研究者詳細 - 赤塚　美樹

講演・口頭発表等 - 赤塚　美樹

分割表示 109 件中 61 - 80 件目／全件表示 >>

第1選択R-CHOP療法が濾胞性リンパ腫患者の免疫に及ぼす影響(Effects of 1st line R-CHOP on the immunity in patients with follicular lymphoma)

Ito Kaori, Okamoto Masataka, Terazawa Tomohiko, Kakumae Yukiko, Okamoto Akinao, Inaguma Yoko, Tokuda Masutaka, Yanada Masamitsu, Morishima Satoko, Kanie Tadaharu, Yamamoto Yukiya, Akatsuka Yoshiki, Mizuta Shuichi, Yamada Shigeki, Emi Nobuhiko

臨床血液 2013年9月 (一社)日本血液学会-東京事務局

当院診療部門における輸血管理状況

荒川章子, 長谷川勝俊, 高須賀広久, 倉橋美千代, 杉浦縁, 村山元秀, 内田由香, 松浦秀哲, 村松知佳, 磯貝聡江, 赤塚美樹, 恵美宣彦

日本輸血細胞治療学会誌 2013年4月 (一社)日本輸血・細胞治療学会

リツキシマブの開発前後の無作為に選んだDLBCL患者の治療成績の違い(Differences in outcome for unselected patients with DLBCL before and after the advent of rituximab)

Okamoto Akinao, Yanada Masamitsu, Inaguma Yoko, Tokuda Masutaka, Morishima Satoko, Kanie Tadaharu, Yamamoto Yukiya, Tuzuki Motohiro, Akatsuka Yoshiki, Shuichi Mizuta, Okamoto Masataka, Emi Nobuhiko

臨床血液 2012年9月 (一社)日本血液学会-東京事務局

NUP98-HOXA9のAML再発患者に見られたt(11;12)(q13;p13)の追加よるETV6-LPXN融合遺伝子(ETV6-LPXN fusion from additional t(11;12) (q13;p13) in a patient relapsing with AML with NUP98-HOXA9)

Akihiro Abe, Kanie Tadaharu, Yamamoto Yukiya, Okamoto Akinao, Tokuda Masutaka, Inaguma Yoko, Yanada Masamitsu, Morishima Satoko, Akatsuka Yoshiki, Mizuta Syuichi, Okamoto Masataka, Emi Nobuhiko

臨床血液 2012年9月 (一社)日本血液学会-東京事務局

当院で検出された抗K抗体の1症例

杉浦縁, 長谷川勝俊, 高須賀広久, 倉橋美千代, 荒川章子, 村山元秀, 内田由香, 松浦秀哲, 村上優佳, 赤塚美樹, 恵美宣彦

日本輸血細胞治療学会誌 2012年4月 (一社)日本輸血・細胞治療学会

劇症型心筋炎に免疫グロブリン大量療法が奏効した1症例

松浦秀哲, 長谷川勝俊, 高須賀広久, 倉橋美千代, 杉浦縁, 荒川章子, 村山元秀, 内田由香, 村上優佳, 赤塚美樹, 恵美宣彦

日本輸血細胞治療学会誌 2012年4月 (一社)日本輸血・細胞治療学会

当科でのDIC症例に関する検討(Single center analysis of DIC with hematological malignancy)

稲熊容子, 岡本晃直, 徳田倍将, 柳田正光, 森島聡子, 蟹江匡治, 山本幸也, 都築基弘, 赤塚美樹, 水田秀一, 岡本昌隆, 恵美宣彦

Thrombosis Medicine 2012年3月 (株)先端医学社

当院におけるPBSCの現状

杉浦縁, 長谷川勝俊, 倉橋美千代, 村山元秀, 七ツ村めぐみ, 水田秀一, 赤塚美樹, 恵美宣彦

日本輸血細胞治療学会誌 2012年2月25日

Intracellular interferon-γ staining analysis of donor-specific t-cell responses in liver transplant recipients

Y. Okanami, K. Tsujimura, S. Mizuno, M. Tabata, S. Isaji, Y. Akatsuka, K. Kuzushima, T. Takahashi, S. Uemoto

Transplantation Proceedings 2012年

血液悪性腫瘍を伴うDICに関する単施設での解析(Single center analysis of DIC with hematologicalmalignancy)

Inaguma Yoko, Okamoto Akinao, Tokuda Masutaka, Yanada Masamitsu, Morishima Satoko, Kanie Tadaharu, Yamamoto Yukiya, Tsuzuki Motohiro, Akatsuka Yoshiki, Mizuta Shuichi, Okamoto Masataka, Emi Nobuhiko

臨床血液 2011年9月 (一社)日本血液学会-東京事務局

FLT3シグナル伝達を直接調節するヒト単クローン抗体の分離(Isolation of human monoclonal antibodies directly modulating FLT3 signaling)

Yamamoto Yukiya, Tsuzuki Sachiko, Akahori Yasushi, Ukai Yoshinori, Sumitomo Mariko, Tokuda Masutaka, Kanie Tadaharu, Abe Akihiro, Akatsuka Yoshiki, Kurosawa Yoshikazu, Emi Nobuhiko

臨床血液 2011年9月 (一社)日本血液学会-東京事務局

Deferasiroxを投与したMDS患者2例における造血に及ぼす好ましい効果(Positive effects on hematopoiesis in two patients with MDS receiving deferasirox)

Tsuzuki Motohiro, Inaguma Youko, Okamoto Akiao, Tokuda Masutaka, Yanada Masamitsu, Morishima Satoko, Kanie Tadaharu, Yamamoto Yukiya, Akatsuka Yoshiki, Mizuta Shuichi, Okamoto Masataka, Emi Nobuhiko

臨床血液 2011年9月 (一社)日本血液学会-東京事務局

マイナー組織適合抗原の重要性招待有り国際会議

赤塚　美樹

第33回日本造血細胞移植学会

当院における輸血関連インシデント事例の検討

松浦秀哲, 長谷川勝俊, 倉橋美千代, 杉浦縁, 荒川章子, 村山元秀, 内田由香, 七ツ村めぐみ, 村上優佳, 高須賀広久, 富井榮江, 赤塚美樹, 恵美宣彦

日本輸血細胞治療学会誌 2011年3月 (一社)日本輸血・細胞治療学会

臍帯血移植後にオセルタミビル耐性新型インフルエンザ(H1N1)感染により死亡した成人APLの1例

都築基弘, 半田幸助, 稲熊容子, 徳田倍将, 長谷川明生, 森島聡子, 蟹江匡治, 山本幸也, 赤塚美樹, 水田秀一, 岡本昌隆, 恵美宣彦

日本造血細胞移植学会総会プログラム・抄録集 2011年

末梢血CD34陽性細胞とCD34陽性細胞収量の相関

杉浦縁, 水田秀一, 長谷川勝俊, 倉橋美千代, 荒川章子, 村山元秀, 七ツ村めぐみ, 内田由香, 村上優佳, 高須賀広久, 富井栄江, 赤塚美樹, 恵美宣彦, 恵美宣彦

日本輸血細胞治療学会誌 2010年4月28日

低悪性度B細胞リンパ腫に対するFludarabinおよびRituximab‐Fludarabin療法の有害事象;免疫機能に与える影響を中心に

熊澤里美, 岡本昌隆, 伊藤佳織, 稲熊容子, 太田秀基, 山本幸也, 都築基弘, 水田秀一, 赤塚美樹, 丸山文夫, 矢野裕章, 恵美宣彦

日本臨床腫瘍学会学術集会プログラム・抄録集 2010年

造血幹細胞移植と組織適合性抗原同種造血幹細胞移植とマイナー組織適合性抗原招待有り国際会議

赤塚　美樹

第18回日本組織適合性学会

網羅的ゲノム解析によるB細胞性リンパ腫における標的遺伝子A20の同定

加藤元博, 真田昌, 加藤格, 佐藤康晴, 滝田順子, 竹内賢吾, 丹羽明, 陳玉彦, 中崎久美, 野本順子, 朝倉義崇, 赤塚美樹, 林泰秀, 五十嵐隆, 黒川峰夫, 千葉滋, 森茂郎, 石川雄一, 岡本康司, 飛内賢正, 中釜斉, 中畑龍俊, 吉野正, 小林幸夫, 小川誠司

日本リンパ網内系学会会誌 2009年6月 (一社)日本リンパ網内系学会

Genome-Wide Association Studies of Genetic Incompatibility That Is Relevant to the Development of GvHD in Unrelated Bone Marrow Transplantation 国際会議

Seishi Ogawa, Aiko Matsubara, Koichi Kashiwase, Makoto Onizuka, Masashi Sanada, Motohiro Kato, Yasuhito Nannya, Yoshiki Akatsuka, Takakazu Kawase, Masahiro Satake, Junko Takita, Yasuo Morishima, Shigeru Chiba, Hiroo Saji, Hidetoshi Inoko, Yoshihisa Kodera, Takehiko Sasazuki

Blood 2008年11月16日 American Society of Hematology

開催年月日： 2008年11月

記述言語：英語会議種別：口頭発表（一般）

<title>Abstract</title>
Allogeneic stem cell transplantation (allo-SCT) is one of the most effective therapeutic options for blood cell cancers. While its major anti-leukemic benefits are obtained from allo-immune reactions against leukemic cells, or GVL, the same kind of allo-reactions could be also directed to normal host tissues, giving rise to a severe complication, know as graft versus host disease (GvHD). In HLA-matched transplantation, the development of both reactions absolutely depends on the presence of one or more mismatched minor histocompatibility antigens (mHAgs) and could be further modified by other genetic as well as environmental factors, including for example, cytokine polymorphisms and GvHD prophylaxis. Thus, in view of better preventing GvHD and specifically targeting allo-immunity to the tumor component, it is critical to understand what mHAgs are mismatched and responsible for the development of GVHD or GVL and what genetic factors can influence the overall reactions. To address these questions, we conducted whole genome association studies by genotyping more than 500,000 SNPs in donors and recipients of 1598 unrelated transplants from Japan Marrow Donation Program (JMDP). All transplants were matched for HLA-A, B, C, DRB1 and DQB1, while 1033 (63%) transplants were mismatched for HLA-DPB1. 656 (41.7%) and 245 (14.9%) of transplants had developed grade II–IV and III–IV of acute GvHD (aGvHD), respectively. Overall call rates exceeded 98% both in donors and in recipients. Unobserved HapMap PhaseII SNPs were rigorously imputed using genotyped SNPs. After excluding those SNPs showing <95% call rate, deviation from Hardy-Weinberg equilibrium, or <5% minor allele frequency, 1,276,699 SNPs were tested for association with development of acute and chronic GvHD, relapse, and overall survival, by calculating LogRank statistics for each SNP according to single genotypes in donors and recipients or based on mismatch in genotypes between donor and recipient. Statistical thresholds for genome-wide-P value of 0.05 were determined empirically by doing 1,000 permutations for each analysis. In the analysis of mismatched genotypes, SNPs around the HLA-DPB1 locus uniquely showed a strong association with the development of >grade II aGvHD with the maximum P-value of 1.81 × 10−9 at rs6937034, and thus, successfully captured the association of DPB1 allele mismatch as directly defined by HLA typing (HR = 1.91, P= 2.88 × 10−13). To facilitate the identification of target mHAgs for aGvHD, we performed subgroup analysis, where association tests were confined to those transplants sharing particular HLA types based on the fact that recognition of mHAgs is restricted to particular HLA contexts (HLA restriction). Six loci was identified as candidate mHAg loci whose mismatch may confer increased risk for development of aGvHD. These included rs17473423 on chr12 associated with an A*2402/B*5201/Cw*1202/DRB1*1501/DQB1*0601 allele set shared in ~40% of unrelated transplants in Japanese (grade III–IV aGvHD with maximum P=3.99 × 10−13), rs9657655 on chr9 associated with another common allele in Japanese, A*3303/B*4403/Cw*1403 (grade III–IV aGvHD with maximum P=8.56 × 10−10), and other four loci associated with DQB1*0501, Cw*0102, B*5201, and Cw*1202. Two SNPs in patients were also found to be associated with aGvHD, rs5998746 on chr22 (P=3.41 × 10−8) and rs11873016 on chr18 (P=1.26 × 10−8), although no donor SNPs showed significant associations). Similarly, we identified four candidate SNPs associated with the development of severe cGvHD or relapse. Current study provided a unique opportunity in that combination of two different genotypes, not merely genotypes of single individuals, that is associated with particular disease phenotypes, is explored by whole genome association scans. Although further replication studies and biological confirmation are required, our results suggest that whole genome association studies of allo-SCT could provide a novel clue to understanding the genetic basis of allo-SCT.

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講演・口頭発表等 - 赤塚 美樹

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講演・口頭発表等 - 赤塚　美樹