IWATA Yoshio
Department of Medicine | Assistant Professor A in Medical School |
Last Updated :2024/09/14
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- Takahiro Haeno; Shinya Rai; Yoshiaki Miyake; Maiko Inoue; Ko Fujimoto; Aki Fujii; Yoshio Iwata; Shuji Minamoto; Takahide Taniguchi; Hiroaki Kakutani; Hiroaki Inoue; Takahiro Kumode; Kentaro Serizawa; Yasuhiro Taniguchi; Chikara Hirase; Yasuyoshi Morita; Hirokazu Tanaka; Yoichi Tatsumi; Takashi Ashida; Itaru MatsumuraJournal of clinical and experimental hematopathology : JCEH 63 (2) 99 - 107 2023/06We retrospectively evaluated long-term outcomes of high dose chemotherapy followed by autologous stem cell transplant (HDC/ASCT) in patients with diffuse large B-cell lymphoma (DLBCL). Between 2004 and 2020, 46 DLBCL patients received HDC/ASCT in our institution, including 12 patients (26.1%), who received as an upfront setting (UFS). At a median follow-up time of 69 months (range, 2-169 months), the 5-year progression-free survival (PFS) rates were 82.5% (95%CI, 46.1-95.3%) in the UFS, and 57.8% (95%CI, 38.1-73.2%) in the relapsed or refractory (R/R) patients (n=34), respectively. The 5-year PFS rates were 62.3% (95%CI, 34.0-81.3%) in primary resistant (n=13) or early relapsing (within 1 year from the initial diagnosis) patients (n=4), and 53.3% (95%CI, 25.9-74.6%) in those relapsing >1 year after the initial diagnosis (n=17), with no statistically significant difference (p=0.498). In R/R patients, multivariate analysis showed that the remission status before HDC/ASCT was an independent poor prognostic factor for progression-free survival (hazard ratio [HR], 17.0; 95%CI, 3.35-86.6; p=0.000630) and high-risk category in the international prognostic index for OS (HR, 9.39; 95%CI, 1.71-51.6; p=0.0100). The incidence of non-relapse mortality by 5 years, and 10 years were 12.2%, and 15.2%, respectively. Eleven patients (23.9%) developed second malignancies, which was the most frequent late complication after HDC/ASCT, with 5-year, and 10-year cumulative incidence of 16.9%, 22.5%, respectively. In conclusion, HDC/ASCT is effective for chemo-sensitive R/R DLBCL regardless of the timing and lines of therapy. However, careful observation is required, considering the long-term complications such as secondary malignancies.
- Ryosuke Fujiwara; Yasuhiro Taniguchi; Shinya Rai; Yoshio Iwata; Aki Fujii; Ko Fujimoto; Takahiro Kumode; Kentaro Serizawa; Yasuyoshi Morita; J Luis Espinoza; Hirokazu Tanaka; Hitoshi Hanamoto; Itaru MatsumuraBiochemical and biophysical research communications 626 156 - 166 2022/10We previously reported that the antipsychotic drug chlorpromazine (CPZ), which inhibits the formation of clathrin-coated vesicles (CCVs) essential for endocytosis and intracellular transport of receptor tyrosine kinase (RTK), inhibits the growth/survival of acute myeloid leukemia cells with mutated RTK (KIT D816V or FLT3-ITD) by perturbing the intracellular localization of these molecules. Here, we examined whether these findings are applicable to epidermal growth factor receptor (EGFR). CPZ dose-dependently inhibited the growth/survival of the non-small cell lung cancer (NSCLC) cell line, PC9 harboring an EGFR-activating (EGFR exon 19 deletion). In addition, CPZ not only suppressed the growth/survival of gefitinib (GEF)-resistant PC9ZD cells harboring T790 M, but also restored their sensitivities to GEF. Furthermore, CPZ overcame GEF resistance caused by Met amplification in HCC827GR cells. As for the mechanism of CPZ-induced growth suppression, we found that although CPZ hardly influenced the phosphorylation of EGFR, it effectively reduced the phosphorylation of ERK and AKT. When utilized in combination with trametinib (a MEK inhibitor), dabrafenib (an RAF inhibitor), and everolimus (an mTOR inhibitor), CPZ suppressed the growth of PC9ZD cells cooperatively with everolimus but not with trametinib or dabrafenib. Immunofluorescent staining revealed that EGFR shows a perinuclear pattern and was intensely colocalized with the late endosome marker, Rab11. However, after CPZ treatment, EGFR was unevenly distributed in the cells, and colocalization with the early endosome marker Rab5 and EEA1 became more apparent, indicating that CPZ disrupted the intracellular transport of EGFR. These results suggest that CPZ has therapeutic potential for NSCLC with mutated EGFR by a novel mechanism different from conventional TKIs alone or in combination with other agents.
- Takahiro Kumode; Hirokazu Tanaka; Jorge Luis Esipinoza; Shinya Rai; Yasuhiro Taniguchi; Ryosuke Fujiwara; Keigo Sano; Kentaro Serizawa; Yoshio Iwata; Yasuyoshi Morita; Itaru MatsumuraInternational journal of hematology 115 (3) 310 - 321 2022/03C-type lectin-like receptor 2 (CLEC-2) expressed on megakaryocytes plays important roles in megakaryopoiesis. We found that CLEC-2 was expressed in about 20% of phenotypical long-term hematopoietic stem cells (LT-HSCs), which expressed lower levels of HSC-specific genes and produced larger amounts of megakaryocyte-related molecules than CLEC-2low LT-HSCs. Although CLEC-2high LT-HSCs had immature clonogenic activity, cultured CLEC-2high LT-HSCs preferentially differentiated into megakaryocytes. CLEC-2high HSCs yielded 6.8 times more megakaryocyte progenitors (MkPs) and 6.0 times more platelets 2 weeks and 1 week after transplantation compared with CLEC-2low LT-HSCs. However, platelet yield from CLEC-2high HSCs gradually declined with the loss of MkPs, while CLEC-2low HSCs self-renewed long-term, indicating that CLEC-2high LT-HSCs mainly contribute to early megakaryopoiesis. Treatment with pI:C and LPS increased the proportion of CLEC-2high LT-HSCs within LT-HSCs. Almost all CLEC-2low LT-HSCs were in the G0 phase and barely responded to pI:C. In contrast, 54% of CLEC-2high LT-HSCs were in G0, and pI:C treatment obliged CLEC-2high LT-HSCs to enter the cell cycle and differentiate into megakaryocytes, indicating that CLEC-2high LT-HSCs are primed for cell cycle entry and rapidly yield platelets in response to inflammatory stress. In conclusion, CLEC-2high LT-HSCs appear to act as a reserve for emergent platelet production under stress conditions.
MISC
- 脳静脈洞血栓症を合併し、開頭減圧術・術後エクリズマブ投与が有効であったPNHの一例(Post-operative treatment with eculizumab for PNH presenting as cerebral venous sinus thrombosis)岩田 吉生; 森田 泰慶; 辻 潔; 頼 晋也; 田崎 貴之; 井上 宏昭; 谷口 康博; 藤本 昂; 田中 宏和; 芦田 隆司; 加藤 天美; 松村 到 臨床血液 59- (9) 1765 -1765 2018/09
- 藤本昂; 頼晋也; 岩田吉生; 平瀬主税; 森田泰慶; 田中宏和; 辰巳陽一; 芦田隆司; 松村到 臨床血液 57- (2) 2016
Lectures, oral presentations, etc.
- COVID-19罹患後に1型糖尿病を発症した2例葉山僚哉; 山下貴史; 村上冴子; 杉本浩嗣; 岩田吉生; 井上宏昭; 花岡郁子日本内分泌学会雑誌 2024
- 骨髄異形成関連変化を伴う急性骨髄性白血病に合併し壊死性筋膜炎との鑑別を要した水疱型壊疽性膿皮症の1例西垣綾子; 河野奈央; 岩田吉生; 前川恭慶; 白鳥隆宏西日本皮膚科 2024
- フォンウィルブランド因子存在下で血腫を来した本態性血小板血症の1例杉本浩嗣; 岩田吉生; 井上宏昭臨床血液 2023
- 末梢血幹細胞採取前のCD34細胞数測定の有用性山田 枝里佳; 斉藤 花往里; 藤本 昂; 角谷 宏明; 岩田 吉生; 谷口 貴英; 源 周治; 大山 泰世; 口分田 貴裕; 井上 宏昭; 芹澤 憲太郎; 谷口 康博; 頼 晋也; 平瀬 主税; 森田 泰慶; 田中 宏和; 岡野 意浩; 坂田 尚己; 芦田 隆司; 松村 到日本アフェレシス学会雑誌 2018/10 (一社)日本アフェレシス学会
- 脳静脈洞血栓症を合併し、開頭減圧術・術後エクリズマブ投与が有効であったPNHの一例(Post-operative treatment with eculizumab for PNH presenting as cerebral venous sinus thrombosis) [Not invited]岩田 吉生; 森田 泰慶; 辻 潔; 頼 晋也; 田崎 貴之; 井上 宏昭; 谷口 康博; 藤本 昂; 田中 宏和; 芦田 隆司; 加藤 天美; 松村 到臨床血液 2018/09 (一社)日本血液学会-東京事務局
- 孤発性皮膚myeloid sarcomaの1例 [Not invited]齋藤花往里; 頼晋也; 岩田吉生; 田中宏和; 辰巳陽一; 芦田隆司; 松村到; 柳原緑; 大磯直毅; 川田暁臨床血液 2016/02
- CLLの経過中に発症したHodgkin variant of Richter syndromeの1例 [Not invited]藤本昂; 頼晋也; 岩田吉生; 平瀬主税; 森田泰慶; 田中宏和; 辰巳陽一; 芦田隆司; 松村到臨床血液 2016/02
- Ph陽性急性リンパ性白血病の同種造血幹細胞移植後の予後はチロシンキナーゼ阻害薬併用寛解導入療法によって改善される [Not invited]芦田隆司; 芦田隆司; 角谷宏明; 末田早苗; 岩田吉生; 福井彩乃; 大山泰世; 井上宏昭; 頼晋也; 平瀬主税; 森田泰慶; 中野勝彦; 福島靖幸; 川野亜美; 山田枝里佳; 井手大輔; 前田岳宏; 菅野知恵美; 椿本祐子; 金光靖; 松村到; 松村到日本造血細胞移植学会総会プログラム・抄録集 2016/02
- Aleukemic solitary cutaneous myeloid sarcomaの1例 [Not invited]柳原緑; 成田智彦; 大磯直毅; 川田暁; 岩田吉生; 田中宏和; 松村到日本皮膚科学会雑誌 2016/01
- 宮武淳一; 岩田吉生; 谷口貴英; 源周治; 大山泰世; 川内超矢; 佐野圭吾; 口分田貴裕; 芹澤憲太郎; 谷口康博; 頼晋也; 金井良高; 平瀬主税; 森田泰慶; 田中宏和; 辰巳陽一; 芦田隆司; 松村到日本造血細胞移植学会総会プログラム・抄録集 2015/02
- KDIGO基準を用いた非進行期造血器疾患患者に対する造血幹細胞移植後の急性腎障害に関する検討 [Not invited]芦田隆司; 岩田吉生; 谷口貴英; 源周治; 芹沢憲太郎; 川内超矢; 大山泰世; 金井良高; 頼晋也; 平瀬主税; 森田泰慶; 竹中孝子; 福島靖幸; 川野亜美; 山田枝里佳; 井手大輔; 菅野知恵美; 加藤祐子; 椿本祐子; 松村到日本造血細胞移植学会総会プログラム・抄録集 2015/02
- 同種造血幹細胞移植前処置におけるフルダラビン併用下での静注ブスルファン使用量の後方視的解析 [Not invited]芹澤憲太郎; 森田泰慶; 谷口貴英; 岩田吉生; 源周治; 大山泰世; 川内超矢; 金井良高; 頼晋也; 平瀬主税; 田中宏和; 宮武淳一; 辰巳陽一; 芦田隆司; 松村到日本造血細胞移植学会総会プログラム・抄録集 2015/02
- IVFで挙児を得た後に脳血管障害を起こしたHIV感染症夫婦 [Not invited]前田裕弘; 岩田吉生; 江口剛; 口分田貴裕; 山口晃史日本エイズ学会誌 2013/11
- 血球貪食症候群を合併した皮膚筋炎の治療中に中枢神経T細胞性リンパ腫を発症した1例 [Not invited]岩田吉生; 口分田貴裕; 江口剛; 山口晃史; 勅使川原悟; 片田圭宣; 星田義彦; 前田裕弘臨床血液 2013/08