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Urinary Bladder Neoplasms: HELP
Articles by Takashi Dejima
Based on 4 articles published since 2008
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Between 2008 and 2019, Takashi Dejima wrote the following 4 articles about Urinary Bladder Neoplasms.
 
+ Citations + Abstracts
1 Article Suppressed Recurrent Bladder Cancer after Androgen Suppression with Androgen Deprivation Therapy or 5α-Reductase Inhibitor. 2017

Shiota, Masaki / Kiyoshima, Keijiro / Yokomizo, Akira / Takeuchi, Ario / Kashiwagi, Eiji / Dejima, Takashi / Takahashi, Ryosuke / Inokuchi, Junichi / Tatsugami, Katsunori / Eto, Masatoshi. ·Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Electronic address: shiota@uro.med.kyushu-u.ac.jp. · Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. ·J Urol · Pubmed #27506696.

ABSTRACT: PURPOSE: We determined whether intravesical recurrence is affected by inhibition of androgen signaling among men with nonmuscle invasive bladder cancer. MATERIALS AND METHODS: We examined the intravesical recurrence rate among men treated with or without androgen suppression therapy by androgen deprivation therapy for prostate cancer or 5α-reductase inhibitor dutasteride for benign prostatic hyperplasia. RESULTS: We studied 228 men, including 32 with and 196 without androgen suppression therapy. During a median followup of 3.6 and 3.0 years intravesical recurrence developed in 4 (12.5%) and 59 men (30.1%) with and without androgen suppression therapy, respectively. On multivariate analysis multiple tumors (HR 1.82, p = 0.027), a large tumor (HR 2.13, p = 0.043) and ever smoking (HR 2.45, p = 0.020) as well as the presence of androgen suppression therapy (HR 0.36, p = 0.024) were independent risk factors for intravesical recurrence. Notably, tumor progressed to muscle invasive bladder cancer in 6 men (3.1%) without androgen suppression therapy. No man with androgen suppression therapy progressed to muscle invasive bladder cancer. CONCLUSIONS: Our study suggests the possibility of androgen suppression therapy as prophylaxis for intravesical recurrence of bladder cancer. Further explorations are warranted of the prophylactic effect of androgen suppression therapy on bladder cancer pathogenesis.

2 Article Antitumor activity of recombinant Bacille Calmette-Guérin secreting interleukin-15-Ag85B fusion protein against bladder cancer. 2016

Takeuchi, Ario / Eto, Masatoshi / Tatsugami, Katsunori / Shiota, Masaki / Yamada, Hisakata / Kamiryo, Yoriyuki / Dejima, Takashi / Kashiwagi, Eiji / Kiyoshima, Keijiro / Inokuchi, Junichi / Takahashi, Ryosuke / Yokomizo, Akira / Ohara, Naoya / Yoshikai, Yasunobu. ·Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. · Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Electronic address: etom@uro.med.kyushu-u.ac.jp. · Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. · Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. ·Int Immunopharmacol · Pubmed #27093372.

ABSTRACT: Mycobacterium bovis Bacillus Calmette-Guérin (BCG) is used for the treatment of bladder cancer. The recruitment of neutrophlis to the bladder after BCG instillation exerts anti-tumor activity against bladder tumor. We have recently demonstrated that interleukin (IL)-17A produced by γδ T cells played a role in the recruitment of neutrophlis to the bladder after BCG instillation. IL-15 is known to play an important role in neutrophil migration during inflammation. We previously constructed a recombinant BCG strain expressing the fusion protein of IL-15 and Ag85B (BCG-IL-15) for prevention of Mycobacterium tuberculosis infection. Here we compared the efficacy of the BCG-IL-15 in protection against bladder cancer with that of rBCG-Ag85B (BCG). Six-week-old female C57BL/6 mice were inoculated with MB49 bladder tumor cells in the bladder and subsequently intravesically inoculated with BCG or BCG-IL-15. BCG-IL-15 treatment significantly prolonged survival of mice inoculated with bladder cancer cells compared with BCG treatment. Infiltration of neutrophils was significantly elevated in BCGB-IL-15 treated mice accompanied by increased chemokines (MIP-2 and MIP-1α) in the bladder. Thus, BCG-IL-15 exerted additive effect on Infiltration of neutrophils in the bladder. BCG-IL-15 may be a promising drug for non-muscle invasive bladder cancer.

3 Article Targeting HER2 with T-DM1, an Antibody Cytotoxic Drug Conjugate, is Effective in HER2 Over Expressing Bladder Cancer. 2015

Hayashi, Tetsutaro / Seiler, Roland / Oo, Htoo Zarni / Jäger, Wolfgang / Moskalev, Igor / Awrey, Shannon / Dejima, Takashi / Todenhöfer, Tilman / Li, Na / Fazli, Ladan / Matsubara, Akio / Black, Peter C. ·Vancouver Prostate Centre and Department of Urologic Sciences, University of British Columbia (TH, RS, HZO, WJ, IM, SA, TD, TT, NL, LF, PCB), Vancouver, British Columbia, Canada · Department of Urology, Institute of Biomedical and Health Science, Hiroshima University (TH), Hiroshima, Japan. ·J Urol · Pubmed #26047983.

ABSTRACT: PURPOSE: Systemic therapy for advanced bladder cancer has not changed substantially in more than 2 decades and mortality rates remain high. The recognition of HER2 over expression in bladder cancer has made HER2 a promising therapeutic target. T-DM1, a new drug consisting of the HER2 antibody trastuzumab conjugated with a cytotoxic agent, has been shown in breast cancer to be superior to trastuzumab. We tested T-DM1 in preclinical models of bladder cancer. MATERIALS AND METHODS: We evaluated the effect of T-DM1 compared to trastuzumab in different in vitro and in vivo models of HER2 over expressing bladder cancer. RESULTS: RT4V6 was the highest HER2 expressing bladder cancer cell line and it showed higher growth inhibition with T-DM1 compared to trastuzumab. T-DM1 but not trastuzumab induced apoptosis of RT4V6 cells after G2/M arrest on cell cycle analysis. HER2 expression was higher in cell lines with acquired cisplatin resistance compared to the corresponding parental cell lines. Resistant cells showed higher sensitivity to T-DM1 by the induction of apoptosis. In addition, cells cultured in anchorage independent conditions increased HER2 expression compared to cells cultured in adherent conditions and T-DM1 significantly inhibited colony formation in soft agar compared to trastuzumab. In an orthotopic bladder cancer xenograft model tumor growth of cisplatin resistant RT112 was significantly inhibited by T-DM1 via the induction of apoptosis compared to treatment with control IgG or trastuzumab. CONCLUSIONS: T-DM1 has promising antitumor effects in preclinical models of HER2 over expressing bladder cancer.

4 Article IL-17 production by γδ T cells is important for the antitumor effect of Mycobacterium bovis bacillus Calmette-Guérin treatment against bladder cancer. 2011

Takeuchi, Ario / Dejima, Takashi / Yamada, Hisakata / Shibata, Kensuke / Nakamura, Risa / Eto, Masatoshi / Nakatani, Tatsuya / Naito, Seiji / Yoshikai, Yasunobu. ·Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. ·Eur J Immunol · Pubmed #21182095.

ABSTRACT: Intravesical inoculation of Mycobacterium bovis bacillus Calmette-Guérin (BCG) has been used for the treatment of bladder cancer. Recent studies implied the requirement of neutrophil infiltration for the antitumor effect. In this study, we found that IL-17 was produced in the bladder after BCG treatment, preceding the infiltration of neutrophils. Neutrophils in the bladder after BCG treatment were reduced in IL-17-deficient mice, in which BCG-induced antitumor effect against intravesically inoculated bladder cancer was abolished. Notably, the level of IL-17 production and the number of neutrophils in BCG-treated bladder was reduced in γδ T-cell-deficient mice but not in CD4-depleted mice. Survival of bladder cancer-inoculated γδ T-cell-deficient mice was not improved by BCG treatment. These results suggest that IL-17-producing γδ T cells play a key role in the BCG-induced recruitment of neutrophils to the bladder, which is essential for the antitumor activity against bladder cancer.