Faculty Profiles - MAEDA Yoshinobu

MISC - MAEDA Yoshinobu

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再発/難治性の非ホジキンリンパ腫への自家末梢血造血幹細胞移植の前処置に,Gemcitanbine,Busulfan,Melphalanを使用した10例

谷勝真, 近藤英生, 石川立則, 清家圭介, 三道康永, 中村真, 藤原英晃, 西森久和, 松岡賢市, 藤井伸治, 藤井伸治, 前田嘉信, 谷本光音, 松本加奈, 曽我賢彦, 高橋郁名代, 川村夢乃, 松田友里, 梶尾利香, 向井裕美子, 三島美鈴

日本造血細胞移植学会総会プログラム・抄録集 37th 2015

Recombinant Thrombomodulin for the Treatment of Transplantation-Associated Coagulopathy after Allogeneic Hematopoietic Stem Cell Transplantation

Kazuyoshi Ishii, Shosaku Nomura, Tomoki Ito, Yuta Katayama, Taiichi Kyo, Shuichi Ota, Masanori Seki, Shigeru Chiba, Yoshinobu Maeda, Mitsune Tanimoto, Takayuki Ikezoe, Hideo Yagi, Yoji Ishida, Naohito Fujishima, Kenichi Sawada

BLOOD 124 ( 21 ) 2014.12

Use of Recombinant Thrombomodulin for Thrombotic Microangiopathy after Hematopoietic Stem Cell Transplantation Ameliorate Disease Severity

Hideaki Fujiwara, Yoshinobu Maeda, Yasuhisa Sando, Makoto Nakamura, Katsuma Tani, Takanori Ishikawa, Hisakazu Nishimori, Ken-ichi Matsuoka, Nobuharu Fujii, Eisei Kondo, Mitsune Tanimoto

BLOOD 124 ( 21 ) 2014.12

Anti-IL-12/23 p40 Antibody Attenuates Chronic Graft Versus Host Disease Via Suppression of IFN-gamma/IL-17-Producing Cells

Taiga Kuroi, Sachiyo Okamoto, Kyosuke Saeki, Yujin Kobayashi, Hisakazu Nishimori, Hideaki Fujiwara, Ken-ichi Matsuoka, Nobuharu Fujii, Eisei Kondo, Mitsune Tanimoto, Yoshinobu Maeda

BLOOD 124 ( 21 ) 2014.12

EBV-POSITIVE MUCOCUTANEOUS ULCER ARISING IN A PATIENT WITH POLYCYTHEMIA VERA TREATED WITH ORAL HYDROXYUREA

Toshihisa Hamada, Mariko Takao, Yoshinobu Maeda, Tadashi Yoshino, Yumi Aoyama, Keiji Iwatsuki

JOURNAL OF DERMATOLOGY 41 41 - 41 2014.10

骨髄移植後肺GVHDに対する両側生体肺葉移植術後にPassenger Lymphocyte Syndromeを呈した一例

大亀剛, 杉本誠一郎, 前田嘉信, 伊賀徳周, 岡田真典, 三好健太郎, 山根正修, 大藤剛宏, 三好新一郎

日本移植学会総会プログラム抄録集 50th 427 2014.8

治療抵抗性DLBCLの自己末梢血幹細胞移植併用大量化学療法(HDT/ASCT)後の再発に対しHLA半合致同種造血幹細胞移植(haploHSCT)を行い完全寛解となった一例

塩手康弘, 近藤英生, 石川立則, 佐伯恭昌, 谷勝真, 山本宜和, 松岡賢市, 西森久和, 藤井伸治, 前田嘉信, 谷本光音, 吉野正

日本リンパ網内系学会会誌 54 122 - 122 2014.6

Overexpression of Smad2 inhibits proliferation of gingival epithelial cells

M. Shimoe, T. Yamamoto, N. Shiomi, K. Tomikawa, S. Hongo, K. Yamashiro, T. Yamaguchi, H. Maeda, S. Takashiba

JOURNAL OF PERIODONTAL RESEARCH 49 ( 3 ) 290 - 298 2014.6

Language：English Publisher：WILEY-BLACKWELL

Background and Objective
Spatiotemporal inhibition of apical migration and proliferation of gingival epithelium are significant factors involved in periodontal regeneration. Transforming growth factor beta (TGF-beta) is important in multiple aspects of wound healing, and Smad2, a downstream transcription factor of TGF-beta, has an inhibitory effect on re-epithelialization during gingival wound healing. Therefore, we investigated the effects on migration and proliferation status, and intra/extracellular signaling regulated by Smad2 overexpression in gingival epithelial cells.
Material and Methods
Gingival epithelial cells were isolated from the palatal gingival tissue of transgenic mice overexpressing Smad2 driven by the Keratin14 promoter. Smad2 expression was identified by western blotting and immunofluorescence analysis. Scratch assay and 5-bromo-2 '-deoxyuridine staining were performed to assess cell migration and proliferation. To inactivate TGF-beta type I receptor, the cultures were supplemented with SB431542. Secreted TGF-beta was quantified by ELISA. Smad2 target gene expression was examined by real-time RT-PCR and in vivo immunofluorescence analysis of gingival junctional epithelium.
Results
Smad2-overexpressing cells were confirmed to have significant phosphorylated Smad2 in the nucleus. Scratch assay and 5-bromo-2 '-deoxyuridine staining indicated that Smad2-overexpressing cells showed no significant differences in migration, but had reduced proliferation rates compared to wild-type controls. SB431542 significantly inhibited Smad2 phosphorylation, which coincided with restoration of the proliferation rate in Smad2-overexpressing cells. ELISA of TGF-beta release did not show any differences between genotypes. The cell cycle inhibitors, p15 and p21, showed significant upregulation in Smad2-overexpressing cells compared to wild-type controls. Moreover, junctional epithelium of the transgenic mice showed increased expression of P-Smad2, p15 and p21.
Conclusion
The signaling activation triggered by overexpression of Smad2 was dependent on TGF-beta type I receptor, and the activated Smad2 increased p15 and p21 expression, responsible for inhibiting cell cycle entry, resulting in antiproliferative effects on gingival epithelial cells. Understanding of Smad2-induced signaling would be useful for possible clinical application to regulate gingival epithelial downgrowth.

DOI： 10.1111/jre.12106

皮膚γδT細胞リンパ腫に対し臍帯血移植を施行した一例

佐伯恭昌, 石川立則, 谷勝真, 松岡賢市, 藤井伸治, 近藤英生, 前田嘉信, 谷本光音

日本リンパ網内系学会会誌 54 121 - 121 2014.6

当院における70歳以上の高齢血液疾患患者に対する同種造血幹細胞移植

近藤正太郎, 前田嘉信, 松岡賢市, 品川克至, 藤井敬子, 藤井伸治, 近藤英生, 谷本光音

日本老年医学会雑誌 51 ( 3 ) 293 - 293 2014.5

Primary cutaneous γδT-cell lymphomaに対し、臍帯血移植を施行した1例

佐伯恭昌, 石川立則, 谷勝真, 山本宜和, 塩手康弘, 松岡賢市, 藤井伸治, 近藤英生, 前田嘉信, 品川克至, 谷本光音

臨床血液 55 ( 5 ) 587 - 587 2014.5

The Impact of HLA-Mismatch Direction on the Outcome of Unrelated Bone Marrow Transplantation: A Retrospective Analysis from the JSHCT HLA Working Group

Junya Kanda, Yoshinobu Maeda, Kazuteru Ohashi, Takahiro Fukuda, Koichi Miyamura, Shin-Ichiro Mori, Yasuo Morishima, Yoshiko Atsuta, Yoshinobu Kanda

BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION 20 ( 2 ) S57 - S57 2014.2

Prospective Multicenter Phase II Study of Myeloablative Conditioning Consisted of Intravenous Busulfan and Fludarabine plus /- Total Body Irradiation for Older Patients (55 years and older): Final Analysis of the JSCT FB09 Study

Naoyuki Uchida, Michihiro Hidaka, Toru Sakura, Toshihiro Miyamoto, Tomoaki Fujisaki, Tetsuya Eto, Yoshinobu Maeda, Kenji Fukuno, Kana Matsumoto, Kunihiko Morita, Junji Kishimoto, Takahiro Fukuda, Takanori Teshima, Shuichi Taniguchi, Shin-Ichiro Mori, Mine Harada

BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION 20 ( 2 ) S253 - S253 2014.2

マウス慢性GVHDモデルにおけるPD-1経路の重要性

藤原英晃, 前田嘉信, 西之原正昭, 岡本幸代, 西森久和, 松岡賢市, 藤井伸治, 近藤英生, 品川克至, 谷本光音

日本造血細胞移植学会総会プログラム・抄録集 36th 2014

Clinicopathological analysis of 17 primary cutaneous T-cell lymphoma of the γδ phenotype from Japan. International journal

Yuka Takahashi, Katsuyoshi Takata, Seiichi Kato, Yasuharu Sato, Naoko Asano, Tetsuro Ogino, Kimio Hashimoto, Yukie Tashiro, Shogo Takeuchi, Taro Masunari, Yasushi Hiramatsu, Yoshinobu Maeda, Mitsune Tanimoto, Tadashi Yoshino

Cancer science 105 ( 7 ) 912 - 923 2014

Language：English

Primary cutaneous γδ T-cell lymphoma (PCGD-TCL) is an aggressive lymphoma consisting of clonal proliferation of mature activated γδ T-cells of a cytotoxic phenotype. Because primary cutaneous γδ T-cell lymphoma is a rare disease, there are few clinicopathological studies. In addition, T-cell receptor (TCR) γδ cells are typically immunostained in frozen sections or determined by TCRβ negativity. We retrospectively analyzed 17 primary cutaneous T-cell lymphomas of the γδ phenotype (CTCL-γδ) in a clinicopathological and molecular study using paraffin-embedded sections. Among 17 patients, 11 had CTCL-γδ without subcutaneous panniculitis-like T-cell lymphoma (SPTCL) features and six had CTCL-γδ with SPTCL features. Immunophenotypically, some significant differences were found in CD8 and CD56 positivity between our patient series of CTCL-γδ patients with SPTCL features and SPTCL-γδ patients described in the previous literature. A univariate analysis of 17 CTCL-γδ patients showed that being more than 60 years old, presence of visceral organ involvement, and small-to-medium cell size were poor prognostic factors. In addition, the 5-year overall survival rate was 42.4% for the CTCL-γδ patients without SPTCL features and 80.0% for those with SPTCL features. Consequently, there was a strikingly significant difference in overall survival among SPTCL, CTCL-γδ with SPTCL features and CTCL-γδ without SPTCL features (P = 0.0005). Our data suggests that an indolent subgroup may exist in CTCL-γδ. Studies on more cases, including those from other countries, are warranted to delineate the clinicopathological features and the significance in these rare lymphomas.

DOI： 10.1111/cas.12439

PubMed

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Duodenal follicular lymphoma: comprehensive gene expression analysis with insights into pathogenesis. International journal

Katsuyoshi Takata, Motohiko Tanino, Daisuke Ennishi, Akira Tari, Yasuharu Sato, Hiroyuki Okada, Yoshinobu Maeda, Naoe Goto, Hiroshi Araki, Mai Harada, Midori Ando, Masaya Iwamuro, Mitsune Tanimoto, Kazuhide Yamamoto, Randy D Gascoyne, Tadashi Yoshino

Cancer science 105 ( 5 ) 608 - 615 2014

Language：English

Follicular lymphoma (FL) of the gastrointestinal tract, particularly duodenal follicular lymphoma (DFL), is a rare variant of FL with indolent clinical behavior, and this disease is included in the 2008 World Health Organization classification system. In contrast to nodal follicular lymphoma (NFL), DFL occurs most frequently in the second part of the duodenum, lacks follicular dendritic cell meshworks and has memory B-cell characteristics. However, its molecular pathogenesis is still unclear. In the present study, we examined 10 DFL, 18 NFL and 10 gastric MALT lymphoma samples using gene expression analysis. Quantitative RT-PCR experiments and immunohistochemical analysis for 72 formalin-fixed, paraffin-embedded tissues from an independent series, including 32 DFL, 19 gastric MALT lymphoma and 27 NFL samples, were performed for validation of microarray data. Gene expression profiles of the three lymphoma types were compared using 2918 differentially expressed genes (DEG) and results suggested that DFL shares characteristics of MALT lymphoma. Among these DEG, CCL20 and MAdCAM-1 were upregulated in DFL and MALT but downregulated in NFL. In contrast, protocadherin gamma subfamily genes were upregulated in DFL and NFL. Quantitative RT-PCR and immunohistochemical studies demonstrated concordant results. Double immunofluorescence studies revealed that CCL20 and CCR6 were co-expressed in both DFL and MALT. We hypothesize that increased expression of CCL20 and MAdCAM-1 and co-expression of CCL20 and CCR6 may play an important role in tumorigenesis.

DOI： 10.1111/cas.12392

PubMed

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Low-grade B-cell lymphoma presenting primarily in the bone marrow. International journal

Kayoko Iwatani, Katsuyoshi Takata, Yasuharu Sato, Tomoko Miyata-Takata, Noriko Iwaki, Wei Cui, Seiko Sawada-Kitamura, Hiroshi Sonobe, Maiko Tamura, Katsuhiko Saito, Katsuya Miyatani, Rie Yamasaki, Ichiro Yamadori, Nobuharu Fujii, Yasushi Terasaki, Yoshinobu Maeda, Mitsune Tanimoto, Naoya Nakamura, Tadashi Yoshino

Human pathology 45 ( 7 ) 1379 - 1387 2014

Language：English

Cases of low-grade B-cell lymphoma presenting primarily in the bone marrow are rare, and its clinicopathology remains unclear. We retrospectively examined patients with low-grade B-cell lymphoma presenting primarily in the bone marrow. Fourteen patients met the inclusion criteria, including 5 with lymphoplasmacytic lymphoma (LPL), 3 with chronic lymphocytic leukemia/small lymphocytic lymphoma, 2 with follicular lymphoma (FL), and 4 with low-grade B-cell lymphoma not otherwise specified (LGBCL-NOS). The median age was 69.5 years (range, 42-89 years), and a slight male predominance was noted (9 men and 5 women, 1.8: 1). Immunohistochemically, all cases were positive for CD20. One case was positive for CD138. Both cases of FL were positive for CD10 and B-cell lymphoma 2 (BCL-2), and immunoglobulin heavy locus (IgH)/B-cell lymphoma 2 rearrangement was observed by fluorescence in situ hybridization. The myeloid differentiation primary response gene (88) leucine to proline mutation was observed in 3 of 5 LPL, 1 of 2 FL, and 2 of 4 LGBCL-NOS patients. Paraproteinemia was observed in 10 patients; IgM and IgG paraproteinemia were observed in 6 and 3 patients, respectively. In this patient series, 3 patients had died at a median follow-up of 36.5 months; the cause of death of 1 LPL patient was malignant lymphoma itself. Thus, low-grade B-cell lymphoma presenting primarily in the bone marrow has various subtypes, and approximately one-third of the patients had LGBCL-NOS. The immunophenotypic features and myeloid differentiation primary response gene (88) leucine to proline mutation data of LGBCL-NOS suggested that some cases present with characteristics similar to those of LPL or marginal zone lymphoma.

DOI： 10.1016/j.humpath.2014.02.010

PubMed

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20年にわたって発熱・皮疹が間欠的に出現した1例.

谷本安, 後藤田裕子, 佐伯恭昌, 近藤英生, 前田嘉信, 品川克至, 木浦勝行, 片岡幹男, 谷本光音

Progress in Medicine 34 ( 1 ) 185 - 192 2014

Host Tissue PD-1 Pathway Contribute To Murine Chronic Graft-Versus-Host Disease Via Th1+Th17+Cells Reviewed

Fujiwara Hideaki, Maeda Yoshinobu, Kobayashi Koichiro, Nishimori Hisakazu, Matsuoka Ken-ichi, Azuma Miyuki, Yagita Hideo, Chen Lieping, Tanimoto Mitsune

BLOOD 122 ( 21 ) 2013.11

Novel Prognostic Model Of Primary Mediastinal Large B-Cell Lymphoma (PMBL): A Multicenter Cooperative Retrospective Study In Japan

Tomohiro Aoki, Koji Izutsu, Ritsuro Suzuki, Chiaki Nakaseko, Hiroshi Arima, Kazuyuki Shimada, Makoto Sasaki, Jun Takizawa, Kinuko Mitani, Tadahiko Igarashi, Yoshinobu Maeda, Fumihiro Ishida, Nozomi Niitsu, Ken Ohmachi, Hirotaka Takasaki, Naoya Nakamura, Tomohiro Kinoshita, Shigeo Nakamura, Michinori Ogura

BLOOD 122 ( 21 ) 2013.11

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MISC - MAEDA Yoshinobu