurement of serum extracellular domain of HER2/neu protein with CLIA method, 紺谷桂一, Rinsho Byori, 58, (6), 541-552,   2010年, [査読有り]
  • Indication for skin-sparing mastectomy with or without nipple preservation for primary breast cancer, 紺谷桂一, 横見瀬裕保, Keiichi Kontani, Hiroyasu Yokomise, Int. Surg., 95, 12-20,   2010年, [査読有り]
  • Inhibition of Transforming Growth Factor-beta-Mediated Immunosuppression in Tumor-Draining Lymph Nodes Augments Antitumor Responses by Various Immunologic Cell Types, Takuya Fujita, Koji Teramoto, Yoshitomo Ozaki, Jun Hanaoka, Noriaki Tezuka, Yasushi Itoh, Tohru Asai, Shozo Fujino, Keiichi Kontani, Kazumasa Ogasawara, CANCER RESEARCH, 69, (12), 5142 - 5150,   2009年06月, [査読有り]
    Tumor-draining lymph nodes (DLN) are the most important priming sites for generation of antitumor immune responses. They are also the location where an immunosuppressive cytokine, transforming growth factor-beta (TGF-beta), plays a critical role in suppressing these antitumor immune responses. We focused on TGF-beta-mediated immunosuppression in DLNs and examined whether local inhibition of TGF-beta augmented antitumor immune responses systemically in tumor-bearing mice models. For inhibition of TGF-beta-mediated immunosuppression in DLNs, C57BL/6 mice subcutaneously bearing E.G7 tumors were administered plasmid DNA encoding the extracellular domain of TGF-beta type II receptor fused to the human IgG heavy chain (TGFR DNA) i.m. near the established tumor. In DLNs, inhibition of TGF-beta suppressed the proliferation of regulatory T cells and increased the number of tumor antigen-specific CD4(+) or CD8(+) cells producing IFN-gamma. Enhancement of antitumor immune responses in DLNs were associated with augmented tumor antigen-specific cytotoxic and natural killer activity in spleen as well as elevated levels of tumor-specific antibody in sera. The growth of the established metastatic as well as primary tumors was effectively suppressed via augmented antitumor immune responses. Inhibition of TGF-beta-mediated immunosuppression in DLNs is significantly associated with augmented antitumor responses by various immunocompetent cell types. This animal model pro-vides a novel rationale for molecular cancer therapeutics targeting TGF-beta. [Cancer Res 2009;69(12):5142-50]
  • CLIAによる血清中HER2/neu蛋白質の測定法, 紺谷桂一, 検査と技術, 37, 446-450,   2009年, [査読有り]
  • 温度応答性培養皿を用いたOK-432誘導成熟樹状細胞培養法の確立, 紺谷桂一, Biotheapy, 22, (5), 339-343,   2008年, [査読有り]
  • Successful tumor eradication was achieved by collaboration of augmented cytotoxic activity and anti-angiogenic effects following therapeutic vaccines containing helper-activating analog-loaded dendritic cells and tumor antigen DNA, Koji Teramoto, Keiichi Kontani, Takuya Fujita, Yoshitomo Ozaki, Satoru Sawai, Noriaki Tezuka, Shozo Fujino, Yasushi Itoh, Osamu Taguchi, Reiji Kannagi, Kazumasa Ogasawara, CANCER IMMUNOLOGY IMMUNOTHERAPY, 56, (3), 331 - 342,   2007年03月, [査読有り]
    We reported previously that pigeon cytochrome c-derived peptides (Pan-IA), which bind broad ranges of MHC class II molecules efficiently, activate T helper (Th) function in mice. In an experimental model, Pan-IA DNA vaccines augmented antitumor immunity in tumor antigen-immunized mice. To elicit more potent antitumor immunity and to eradicate tumors in a therapeutic setting, Pan-IA-loaded dendritic cells (DCs) were inoculated in combination with vaccines including ovalbumin (OVA) antigen DNA in tumor-bearing mice. Seventy percent of the immunized mice survived tumor-free for at least 4 months after treatment. In contrast, mice vaccinated with OVA DNA, either with or without naive DCs, did not eliminate the tumors and died within 5 weeks. Only in mice vaccinated with OVA DNA and Pan-IA-loaded DCs were both cytotoxic and helper responses specific for OVA induced at the spleen and tumor sites as well as at the vaccination sites. Furthermore, accumulation of OVA-specific CD4(+) and CD8(+) T lymphocytes and interferon-gamma-mediated anti-angiogenesis were observed in the tumors of these mice. Thus, the combined vaccination primed both tumor-specific cytotoxicity and helper immunity resulting in augmented tumor lysis ability and anti-angiogenic effects. This is the first report to show that most established tumors were successfully eradicated by collaboration of potent antitumor immunity and anti-angiogenic effects by vaccination with tumor antigens and helper-activating analogs. This novel vaccination strategy is broadly applicable, regardless of identifying helper epitopes in target molecules, and contributes to the development of therapeutic cancer vaccines.
  • Preparation of fully activated dendritic cells capable of priming tumor-specific cytotoxic T lymphocytes in patients with metastatic cancer using penicillin-killed streptococcus pyogenes (OK432) and anti-CD40 antibody., 紺谷桂一, Oncology Report, 17, (4), 895-902,   2007年, [査読有り]
  • Spontaneous elicitation of potent antitumor immunity and eradication of established tumors by administration of DNA encoding soluble transforming growth factor-b II receptor without active antigen-sensitization, K Kontani, K Kajino, CL Huangi, S Fujino, O Taguchi, A Yamauchi, H Yokomise, K Ogasawara, CANCER IMMUNOLOGY IMMUNOTHERAPY, 55, (5), 579 - 587,   2006年05月, [査読有り]
    Since immunity is generally suppressed by immunoregulatory factors, such as transforming growth factor-beta (TGF-beta), interleukin (IL)-10, and vascular endothelial growth factor (VEGF), produced by tumor cells or stromal cells surrounding tumor cells, various kinds of cancer immunotherapy mostly fail to elicit potent antitumor immunity. Herein, we tested whether neutralization of TGF-beta can elicit strong antitumor immune responses and tumor regression in tumor-bearing mice. A plasmid DNA, pcDNA-sTGF beta R/huIg, encoding a fusion protein consisting of the extracellular domain of TGF-beta type II receptor (TGF beta RII) and the Fc portion of human IgG heavy chain, was injected through different routes into B6 mice carrying established tumors of E.G7 cells, which consist of the poorly immunogenic tumor cells EL4, transfected with the ovalbumin (OVA) gene. The frequency of OVA-specific cytotoxic T lymphocytes (CTL), in the treated mice. increased resulting in the tumor eradication and relapse-free survival in around 70% of the E.G7-bearing mice. In contrast, administration of mock DNA into E.G7-bearing mice did not elicit tumor-specific immune responses. Therefore, administration of DNA encoding TGF beta RII allowed tumor-bearing hosts to elicit sufficiently potent antitumor immune responses without requirement of further active antigen-immunization. This strategy seems to be applicable to clinical therapy against cancer, because it is low-cost, safe, and easy to manipulate.
  • Galectin-9 induces maturation of human monocyte-derived dendritic cells., DAI, Syu-Yan, NAKAGAWA, Ryusuke, ITOH, Aiko, MURAKAMI, Hiromoto, KASHIO, Yumiko, ABE, Hiroko, KATOH, Shigeki, KONTANI, Keiichi, KIHARA, Minoru, ZHANG, Shu-Lan, HATA, Toshiyuki, NAKAMURA, Takanori, YAMAUCHI, Akira, HIRASHIMA, Mitsuomi, J. Immunol., 175, 2974?2981,   2005年11月, [査読有り]
  • Autologous dendritic cells or cells expressing both B7-1 and MUC1 can rescue tumor-specific cytotoxic T lymphocytes from MUC1-mediated apoptotic cell death, K Kontani, O Taguchi, T Narita, N Hiraiwa, S Sawai, J Hanaoka, M Ichinose, N Tezuka, S Inoue, S Fujino, R Kannagi, JOURNAL OF LEUKOCYTE BIOLOGY, 68, (2), 225 - 232,   2000年08月
    We attempted to induce MUC1-specific cytotoxic T lymphocytes (CTLs) by mixed-lymphocyte tumor cell culture (MLTC) using two allogeneic MUC1-positive cancer cell lines, T-47D and MCF7. The induced CTLs exhibited MUC1-specific cytotoxicity 16 days after the initial stimulation. However, these CTLs underwent apoptotic death within 16 days. To examine whether the B7-1 molecule is required for the expansion of the responder cells, a B7-1(+)/MUC1(-) cell line was transfected with MUC1 cDNA, and the resulting transfectant was employed as a stimulator in an autologous MLTC. The CTLs exhibited MUC1 specificity but also continued to propagate. In parallel, autologous dendritic cells (DCs) were added to all MLTC containing peripheral blood lymphocytes (PBLs) and the allogeneic MUC1-positive stimulators. The CTLs demonstrated MUC1 specificity and their number increased. This suggests that the B7-1 molecule is required for rescuing CTLs front MUC1-mediated apoptotic death, but not for the induction of MUC1-specific responsiveness. This strategy to obtain the CTLs efficiently may be useful for adoptive immunotherapy against cancer.
  • 癌抗原MUC1ムチンを標的とした樹状細胞ワクチン療法-進行再発乳癌を中心に-, 癌の臨床, 46, (8), 961 - 965,   2000年
  • Involvement of the H1/K1-ATPase alpha subunit as a major antigenic protein in autoimmune gastritis induced by neonatal thymectomy in mice., Clinical and Experimental Immunology, 89, 63 - 69,   1992年

講演・口頭発表等

  • Identification of prognostic factors responsible for long-term survival in metastatic breast cancer, The 11th international conference of the Asian Clinical Oncology Society,   2014年
  • Detection of prognostic factors in metastatic breast cancer from the result comparing clinicopathological factors between long survivors and short survivors, Global Breast Cancer Conference 2013,   2013年
  • 乳癌におけるTrastuzumab効果予測因子, 第112回日本外科学会学術総会,   2012年
  • 当科におけるセンチネルリンパ節陽性例の検討, 第20回日本乳癌学会学術総会,   2012年
  • 転移再発乳癌に対するtime to treatment failure延長を目指した治療戦略, 第20回日本乳癌学会学術総会,   2012年
  • 当院におけるT4M0乳癌の検討, 第20回日本乳癌学会学術総会,   2012年
  • Clinical efficacy of metronomic chemotherapy for advanced or recurrent breast cancer, The 10th international conference of the Asian Clinical Oncology Society,   2012年
  • Clinicopathologic factors involved in positive surgical margins after breast-conserving surgery in patients with primary breast cancer, The 10th international conference of the Asian Clinical Oncology Society,   2012年
  • Clinical use of HER2 extracellular domain as a marker to monitor cancer status and predict the response to anti-cancer treatment in breast cancer, 22nd Biennial Congress of the European Association of Cancer Research,   2012年
  • Trastuzumab+Capecitabineが奏功したHER2陽性進行・再発乳癌4例の検討, 第9回日本乳癌学会中国四国地方会,   2012年
  • Paget病と髄様癌を併発した1症例, 第9回日本乳癌学会中国四国地方会,   2012年
  • HER2強陽性進行・再発転移乳癌に対するtrastuzumab効果予測因子の探索, 第19回日本乳癌学会学術総会,   2011年
  • Clinicopathologic factors that predict responses to trastuzumab in HER2-overecpressed breast cancer, Global Breast Cancer Conference 2011,   2011年
  • Clinicopathologic assessments and postoperative outcomes of patients with positive surgical margins who underwent breast-conserving surgery for primary breast cancer, Global Breast Cancer Conference 2011,   2011年
  • 乳癌薬物治療の変遷とバイオマーカーの役割, 第50回日本薬剤師会・日本薬剤師会中国四国支部学術大会,   2011年
  • Clinicopathologic factors that predict responses to trastuzumab in HER2-overecpressed breast cancer, Global Breast Cancer Conference 2011,   2011年
  • Clinicopathologic assessments and postoperative outcomes of patients with positive surgical margins who underwent breast-conserving surgery for primary breast cancer, Global Breast Cancer Conference 2011,   2011年
  • バイオマーカーとしてのHER2細胞外ドメインの臨床応用, 第18回日本乳癌学会学術総会,   2010年
  • ハーセプチンとゼローダ併用治療が無効であったがTS-1変更により著効を示した再発乳癌の1症例, 第18回日本乳癌学会学術総会,   2010年
  • HER2強陽性乳癌に対するTrastuzumabの治療効果に関する検討, 第18回日本乳癌学会学術総会,   2010年
  • 高感度乳癌腫瘍マーカーの開発, 第18回日本乳癌学会学術総会,   2010年
  • 乳癌における可溶性HER2分子の腫瘍マーカーとしての臨床応用, 第109回日本外科学会定期学術集会,   2009年
  • 乳癌に対するカペペシタビンの適応:当科使用経験からの検討, 第17回日本乳癌学会学術総会,   2009年
  • Clinical use of serum HER2/neu level as a tumor marker in breast cancer, 7th biennial meeting of the Asian Breast Cancer Society,   2009年
  • Wnt signal pathways are down-regulated by MRP-1/CD9 gene transduction, 96th Annual Meeting of American Association for Cancer Research,   2005年
  • MRP-1/CD9遺伝子導入によるWntシグナル抑制, 第64回日本癌学会学術総会,   2005年
  • Clinical application of biological markers for treatments of non-small cell lung cancer patients, 9th World Congress on Advances in Oncology,   2004年

競争的資金

  • 癌免疫療法に関する研究
  • Development of Cancer Immunotherapy
  • 腫瘍免疫学、癌免疫治療の開発、癌抑制遺伝子解析
  • tumor immunology, oncology