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  日本消化器内視鏡学会

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  日本臨床血液学会

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  肝臓

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  日本消化器病学会

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  日本内科学会

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• 札幌医科大学   医学部 医学科 内科学第四講座   大学院生  

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• Increased mitochondrial apoptotic priming of human regulatory T cells after allogeneic hematopoietic stem cell transplantation

  Kazuyuki Murase, Haesook T. Kim, O. R. Gregory Bascug, Yutaka Kawano, Jeremy Ryan, Ken-ichi Matsuoka, Matthew S. Davids, John Koreth, Vincent T. Ho, Corey Cutler, Philippe Armand, Edwin P. Alyea, Bruce R. Blazar, Joseph H. Antin, Robert J. Soiffer, Anthony Letai, Jerome Ritz

  HAEMATOLOGICA ( FERRATA STORTI FOUNDATION )  99 ( 9 ) 1499 - 1508  2014年09月  [査読有り]

  　概要を見る

  CD4 regulatory T cells play a critical role in establishment of immune tolerance and prevention of graft-versus-host disease after allogeneic hematopoietic stem cell transplantation. The recovery and maintenance of regulatory T cells is dependent on homeostatic factors including the generation of naive regulatory T cells from hematopoietic precursor cells, the proliferation and expansion of mature regulatory T cells, and the survival of regulatory T cells in vivo. In this study, quantitation of mitochondrial apoptotic priming was used to compare susceptibility of regulatory T cells, conventional CD4 T cells and CD8 T cells to intrinsic pathway apoptosis in 57 patients after allogeneic hematopoietic stem cell transplantation and 25 healthy donors. In healthy donors, regulatory T cells are more susceptible to mitochondrial priming than conventional T cells. Mitochondrial priming is increased after hematopoietic stem cell transplantation in all T-cell subsets and particularly in patients with chronic graft-versus-host disease. Regulatory T cells express high levels of CD95 and are also more susceptible than conventional T cells to apoptosis through the extrinsic pathway. However, CD95 expression and extrinsic pathway apoptosis is not increased after hematopoietic stem cell transplantation. Decreased expression of BCL2 and increased expression of BIM, a mitochondrial cell death activator protein, in regulatory T cells contributes to increased mitochondrial priming in this T-cell subset but additional factors likely contribute to increased mitochondrial priming following hematopoietic stem cell transplantation.

  DOI PubMed

• Effective Treatment of Metastatic Rhabdomyosarcoma with Pazopanib

  Akari Hashimoto, Kohichi Takada, Rishu Takimoto, Hiroto Horiguchi, Tsutomu Sato, Satoshi Iyama, Kazuyuki Murase, Kaoru Ono, Ayumi Tatekoshi, Tsuyoshi Hayashi, Koji Miyanishi, Yasushi Sato, Masayoshi Kobune, Yasuo Hirayama, Hiroshi Kitamura, Katsuya Nakanishi, Naoya Masumori, Tadashi Hasegawa, Junji Kato

  Japanese Journal of Cancer and Chemotherapy ( Japanese Journal of Cancer and Chemotherapy Publishers Inc. )  41 ( 8 ) 1041 - 1044  2014年08月  [査読有り]

  　概要を見る

  Pazopanib, an oral tyrosine kinase inhibitor, is the first molecular-Targeted agent approved for the treatment of advanced soft tissue sarcoma (STS). Rhabdomyosarcoma in adults is rare, accounting for less than 3% of all adult STS cases. A 57-year-old woman presented with cervical lymphadenopathy. Computed tomography revealed a heterogeneous mass in the retro-peritoneum, replacing the entire right kidney. On the basis of the above findings, the patient was diagnosed with alveolar rhabdomyosarcoma. She was first treated with 4 courses of vincristine, actinomycin D, and cyclophosphamide (VAC), which resulted in a partial response. Dose reduction and delay occurred owing to hematological toxicity and febrile neutropenia. As second-line chemotherapy, the patient was administered a single daily dose of 800 mg of pazopanib. Because of an episode of hand-foot syndrome and hepatic impairment, the 800-mg daily dose of pazopanib was reduced to a daily dose of 600 mg, which had to be further reduced to a daily dose of 400 mg owing to fatigue and anorexia. The patient maintained a partial response for a total of 4.3 months when treated with pazopanib. Therefore, this drug may be a new treatment option for patients showing metastatic STS after previous chemotherapy.

  PubMed

• Activated Hepatic Stellate Cells Are Dependent on Self-collagen, Cleaved by Membrane Type 1 Matrix Metalloproteinase for Their Growth

  Naoko Kubo Birukawa, Kazuyuki Murase, Yasushi Sato, Akemi Kosaka, Akihiro Yoneda, Hiroki Nishita, Ryosuke Fujita, Miyuki Nishimura, Takafumi Ninomiya, Keiko Kajiwara, Miyono Miyazaki, Yusuke Nakashima, Sigenori Ota, Yuya Murakami, Yasunobu Tanaka, Kenjiro Minomi, Yasuaki Tamura, Yoshiro Niitsu

  JOURNAL OF BIOLOGICAL CHEMISTRY ( AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC )  289 ( 29 ) 20209 - 20221  2014年07月  [査読有り]

  　概要を見る

  Stellate cells are distributed throughout organs, where, upon chronic damage, they become activated and proliferate to secrete collagen, which results in organ fibrosis. An intriguing property of hepatic stellate cells (HSCs) is that they undergo apoptosis when collagen is resolved by stopping tissue damage or by treatment, even though the mechanisms are unknown. Here we disclose the fact that HSCs, normal diploid cells, acquired dependence on collagen for their growth during the transition from quiescent to active states. The intramolecular RGD motifs of collagen were exposed by cleavage with their own membrane type 1 matrix metalloproteinase (MT1-MMP). The following evidence supports this conclusion. When rat activated HSCs (aHSCs) were transduced with siRNA against the collagen-specific chaperone gp46 to inhibit collagen secretion, the cells underwent autophagy followed by apoptosis. Concomitantly, the growth of aHSCs was suppressed, whereas that of quiescent HSCs was not. These in vitro results are compatible with the in vivo observation that apoptosis of aHSCs was induced in cirrhotic livers of rats treated with siRNAgp46. siRNA against MT1-MMP and addition of tissue inhibitor of metalloproteinase 2 (TIMP-2), which mainly inhibits MT1-MMP, also significantly suppressed the growth of aHSCs in vitro. The RGD inhibitors echistatin and GRGDS peptide and siRNA against the RGD receptor alpha V beta 1 resulted in the inhibition of aHSCs growth. Transduction of siRNAs against gp46, alpha V beta 1, and MT1-MMP to aHSCs inhibited the survival signal of PI3K/AKT/I kappa B. These results could provide novel antifibrosis strategies.

  DOI PubMed

• Narrowband ultraviolet B phototherapy ameliorates acute graft-versus-host disease by a mechanism involving in vivo expansion of CD4+CD25+Foxp3+regulatory T cells

  Satoshi Iyama, Kazuyuki Murase, Tsutomu Sato, Akari Hashimoto, Ayumi Tatekoshi, Hiroto Horiguchi, Yusuke Kamihara, Kaoru Ono, Shohei Kikuchi, Kohichi Takada, Yutaka Kawano, Tsuyoshi Hayashi, Koji Miyanishi, Yasushi Sato, Rishu Takimoto, Masayoshi Kobune, Satoru Mori, Junji Kato, Toshiharu Yamashita, Junji Kato

  INTERNATIONAL JOURNAL OF HEMATOLOGY ( SPRINGER JAPAN KK )  99 ( 4 ) 471 - 476  2014年04月  [査読有り]

  　概要を見る

  Narrowband ultraviolet B phototherapy (NB-UVB) is a therapeutic alternative for haematopoietic stem cell transplantation-related skin graft-versus-host disease (GVHD). The beneficial effects of this intervention may be induced by direct irradiation of inflammatory cells in the skin; however, the putative involvement of indirect effects on systemic immunity has not been elucidated. To address this issue, 11 acute skin GVHD patients refractory to standard corticosteroid treatment and with no gut/liver involvement were treated with NB-UVB irradiation. The median number of treatments was 10 times, with a mean cumulative exposure of 6.36 J/cm(2). No other immunosuppressive therapy was initiated during irradiation. Eight patients achieved an objective complete response, two had a partial response, and one showed no change. None of the patients experienced progressive skin GVHD or newly diagnosed gut/liver GVHD. NB-UVB was well tolerated, with no patients discontinuing irradiation due to toxicity. We additionally demonstrated by flow cytometry that NB-UVB irradiation induces the increment of the proportion of regulatory T cell (Tregs) in patients' peripheral blood. These results suggest that NB-UVB may exert beneficial effects on steroid-refractory skin GVHD through the expansion of Tregs.

  DOI PubMed

• Combination chemotherapy of azacitidine and cetuximab for therapy-related acute myeloid leukemia following oxaliplatin for metastatic colorectal cancer

  Akari Hashimoto, Kohichi Takada, Hiroto Horiguchi, Tsutomu Sato, Satoshi Iyama, Kazuyuki Murase, Yusuke Kamihara, Kaoru Ono, Ayumi Tatekoshi, Tsuyoshi Hayashi, Koji Miyanishi, Yasushi Sato, Tomohisa Furuhata, Masayoshi Kobune, Rishu Takimoto, Koichi Hirata, Junji Kato

  Case Reports in Oncology ( S. Karger AG )  7 ( 2 ) 316 - 322  2014年03月  [査読有り]

  　概要を見る

  Therapy-related leukemia (TRL) has been reported to occur after treatment with alkylating agents and/or topoisomerase II inhibitors. Oxaliplatin (OXP) is used as a key drug for the treatment of colorectal cancer (CRC). Cisplatin and carboplatin have been linked with TRL, but the involvement of OXP is questionable. A 74-year-old male was diagnosed with peritoneal metastasis from CRC in July 2011. The patient received nine cycles of 5-fluorouracil (5-FU), leucovorin (LV), and OXP (mFOLFOX-6 regimen) and three cycles of 5-FU and LV only, resulting in a clinical complete response. However, recurrence of CRC was detected by CT within 3 months after the last course of chemotherapy. In April 2013, laboratory tests showed pancytopenia and 15% blast cells. A bone marrow examination revealed multilineage dysplasia and 20.4% myeloblasts. Cytogenetic analysis indicated a complex karyotype that included chromosome 5 and 7 abnormalities. The patient was diagnosed with TRL and treated with a combination of azacitidine (AZA) and cetuximab (Cmab) for both cancers. AZA might be useful in TRL when a patient needs to be treated simultaneously for more than one primary cancer because of its low toxicity. Moreover, Cmab is an effective therapeutic tool in TRL patients with metastatic CRC with the wild-type K-ras gene.

  DOI PubMed

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• P-0322 多発性骨髄腫に対するレナリドミド療法の有害事象の解析と薬剤管理指導(一般演題 ポスター発表,がん薬物療法(その他),Enjoy Pharmacists' Lifestyles)

  中村 勝之, 野田 師正, 安井 寛, 池田 博, 林 敏昭, 石田 禎夫, 篠村 恭久, 村瀬 和幸, 井山 諭, 佐藤 勉, 瀧本 理修, 小船 雅義, 加藤 淳二, 中田 浩雅, 宮本 篤

  日本医療薬学会年会講演要旨集 ( 日本医療薬学会 )  21   235 - 235  2011年09月

  CiNii

• 症例 壊疽性膿皮症を合併した骨髄異形成症候群の2例

  村瀬 和幸, 佐藤 勉, 瀧本 理修

  内科 ( 南江堂 )  108 ( 3 ) 558 - 560  2011年09月

  CiNii

• 潰瘍性大腸炎の治療経過中に骨髄異形成症候群を発症しシクロスポリンが奏功した1例

  高橋 祥, 佐藤 康史, 佐川 保, 田中 信悟, 村瀬 和幸, 高田 弘一, 井山 諭, 佐藤 勉, 瀧本 理修, 小船 雅義, 黒岩 巌志, 平山 眞章, 岡本 哲郎, 加藤 淳二

  日本消化器病學會雜誌 = The Japanese journal of gastro-enterology ( The Japanese Society of Gastroenterology )  108 ( 8 ) 1405 - 1412  2011年08月

  　概要を見る

  症例は64歳，男性．前医にて全大腸炎型潰瘍性大腸炎（UC）重症と診断され，経口PSL 45mg，5-ASA 3gを併用し治療開始．高アミラーゼ血症をきたしPSLを減量されたところ，20mg/日の時点で病状の再燃と血小板減少が出現し，その後大量下血による出血性ショックをきたし搬送された．サイトメガロウイルス（CMV）antigenemiaに対する抗ウイルス療法と，UCに対するシクロスポリン（CsA）持続静注にて下血も改善し，血小板も改善傾向であった．その後急性腎不全から心不全をきたし，一時集中治療室管理となるも全身管理にて改善した．経過中CsA濃度低下とともに白血球減少が出現，骨髄生検にて低形成骨髄で，かつ，2血球系統以上の異型細胞を認め，芽球が5.1％を占めることから骨髄異形成症候群（MDS；RAEB-1）と診断された．CsAの血中濃度維持によりUCとMDSの病状はともに安定した．

  DOI CiNii

• 食道癌に対する化学放射線療法後に難治性胸水として発症した結核性胸膜炎の1例

  平川 昌宏, 佐藤 康史, 大沼 啓之, 佐川 保, 石渡 裕俊, 村瀬 和幸, 井山 諭, 林 毅, 佐藤 勉, 宮西 浩嗣, 小船 雅義, 瀧本 理修, 加藤 淳二

  日本消化器病學會雜誌 = The Japanese journal of gastro-enterology ( The Japanese Society of Gastroenterology )  108 ( 2 ) 231 - 237  2011年02月

  　概要を見る

  75歳，男性．前医で食道癌stage IVaに対し化学放射線療法（CRT）を施行され完全奏効が得られたが，照射野外食道に再発し精査加療目的で当科紹介となった．入院後左胸水の増加を認め，最終的に胸腔鏡下生検にて結核性胸膜炎と診断した．CRT後の胸水に対しては，その成因によって治療が大きく異なり，的確な診断を行うことが必要である．特に結核既往歴のある患者では結核性胸膜炎の発症にも注意を要すると考えられた.

  DOI PubMed CiNii

• 抗体薬 ゲムツズマブ オゾガマイシン (分子標的治療薬--最新の選び方・使い方) -- (がん分子標的治療薬の使い方)

  佐藤 勉, 村瀬 和幸, 加藤 淳二

  がん治療レクチャー ( 総合医学社 )  2 ( 2 ) 272 - 274  2011年

  CiNii

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