2024/06/11 更新

写真a

タケダ タツアキ
武田 達明
Tatsuaki Takeda
所属
医歯薬学域 助教
職名
助教
外部リンク

学位

  • 博士(医学) ( 2020年6月   岡山大学 )

研究分野

  • ライフサイエンス / 医療薬学

  • ライフサイエンス / 腫瘍生物学

学歴

  • 岡山大学   Graduate School of Medicine , Dentistry and Pharmaceutical Sciences  

    2016年4月 - 2020年6月

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  • 岡山大学   Faculty of Pharmaceutical Sciences   Department of Pharmacy

    2010年4月 - 2016年3月

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経歴

  • 岡山大学   臨床薬学教育研究センター   助教

    2022年9月 - 現在

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  • 岡山大学病院   薬剤部   薬剤師

    2016年4月 - 現在

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所属学協会

  • 日本臨床疫学会

    2022年6月 - 現在

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  • 日本アカデミック・ディテーリング研究会

    2022年5月 - 現在

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  • 日本医療薬学会

    2016年7月 - 現在

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  • 日本病院薬剤師会

    2016年4月 - 現在

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論文

  • Adverse events of nivolumab plus ipilimumab versus nivolumab plus cabozantinib: a real-world pharmacovigilance study. 国際誌

    Yurie Oka, Jun Matsumoto, Tatsuaki Takeda, Naohiro Iwata, Takahiro Niimura, Aya Fukuma Ozaki, Kensuke Bekku, Hirofumi Hamano, Motoo Araki, Keisuke Ishizawa, Yoshito Zamami, Noritaka Ariyoshi

    International journal of clinical pharmacy   2024年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: No head-to-head clinical trials have compared the differences in adverse events (AEs) between nivolumab plus ipilimumab (NIVO-IPI) and nivolumab plus cabozantinib (NIVO-CABO) in the treatment of metastatic renal cell carcinoma (mRCC). AIM: We analysed the two largest real-world databases, the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) and the World Health Organization's VigiBase, to elucidate the differences in AEs between NIVO-IPI and NIVO-CABO. METHOD: In total, 40,376 and 38,022 records were extracted from FAERS and VigiBase, and 193 AEs were analysed. The reporting odds ratios (ROR) with 95% confidence interval were calculated using a disproportionality analysis (NIVO-CABO/NIVO-IPI). RESULTS: The reported numbers of immune-related AEs, including myocarditis, colitis, and hepatitis, were significantly higher with NIVO-IPI (ROR = 0.18 for FAERS and 0.13 for VigiBase). Contrarily, the reported numbers of other AEs, including gastrointestinal disorders (ROR = 2.68 and 2.92) and skin and subcutaneous tissue disorders (ROR = 2.94 and 3.55), considered to be potentiated by the combination of NIVO and CABO, were higher with NIVO-CABO. CONCLUSION: Our findings contribute to the selection and clinical management of NIVO-IPI and NIVO-CABO, which minimizes the risk of AEs for individual patients with mRCC by considering distinctive differences in the AE profiles.

    DOI: 10.1007/s11096-024-01713-1

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  • A comparison between the adverse event profiles of patients receiving palbociclib and abemaciclib: analysis of two real-world databases 査読

    Tatsuaki Takeda, Shiho Sugimoto, Jun Matsumoto, Naohiro Iwata, Akihiko Nakamoto, Aya Fukuma Ozaki, Hirofumi Hamano, Noritaka Ariyoshi, Yoshito Zamami

    International Journal of Clinical Pharmacy   2023年12月

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    担当区分:筆頭著者  

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  • Influence of vasopressin receptor antagonists on triple-whammy acute kidney injury: A VigiBase analysis. 国際誌

    Satoru Mitsuboshi, Kenji Hayakawa, Hirofumi Hamano, Ayako Oshima, Tatsuaki Takeda, Kiminaka Murakawa, Hideki Mori, Yoshito Zamami

    British journal of clinical pharmacology   2023年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Although diuretics play an important role in triple-whammy acute kidney injury (AKI), it is unclear whether the type of diuretic influences the risk of triple-whammy AKI. The aim of this study was to evaluate whether vasopressin receptor antagonists affect triple-whammy AKI. This cross-sectional study used disproportionality analysis of VigiBase data to assess the risk of AKI with various diuretics. Although multiple logistic regression analysis showed that aldosterone antagonists (odds ratio [OR] 2.19, 95% CI 2.01-2.37), loop diuretics (OR 4.40, 95% CI 4.07-4.76) and thiazide diuretics (OR 1.98, 95% CI 1.83-2.15) increased the risk of AKI in patients who received non-steroidal anti-inflammatory drugs (NSAIDs) and renin-angiotensin system inhibitors (RASi), vasopressin receptor antagonists did not increase the risk of AKI in those patients. Vasopressin receptor antagonists might not influence the development of triple-whammy AKI.

    DOI: 10.1111/bcp.15974

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  • Proton Pump Inhibitors and Rhabdomyolysis: Analysis of Two Different Cross-Sectional Databases. 国際誌

    Satoru Mitsuboshi, Hirofumi Hamano, Yurika Kuniki, Takahiro Niimura, Masayuki Chuma, Soichiro Ushio, Tsung-Jen Lin, Jun Matsumoto, Tatsuaki Takeda, Makoto Kajizono, Yoshito Zamami, Keisuke Ishizawa

    The Annals of pharmacotherapy   57 ( 11 )   10600280231156270 - 10600280231156270   2023年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: It is unclear whether use of a proton pump inhibitors (PPIs) increases the risk of rhabdomyolysis. OBJECTIVE: To clarify whether use of PPIs increases the risk of rhabdomyolysis. METHODS: This cross-sectional study analyzed data entered into the Medical Data Vision (MDV) database in Japan and into the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). The MDV data were analyzed to evaluate the association between use of PPIs and rhabdomyolysis. Then, the FAERS data were analyzed to evaluate whether the risk of rhabdomyolysis was increased further when a statin or fibrate was used concomitantly with a PPI. In both analyses, histamine-2 receptor antagonist was set as a comparator because it is used to treat gastric disease. In the MDV analysis, Fisher's exact test and multiple logistic regression analysis were performed. In the FAERS analysis, a disproportionality analysis using Fisher's exact test and multiple logistic regression analysis were performed. RESULTS: Multiple logistic regression analysis of both databases showed a significant association between use of PPIs and an increased risk of rhabdomyolysis (odds ratio [OR] = 1.74-1.95, P ≤ 0.01). However, use of a histamine-2 receptor antagonist was not significantly associated with increased risk of rhabdomyolysis. In the sub-analysis of the FAERS data, use of a PPI did not increase the risk of rhabdomyolysis in patients receiving a statin. CONCLUSION AND RELEVANCE: The data in 2 separate databases consistently suggest that PPIs may increase the risk of rhabdomyolysis. The evidence for this association should be assessed in further drug safety studies.

    DOI: 10.1177/10600280231156270

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  • Significance of UGT1A6, UGT1A9, and UGT2B7 genetic variants and their mRNA expression in the clinical outcome of renal cell carcinoma. 国際誌

    Jun Matsumoto, Anzu Nishimoto, Shogo Watari, Hideo Ueki, Shoya Shiromizu, Naohiro Iwata, Tatsuaki Takeda, Soichiro Ushio, Makoto Kajizono, Masachika Fujiyoshi, Toshihiro Koyama, Motoo Araki, Koichiro Wada, Yoshito Zamami, Yasutomo Nasu, Noritaka Ariyoshi

    Molecular and cellular biochemistry   478 ( 8 )   1779 - 1790   2022年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    UDP-glucuronosyltransferase (UGT) metabolizes a number of endogenous and exogenous substrates. Renal cells express high amounts of UGT; however, the significance of UGT in patients with renal cell carcinoma (RCC) remains unknown. In this study, we profile the mRNA expression of UGT subtypes (UGT1A6, UGT1A9, and UGT2B7) and their genetic variants in the kidney tissue of 125 Japanese patients with RCC (Okayama University Hospital, Japan). In addition, we elucidate the association between the UGT variants and UGT mRNA expression levels and clinical outcomes in these patients. The three representative genetic variants, namely, UGT1A6 541A > G, UGT1A9 i399C > T, and UGT2B7-161C > T, were genotyped, and their mRNA expression levels in each tissue were determined. We found that the mRNA expression of the three UGTs (UGT1A6, UGT1A9, and UGT2B7) are significantly downregulated in RCC tissues. Moreover, in patients with RCC, the UGT2B7-161C > T variant and high UGT2B7 mRNA expression are significantly correlated with preferable cancer-specific survival (CSS) and overall survival (OS), respectively. As such, the UGT2B7-161C > T variant and UGT2B7 mRNA expression level were identified as significant independent prognostic factors of CSS and CSS/OS, respectively. Taken together, these findings indicate that UGT2B7 has a role in RCC progression and may, therefore, represent a potential prognostic biomarker for patients with RCC.

    DOI: 10.1007/s11010-022-04637-4

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  • Adverse Events of Axitinib plus Pembrolizumab Versus Lenvatinib plus Pembrolizumab: A Pharmacovigilance Study in Food and Drug Administration Adverse Event Reporting System. 国際誌

    Jun Matsumoto, Naohiro Iwata, Shogo Watari, Soichiro Ushio, Shoya Shiromizu, Tatsuaki Takeda, Hirofumi Hamano, Makoto Kajizono, Motoo Araki, Yasutomo Nasu, Noritaka Ariyoshi, Yoshito Zamami

    European urology focus   9 ( 1 )   141 - 144   2022年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    No head-to-head postmarket surveillance study has compared the differences in adverse events (AEs) between two combination therapies, axitinib (AXI) + pembrolizumab (PEMBRO) and lenvatinib (LEN) + PEMBRO, against metastatic renal cell carcinoma. This study aims to highlight the comprehensive differences in AEs between these two therapies based on the real-world big data from the Food and Drug Administration Adverse Event Reporting System (FAERS) database. In total, 28 937 records were extracted from the FAERS database, and 139 AEs grouped into the System Organ Class according to the Medical Dictionary for Regulatory Activities were analysed. Logistic regression analyses were performed, and the reporting odds ratio with a 95% confidence interval was determined. We found that the incidences of cardiac and hepatobiliary disorders for AXI + PEMBRO, and blood and lymphatic system, metabolism and nutrition, and vascular disorders for LEN + PEMBRO, all of which were associated with serious AEs, were higher than those for LEN + PEMBRO and AXI + PEMBRO, respectively. The differences in the AEs between AXI + PEMBRO and LEN + PEMBRO were not derived merely from those between AXI and LEN monotherapies. Furthermore, remarkable AE potentiation was observed for AXI + PEMBRO. As FAERS is a spontaneous reporting system comprising partially limited information, analysing more detailed relationships between AEs and patient or treatment characteristics was challenging in this study. The present study is the first to show the overall real-world postmarketing differences in AEs between AXI + PEMBRO and LEN + PEMBRO. Our novel findings will substantially improve clinical practice; we recommend comparing patients' conditions associated with the above AEs when selecting between these two therapies. PATIENT SUMMARY: Herein, we highlight the differences in adverse events (AEs) between axitinib + pembrolizumab and lenvatinib + pembrolizumab therapies using data from the real-world Food and Drug Administration Adverse Event Reporting System database aimed at patients with metastatic renal cell carcinoma. We identified AEs that needed attention in each combination. We recommend the differences in AEs to be considered when selecting these two therapies.

    DOI: 10.1016/j.euf.2022.07.003

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  • Drug repositioning of tranilast to sensitize a cancer therapy by targeting cancer-associated fibroblast. 国際誌

    Kosuke Ochi, Ken Suzawa, Yin Min Thu, Fumiaki Takatsu, Shimpei Tsudaka, Yidan Zhu, Kentaro Nakata, Tatsuaki Takeda, Kazuhiko Shien, Hiromasa Yamamoto, Mikio Okazaki, Seiichiro Sugimoto, Tadahiko Shien, Yoshiharu Okamoto, Shuta Tomida, Shinichi Toyooka

    Cancer science   2022年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cancer-associated fibroblasts (CAFs) are a major component of the tumor microenvironment that mediate resistance of cancer cells to anticancer drugs. Tranilast is an antiallergic drug that suppresses the release of cytokines from various inflammatory cells. In this study, we investigated the inhibitory effect of tranilast on the interactions between non-small cell lung cancer (NSCLC) cells and the CAFs in the tumor microenvironment. Three EGFR-mutant NSCLC cell lines, two KRAS-mutant cell lines, and three CAFs derived from NSCLC patients were used. To mimic the tumor microenvironment, the NSCLC cells were cocultured with the CAFs in vitro, and the molecular profiles and sensitivity to molecular targeted therapy were assessed. Crosstalk between NSCLC cells and CAFs induced multiple biological effects on the NSCLC cells both in vivo and in vitro, including activation of the STAT3 signaling pathway, promotion of xenograft tumor growth, induction of epithelial-mesenchymal transition (EMT), and acquisition of resistance to molecular-targeted therapy, including EGFR-mutant NSCLC cells to osimertinib and of KRAS-mutant NSCLC cells to selumetinib. Treatment with tranilast led to inhibition of IL-6 secretion from the CAFs, which, in turn, resulted in inhibition of CAF-induced phospho-STAT3 upregulation. Tranilast also inhibited CAF-induced EMT in the NSCLC cells. Finally, combined administration of tranilast with molecular-targeted therapy reversed the CAF-mediated resistance of the NSCLC cells to the molecular-targeted drugs, both in vitro and in vivo. Our results showed that combined administration of tranilast with molecular-targeted therapy is a possible new treatment strategy to overcome drug resistance caused by cancer-CAF interaction.

    DOI: 10.1111/cas.15502

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  • YES1 as a Therapeutic Target for HER2-Positive Breast Cancer after Trastuzumab and Trastuzumab-Emtansine (T-DM1) Resistance Development. 国際誌

    Miwa Fujihara, Tadahiko Shien, Kazuhiko Shien, Ken Suzawa, Tatsuaki Takeda, Yidan Zhu, Tomoka Mamori, Yusuke Otani, Ryo Yoshioka, Maya Uno, Yoko Suzuki, Yuko Abe, Minami Hatono, Takahiro Tsukioki, Yuko Takahashi, Mariko Kochi, Takayuki Iwamoto, Naruto Taira, Hiroyoshi Doihara, Shinichi Toyooka

    International journal of molecular sciences   22 ( 23 )   2021年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Trastuzumab-emtansine (T-DM1) is a therapeutic agent molecularly targeting human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC), and it is especially effective for MBC with resistance to trastuzumab. Although several reports have described T-DM1 resistance, few have examined the mechanism underlying T-DM1 resistance after the development of acquired resistance to trastuzumab. We previously reported that YES1, a member of the Src family, plays an important role in acquired resistance to trastuzumab in HER2-amplified breast cancer cells. We newly established a trastuzumab/T-DM1-dual-resistant cell line and analyzed the resistance mechanisms in this cell line. At first, the T-DM1 effectively inhibited the YES1-amplified trastuzumab-resistant cell line, but resistance to T-DM1 gradually developed. YES1 amplification was further enhanced after acquired resistance to T-DM1 became apparent, and the knockdown of the YES1 or the administration of the Src inhibitor dasatinib restored sensitivity to T-DM1. Our results indicate that YES1 is also strongly associated with T-DM1 resistance after the development of acquired resistance to trastuzumab, and the continuous inhibition of YES1 is important for overcoming resistance to T-DM1.

    DOI: 10.3390/ijms222312809

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  • Overcoming epithelial-mesenchymal transition-mediated drug resistance with monensin-based combined therapy in non-small cell lung cancer. 国際誌

    Kosuke Ochi, Ken Suzawa, Shuta Tomida, Kazuhiko Shien, Jui Takano, Shunsaku Miyauchi, Tatsuaki Takeda, Akihiro Miura, Kota Araki, Kentaro Nakata, Hiromasa Yamamoto, Mikio Okazaki, Seiichiro Sugimoto, Tadahiko Shien, Masaomi Yamane, Kazuo Azuma, Yoshiharu Okamoto, Shinichi Toyooka

    Biochemical and biophysical research communications   529 ( 3 )   760 - 765   2020年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: The epithelial-mesenchymal transition (EMT) is a key process in tumor progression and metastasis and is also associated with drug resistance. Thus, controlling EMT status is a research of interest to conquer the malignant tumors. MATERIALS AND METHODS: A drug repositioning analysis of transcriptomic data from a public cell line database identified monensin, a widely used in veterinary medicine, as a candidate EMT inhibitor that suppresses the conversion of the EMT phenotype. Using TGF-β-induced EMT cell line models, the effects of monensin on the EMT status and EMT-mediated drug resistance were assessed. RESULTS: TGF-β treatment induced EMT in non-small cell lung cancer (NSCLC) cell lines and the EGFR-mutant NSCLC cell lines with TGF-β-induced EMT acquired resistance to EGFR-tyrosine kinase inhibitor. The addition of monensin effectively suppressed the TGF-β-induced-EMT conversion, and restored the growth inhibition and the induction of apoptosis by the EGFR-tyrosine kinase inhibitor. CONCLUSION: Our data suggested that combined therapy with monensin might be a useful strategy for preventing EMT-mediated acquired drug resistance.

    DOI: 10.1016/j.bbrc.2020.06.077

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  • Antitumor Effects of Pan-RAF Inhibitor LY3009120 Against Lung Cancer Cells Harboring Oncogenic BRAF Mutation. 国際誌

    Shunsaku Miyauchi, Kazuhiko Shien, Tatsuaki Takeda, Kota Araki, Kentaro Nakata, Akihiro Miura, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Kei Namba, Ken Suzawa, Hiromasa Yamamoto, Mikio Okazaki, Junichi Soh, Shuta Tomida, Masaomi Yamane, Masakiyo Sakaguchi, Shinichi Toyooka

    Anticancer research   40 ( 5 )   2667 - 2673   2020年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND/AIM: The therapeutic strategy for patients with non-small-cell lung cancer (NSCLC) harboring the BRAF non-V600E mutation has not been established. LY3009120, a newly discovered pan-RAF inhibitor, has shown strong antitumor effects in cancers with various BRAF genotypes. This study investigated the antitumor effects of LY3009120 in NSCLC cells harboring the BRAF non-V600E mutation. MATERIALS AND METHODS: We examined the antitumor effects of LY3009120 by MTS assay and flow cytometry. We analyzed the expression status of proteins by western blot. The mouse xenograft models were used for the in vivo experiments. RESULTS: LY3009120 suppressed BRAF-related downstream pathway molecules and induced cleavage of poly ADP-ribose polymerase in all examined NSCLC cell lines. LY3009120 also inhibited in vivo tumor growth in NSCLC cells harboring the BRAF non-V600E mutation. CONCLUSION: LY3009120 is a potent therapeutic agent for patients with BRAF non-V600E mutant NSCLC.

    DOI: 10.21873/anticanres.14237

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  • YES1 activation induces acquired resistance to neratinib in HER2-amplified breast and lung cancers. 国際誌

    Tatsuaki Takeda, Hiromasa Yamamoto, Ken Suzawa, Shuta Tomida, Shunsaku Miyauchi, Kota Araki, Kentaro Nakata, Akihiro Miura, Kei Namba, Kazuhiko Shien, Junichi Soh, Tadahiko Shien, Yoshihisa Kitamura, Toshiaki Sendo, Shinichi Toyooka

    Cancer science   111 ( 3 )   849 - 856   2020年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Molecular-targeted therapies directed against human epidermal growth factor receptor 2 (HER2) are evolving for various cancers. Neratinib is an irreversible pan-HER tyrosine kinase inhibitor and has been approved by the FDA as an effective drug for HER2-positive breast cancer. However, acquired resistance of various cancers to molecular-targeted drugs is an issue of clinical concern, and emergence of resistance to neratinib is also considered inevitable. In this study, we established various types of neratinib-resistant cell lines from HER2-amplified breast and lung cancer cell lines using several drug exposure conditions. We analyzed the mechanisms of emergence of the resistance in these cell lines and explored effective strategies to overcome the resistance. Our results revealed that amplification of YES1, which is a member of the SRC family, was amplified in two neratinib-resistant breast cancer cell lines and one lung cancer cell line. Knockdown of YES1 by siRNA and pharmacological inhibition of YES1 by dasatinib restored the sensitivity of the YES1-amplified cell lines to neratinib in vitro. Combined treatment with dasatinib and neratinib inhibited tumor growth in vivo. This combination also induced downregulation of signaling molecules such as HER2, AKT and MAPK. Our current results indicate that YES1 plays an important role in the emergence of resistance to HER2-targeted drugs, and that dasatinib enables such acquired resistance to neratinib to be overcome.

    DOI: 10.1111/cas.14289

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  • Acquired resistance mechanisms to afatinib in HER2-amplified gastric cancer cells. 国際誌

    Takahiro Yoshioka, Kazuhiko Shien, Tatsuaki Takeda, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Kei Namba, Hidejiro Torigoe, Hiroki Sato, Shuta Tomida, Hiromasa Yamamoto, Junichi Soh, Toshiyoshi Fujiwara, Shinichi Toyooka

    Cancer science   110 ( 8 )   2549 - 2557   2019年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cancer treatment, especially that for breast and lung cancer, has entered a new era and continues to evolve, with the development of genome analysis technology and the advent of molecular targeted drugs including tyrosine kinase inhibitors. Nevertheless, acquired drug resistance to molecular targeted drugs is unavoidable, creating a clinically challenging problem. We recently reported the antitumor effect of a pan-HER inhibitor, afatinib, against human epidermal growth factor receptor 2 (HER2)-amplified gastric cancer cells. The purpose of the present study was to identify the mechanisms of acquired afatinib resistance and to investigate the treatment strategies for HER2-amplified gastric cancer cells. Two afatinib-resistant gastric cancer cell lines were established from 2 HER2-amplified cell lines, N87 and SNU216. Subsequently, we investigated the molecular profiles of resistant cells. The activation of the HER2 pathway was downregulated in N87-derived resistant cells, whereas it was upregulated in SNU216-derived resistant cells. In the N87-derived cell line, both MET and AXL were activated, and combination treatment with afatinib and cabozantinib, a multikinase inhibitor that inhibits MET and AXL, suppressed the cell growth of cells with acquired resistance both in vitro and in vivo. In the SNU216-derived cell line, YES1, which is a member of the Src family, was remarkably activated, and dasatinib, a Src inhibitor, exerted a strong antitumor effect in these cells. In conclusion, we identified MET and AXL activation in addition to YES1 activation as novel mechanisms of afatinib resistance in HER2-driven gastric cancer. Our results also indicated that treatment strategies targeting individual mechanisms of resistance are key to overcoming such resistance.

    DOI: 10.1111/cas.14089

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  • Ganetespib in Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor-resistant Non-small Cell Lung Cancer. 国際誌

    Eisuke Kurihara, Kazuhiko Shien, Hidejiro Torigoe, Tatsuaki Takeda, Yuta Takahashi, Yusuke Ogoshi, Takahiro Yoshioka, Kei Namba, Hiroki Sato, Ken Suzawa, Hiromasa Yamamoto, Junichi Soh, Mikio Okazaki, Tadahiko Shien, Shuta Tomida, Shinichi Toyooka

    Anticancer research   39 ( 4 )   1767 - 1775   2019年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: The 90-kDa heat-shock protein (HSP90) is a chaperone protein expressed at high levels in cancer cells and is involved in the folding or stabilization of several client proteins, including epidermal growth factor receptor (EGFR). Ganetespib is a second-generation HSP90 inhibitor with a potent antitumor effect against various cancer types. MATERIALS AND METHODS: This study examined the antitumor effect of ganetespib in EGFR-mutant non-small cell lung cancer (NSCLC) cells and experimentally established EGFR-tyrosine kinase inhibitor (TKI)-resistant cells harboring various resistance mechanisms, including EGFR T790M mutation, met proto-oncogene amplification, and epithelial-mesenchymal transition. RESULTS: Ganetespib showed a potent antitumor effect at low concentrations, suppressing EGFR-related downstream pathway molecules and inducing cleavage of poly ADP-ribose polymerase in all examined EGFR-TKI-resistant cell lines in vitro. Ganetespib also inhibited in vivo tumor growth in resistant cells harboring EGFR T790M. CONCLUSION: Ganetespib might be a promising therapeutic option for the treatment of patients with EGFR-TKI-resistant NSCLC.

    DOI: 10.21873/anticanres.13283

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  • Application of amplicon-based targeted sequencing with the molecular barcoding system to detect uncommon minor EGFR mutations in patients with treatment-naïve lung adenocarcinoma. 国際誌

    Kei Namba, Shuta Tomida, Takehiro Matsubara, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Takahiro Yoshioka, Tatsuaki Takeda, Hidejiro Torigoe, Hiroki Sato, Kazuhiko Shien, Hiromasa Yamamoto, Junichi Soh, Kazunori Tsukuda, Shinichi Toyooka

    BMC cancer   19 ( 1 )   175 - 175   2019年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: In lung cancer, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor sensitizing mutations co-existing with rare minor EGFR mutations are known as compound mutations. These minor EGFR mutations can lead to acquired resistance after EGFR tyrosine kinase inhibitor treatment, so determining the mutation status of patients is important. However, using amplicon-based targeted deep sequencing based on next-generation sequencing to characterize mutations is prone to sequencing error. We therefore assessed the benefit of incorporating molecular barcoding with high-throughput sequencing to investigate genomic heterogeneity in treatment-naïve patients who have undergone resection of their non-small cell lung cancer (NSCLC) EGFR mutations. METHODS: We performed amplicon-based targeted sequencing with the molecular barcoding system (MBS) to detect major common EGFR mutations and uncommon minor mutations at a 0.5% allele frequency in fresh-frozen lung cancer samples. RESULTS: Profiles of the common mutations of EGFR identified by MBS corresponded with the results of clinical testing in 63 (98.4%) out of 64 cases. Uncommon mutations of EGFR were detected in seven cases (10.9%). Among the three types of major EGFR mutations, patients with the G719X mutation had a significantly higher incidence of compound mutations than those with the L858R mutation or exon 19 deletion (p = 0.0052). This was validated in an independent cohort from the Cancer Genome Atlas dataset (p = 0.018). CONCLUSIONS: Our findings demonstrate the feasibility of using the MBS to establish an accurate NSCLC patient genotype. This work will help understand the molecular basis of EGFR compound mutations in NSCLC, and could aid the development of new treatment modalities.

    DOI: 10.1186/s12885-019-5374-1

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  • Activation of AXL as a Preclinical Acquired Resistance Mechanism Against Osimertinib Treatment in EGFR-Mutant Non-Small Cell Lung Cancer Cells. 国際誌

    Kei Namba, Kazuhiko Shien, Yuta Takahashi, Hidejiro Torigoe, Hiroki Sato, Takahiro Yoshioka, Tatsuaki Takeda, Eisuke Kurihara, Yusuke Ogoshi, Hiromasa Yamamoto, Junichi Soh, Shuta Tomida, Shinichi Toyooka

    Molecular cancer research : MCR   17 ( 2 )   499 - 507   2019年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Osimertinib (AZD9291) has an efficacy superior to that of standard EGFR-tyrosine kinase inhibitors for the first-line treatment of patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC). However, patients treated with osimertinib eventually acquire drug resistance, and novel therapeutic strategies to overcome acquired resistance are needed. In clinical or preclinical models, several mechanisms of acquired resistance to osimertinib have been elucidated. However, the acquired resistance mechanisms when osimertinib is initially used for EGFR-mutant NSCLC remain unclear. In this study, we experimentally established acquired osimertinib-resistant cell lines from EGFR-mutant NSCLC cell lines and investigated the molecular profiles of resistant cells to uncover the mechanisms of acquired resistance. Various resistance mechanisms were identified, including the acquisition of MET amplification, EMT induction, and the upregulation of AXL. Using targeted next-generation sequencing with a multigene panel, no secondary mutations were detected in our resistant cell lines. Among three MET-amplified cell lines, one cell line was sensitive to a combination of osimertinib and crizotinib. Acquired resistance cell lines derived from H1975 harboring the T790M mutation showed AXL upregulation, and the cell growth of these cell lines was suppressed by a combination of osimertinib and cabozantinib, an inhibitor of multiple tyrosine kinases including AXL, both in vitro and in vivo. Our results suggest that AXL might be a therapeutic target for overcoming acquired resistance to osimertinib. IMPLICATIONS: Upregulation of AXL is one of the mechanisms of acquired resistance to osimertinib, and combination of osimertinib and cabozantinib might be a key treatment for overcoming osimertinib resistance.

    DOI: 10.1158/1541-7786.MCR-18-0628

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  • Therapeutic strategies for afatinib-resistant lung cancer harboring HER2 alterations. 国際誌

    Hidejiro Torigoe, Kazuhiko Shien, Tatsuaki Takeda, Takahiro Yoshioka, Kei Namba, Hiroki Sato, Ken Suzawa, Hiromasa Yamamoto, Junichi Soh, Masakiyo Sakaguchi, Shuta Tomida, Kazunori Tsukuda, Shinichiro Miyoshi, Shinichi Toyooka

    Cancer science   109 ( 5 )   1493 - 1502   2018年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Human epidermal growth factor receptor 2 (HER2) plays an important role in the pathogenesis of various cancers. HER2 alterations have been suggested to be a therapeutic target in non-small-cell lung cancer (NSCLC), just as in breast and gastric cancers. We previously reported that the pan-HER inhibitor afatinib could be a useful therapeutic agent as HER2-targeted therapy for patients with NSCLC harboring HER2 alterations. However, acquired resistance to afatinib was observed in the clinical setting, similar to the case for other HER inhibitors. Thus, elucidation of the mechanisms underlying the development of acquired drug resistance and exploring means to overcome acquired drug resistance are important issues in the treatment of NSCLC. In this study, we experimentally established afatinib-resistant cell lines from NSCLC cell lines harboring HER2 alterations, and investigated the mechanisms underlying the acquisition of drug resistance. The established cell lines showed several unique afatinib-resistance mechanisms, including MET amplification, loss of HER2 amplification and gene expression, epithelial-to-mesenchymal transition (EMT) and acquisition of cancer stem cell (CSC)-like features. The afatinib-resistant cell lines showing MET amplification were sensitive to the combination of afatinib plus crizotinib (a MET inhibitor), both in vitro and in vivo. The resistant cell lines which showed EMT or had acquired CSC-like features remained sensitive to docetaxel, like the parental cells. These findings may provide clues to countering the resistance to afatinib in NSCLC patients with HER2 alterations.

    DOI: 10.1111/cas.13571

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  • Yes1 signaling mediates the resistance to Trastuzumab/Lap atinib in breast cancer. 国際誌

    Tatsuaki Takeda, Hiromasa Yamamoto, Hirotaka Kanzaki, Ken Suzawa, Takahiro Yoshioka, Shuta Tomida, Xiaojiang Cui, Ramachandran Murali, Kei Namba, Hiroki Sato, Hidejiro Torigoe, Mototsugu Watanabe, Kazuhiko Shien, Junichi Soh, Hiroaki Asano, Kazunori Tsukuda, Yoshihisa Kitamura, Shinichiro Miyoshi, Toshiaki Sendo, Shinichi Toyooka

    PloS one   12 ( 2 )   e0171356   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Overexpression of human epidermal growth factor receptor 2 (HER2) is observed in approximately 15-23% of breast cancers and these cancers are classified as HER2-positive breast cancer. Trastuzumab is the first-line targeted therapeutic drug for HER2-positive breast cancer and has improved patient overall survival. However, acquired resistance to trastuzumab is still a critical issue in breast cancer treatment. We previously established a trastuzumab-resistant breast cancer cell line (named as BT-474-R) from a trastuzumab-sensitive HER2-amplified cell line BT-474. Lapatinib is also a molecular-targeted drug for HER2-positive breast cancer, which acquired the resistance to trastuzumab. Acquired resistance to lapatinib is also an issue to be conquered. METHODS: We established trastuzumab/lapatinib-dual resistant cell line (named as BT-474-RL2) by additionally treating BT-474-R with lapatinib. We analyzed the mechanisms of resistance to trastuzumab and lapatinib. Besides, we analyzed the effect of the detected resistance mechanism in HER2-positive breast cancer patients. RESULTS: Proto-oncogene tyrosine-protein kinase Yes1, which is one of the Src family members, was amplified, overexpressed and activated in BT-474-R and BT-474-RL2. Silencing of Yes1 by siRNA induced both BT-474-R and BT-474-RL2 to restore the sensitivity to trastuzumab and lapatinib. Pharmaceutical inhibition of Yes1 by the Src inhibitor dasatinib was also effective to restore the sensitivity to trastuzumab and lapatinib in the two resistant cell lines. Combination treatment with dasatinib and trastuzumab induced down-regulation of signaling molecules such as HER2 and Akt. Moreover, the combination treatments induced G1-phase cell-cycle arrest and apoptosis. Consistent with cell line data, high expression of Yes1 mRNA was correlated with worse prognosis in patients with HER2-positive breast cancer. CONCLUSION: Yes1 plays an important role in acquired resistance to trastuzumab and lapatinib in HER2-positive breast cancer. Our data suggest that pharmacological inhibition of Yes1 may be an effective strategy to overcome resistance to trastuzumab and lapatinib.

    DOI: 10.1371/journal.pone.0171356

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  • Differential combined effect of COX inhibitors on cell survival suppressed by sorafenib in the HepG2 cell line.

    Kenta Yagi, Yoichi Kawasaki, Hiroko Nakamura, Taro Miura, Tatsuaki Takeda, Satoru Esumi, Hisashi Matsunaga, Yoshihisa Kitamura, Toshiaki Sendo

    Biological & pharmaceutical bulletin   37 ( 7 )   1234 - 40   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Sorafenib, a molecular-targeted drug, is a multi-target oral anti-neoplastic drug that is used as a first-line treatment for patients with advanced Human HCC. An increase in the expression of the cyclooxygenase-2 (COX-2) protein and sequential production of prostaglandin (PG) E2 were previously shown to significantly enhance carcinogenesis. Although the synergistic and/or additive effects of various COX inhibitors have been demonstrated in HCC, those of a combination of sorafenib and COX inhibitors remain unclear. The aim of the present study was to examine the antitumor effects of a combination of sorafenib and COX inhibitors on HCC HepG2 cells. Various COX inhibitors suppressed HepG2 cell survival, and exhibited a combined effect with sorafenib. However, COX-2 selectivity had little relevance. The co-administration of COX inhibitors and sorafenib increased the frequency of apoptosis. Moreover, the combination of sorafenib and diclofenac significantly increased Bax protein expression levels. The results of the present study indicate that COX inhibitors can be administered in combination with sorafenib for HCC therapy.

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MISC

  • 医療ビッグデータを活用した免疫関連心筋炎の予防法の構築

    座間味義人, 武田達明, 牛尾聡一郎, 濱野裕章

    日本薬剤学会年会講演要旨集(CD-ROM)   38th   2023年

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  • 医薬品副作用情報データベースの活用によるバイオシミラーの安全性評価

    藤井緑, 濱野裕章, 濱野裕章, 武田達明, 谷岡真樹, 鍛治園誠, 西原茂樹, 村川公央, 座間味義人, 座間味義人

    次世代を担う若手のための創薬・医療薬理シンポジウムプログラム・要旨集   2023   2023年

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  • パンデミック後の薬学部病院実務実習の変化

    猪田宏美, 武田達明, 西原茂樹, 松本 准, 有吉範高, 座間味義人

    医学教育   2023年

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  • 癌関連線維芽細胞を標的としたトラニラストの癌治療増感効果 国際誌

    大智宏祐, 大智宏祐, 諏澤憲, 枝園和彦, 武田達明, 山本寛斉, 岡本芳晴, 豊岡伸一, 豊岡伸一

    日本癌学会学術総会抄録集(Web)   79th ( 10 )   3428 - 3436   2022年7月

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  • 薬物相互作用(52-利尿薬の薬物相互作用)

    武田達明, 江角悟, 村川公央

    岡山医学会雑誌   133 ( 3 )   2021年

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  • 再生医療等製品の治験製品管理・調製の現状と市販化に向けた課題

    武田達明, 晴田佑介, 河崎陽一, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   21st   2021年

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  • がんゲノム医療におけるCRCの取り組みと役割

    宮本理史, 奥田浩人, 武田達明, 宮本理史, 奥田浩人, 武田達明, 難波志穂子, 黒田智, 黒田智, 平沢晃, 千堂年昭, 四方賢一

    薬理と治療   49 ( 6 )   2021年

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  • 組織・遺伝子診断 肉腫におけるがんゲノム医療の意義

    中田英二, 藤原智洋, 国定俊之, 尾崎敏文, 遠西大輔, 冨田秀太, 平沢晃, 二川摩周, 武田達明

    別冊整形外科   ( 79 )   2021年

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  • The activation of YES1 leads to the acquired resistance to neratinib in HER2-amplified breast and lung cancers

    Hiromasa Yamamoto, Tatsuaki Takeda, Ken Suzawa, Shuta Tomida, Shunsaku Miyauchi, Kota Araki, Kentaro Nakata, Akihiro Miura, Tadahiko Shien, Yoshihisa Kitamura, Toshiaki Sendo, Shinichi Toyooka

    CANCER RESEARCH   80 ( 16 )   2020年8月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:AMER ASSOC CANCER RESEARCH  

    DOI: 10.1158/1538-7445.AM2020-1884

    Web of Science

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  • がんゲノム医療におけるCRCの取り組みと役割

    宮本理史, 奥田浩人, 奥田浩人, 武田達明, 難波志穂子, 黒田智, 黒田智, 平沢晃, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   20th   2020年

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  • パクリタキセル注射薬の不溶物に対するプラスチック針の有用性

    八木健太, 武田達明, 牛尾聡一郎, 江角悟, 鍛治園誠, 北村佳久, 千堂年昭

    日本注射薬臨床情報学会誌   ( 7 )   2019年

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  • ネラチニブ耐性乳がんにおけるYES1の重要性

    武田達明, 山本寛斉, 諏澤憲, 北村佳久, 千堂年昭, 豊岡伸一

    日本癌学会学術総会抄録集(Web)   78th   2019年

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  • 非小細胞肺癌におけるモネンシン併用療法によるEMT関連薬剤耐性の克服

    大智宏祐, 諏澤憲, 冨田秀太, 荒木恒太, 宮内俊策, 三浦章博, 武田達明, 難波圭, 枝園和彦, 山本寛斉, 岡崎幹生, 枝園忠彦, 豊岡伸一

    日本癌学会学術総会抄録集(Web)   78th   2019年

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  • EGFR-TKI耐性NSCLCに対するHSP90阻害剤ganetespibの有用性の検討

    栗原英祐, 枝園和彦, 鳥越英次郎, 武田達明, 荒木恒太, 宮内俊策, 三浦章博, 高橋優太, 諏澤憲, 山本寛斉, 宗淳一, 冨田秀太, 豊岡伸一

    日本呼吸器外科学会総会(Web)   36th   2019年

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  • 乳がんにおけるネラチニブ耐性化の機序解析(Analyses of the mechanisms of the resistance to neratinib in breast cancer)

    武田 達明, 山本 寛斉, 冨田 秀太, 高橋 優太, 栗原 英祐, 大越 祐介, 枝園 和彦, 宗 淳一, 北村 佳久, 千堂 年昭, 豊岡 伸一

    日本癌学会総会記事   77回   839 - 839   2018年9月

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    記述言語:英語   出版者・発行元:日本癌学会  

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  • パクリタキセル調製時に発生する不溶性異物に対するプラスチック針の有用性

    八木健太, 武田達明, 牛尾聡一郎, 江角悟, 鍛治園誠, 北村佳久, 千堂年昭

    日本医療薬学会年会講演要旨集(Web)   27   2017年

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  • 小児急性骨髄性白血病(AML)における脱メチル化薬の有効性

    竹井絵莉菜, 嶋田明, 神崎浩孝, 渡部友紀, 武田達明, 八木健太, 槙田祟志, 正岡康幸, 北村佳久, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   135th   2015年

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  • 乳癌におけるHER2標的治療薬に対する耐性化機構

    武田達明, 神崎浩孝, 豊岡伸一, 豊岡伸一, 宋淳一, 宋淳一, 山本寛斉, 山本寛斉, 橋田真輔, 橋田真輔, 北村佳久, 北村佳久, 三好新一郎, 千堂年昭, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   135th   2015年

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  • トラスツズマブに耐性化したHER2陽性乳癌対するNF-κB阻害薬の有効性

    神崎浩孝, MURALI Ramachandran, CUI Xiaojiang, 武田達明, 北村佳久, 北村佳久, 千堂年昭, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   135th   2015年

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  • 小児急性骨髄性白血病における癌抑制遺伝子のDNAメチル化と脱メチル化剤の抗腫瘍効果(Promotor Hypermethylation of Tumor Suppressor Genes in Pediatric Acute Myeloid Leukemia and Anti-Tumor Effect of Demethylating Agent)

    竹井 絵莉菜, 神崎 浩孝, 武田 達明, 八木 健太, 槇田 崇志, 正岡 康幸, 北村 佳久, 千堂 年昭, 嶋田 明

    日本小児血液・がん学会雑誌   51 ( 4 )   269 - 269   2014年10月

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    記述言語:英語   出版者・発行元:(一社)日本小児血液・がん学会  

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  • 慢性骨髄性白血病細胞株を用いたイマチニブとJAK阻害剤併用の有用性に関する基礎的検討

    八木健太, 河崎陽一, 嶋田明, 竹井絵莉菜, 武田達明, 江角悟, 北村佳久, 北村佳久, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   134th   2014年

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  • 入院患者における緩和ケア介入による痛み・気持ちのつらさの改善に関する検討

    武田達明, 鍛治園誠, 河崎陽一, 高下典子, 江角悟, 北村佳久, 北村佳久, 松岡順治, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   134th   2014年

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講演・口頭発表等

  • 乳がん・肺がんにおけるHER2阻害薬ネラチニブに対する獲得耐性へのYES1の重要性

    武田 達明, 山本 寛斉, 千堂 年昭, 豊岡 伸一

    第14回次世代を担う若手のための医療薬科学シンポジウム 

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    開催年月日: 2020年11月28日

    会議種別:口頭発表(一般)  

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  • 遺伝子パネル検査におけるレポートの読み方

    ゲノム医療薬剤師研修会 in 岡山 

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    開催年月日: 2020年2月23日

    会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • がんゲノム医療と薬剤師

    第2回がんゲノム医療従事者多職種合同セミナー 

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    開催年月日: 2020年1月25日

    会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • がんゲノム医療における薬剤師の関わり 招待

    広島県がん診療連携拠点病院薬剤師研修会 

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    開催年月日: 2020年1月22日

    会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • がんゲノム医療における薬剤師の役割 招待

    第12回薬剤師セミナー 

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    開催年月日: 2020年1月18日

    会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • がんゲノム医療と薬剤師

    がんゲノム医療従事者多職種合同セミナー 

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    開催年月日: 2019年9月8日

    会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • がんゲノム医療における薬剤師の関わり 招待

    武田達明, 河内麻里子, 遠西大輔, 久保寿夫, 冨田秀太, 北村佳久, 千堂年昭, 平沢 晃, 豊岡伸一

    第5回クリニカルバイオバンク学会シンポジウム 

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    開催年月日: 2019年7月7日

    会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • trastuzumab/lapatinib 耐性乳癌におけるYes1の重要性

    武田達明, 山本寛斉, 神崎浩孝, 諏澤 憲, 吉岡貴裕, 冨田秀太, 北村佳久, 豊岡伸一, 千堂年昭

    日本医療薬学会 第1回フレッシャーズ・カンファランス 

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    開催年月日: 2017年5月25日

    会議種別:口頭発表(一般)  

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  • 乳癌におけるトラスツズマブ耐性化の要因解析とその克服に向けた新規アプローチ

    武田達明, 神崎浩孝, 山本寛斎, 北村佳久, 豊岡伸一, 三好耕一郎, 千堂年昭

    日本薬学会第136年会 シンポジウム:患者のQOL改善を目指した薬学基礎研究 

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    開催年月日: 2016年3月29日

    会議種別:シンポジウム・ワークショップ パネル(公募)  

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  • Anti-tumor effect of dasatinib in HER2-positive brast cancer with trastuzumab resistance

    Tatsuaki Takeda, Hirotaka Kanzaki, Shinichi Toyooka, Mototsugu Watanabe, Tomoaki Ohtsuka, Ken Suzawa, Shinsuke Hashida, Yuho Maki, Hiromasa Yamamoto, Junichi Soh, Hiroaki Asano, Kazunori Tsukada, Shinichiro Miyoshi, Yoshihisa Kitamura, Toshiaki Sendo

    American Association for Cancer Research Annual Meeting 2015 

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    開催年月日: 2015年4月

    会議種別:ポスター発表  

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受賞

  • 優秀演題発表賞

    2017年6月   第1回フレッシャーズ・カンファランス  

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共同研究・競争的資金等の研究

  • 抗HER2分子標的薬治療薬耐性におけるHippoシグナルの関連性の解明

    2023年07月 - 2024年03月

    公益財団法人川崎医学・医療福祉学振興会 

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    担当区分:研究代表者 

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  • 既存薬を活用した分子標的治療薬の耐性克服に向けた新たな治療法の確立

    研究課題/領域番号:23K14412  2023年04月 - 2026年03月

    日本学術振興会  科学研究費助成事業  若手研究

    武田 達明

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    配分額:4680000円 ( 直接経費:3600000円 、 間接経費:1080000円 )

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  • 抗HER2薬耐性細胞株に対するトラスツズマブ デルクステカンの有効性の検討

    研究課題/領域番号:21H04182  2021年04月 - 2022年03月

    日本学術振興会  科学研究費助成事業 奨励研究  奨励研究

    武田 達明

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    配分額:470000円 ( 直接経費:470000円 )

    トラスツズマブ デルクステカン(T-DXd)は乳がん、胃がんに使用される薬剤である。本研究では、細胞の遺伝子的な特徴の観点から、T-DXdの有効性を評価した。その結果、YES1の遺伝子増幅、HER2の遺伝子消失、METの遺伝子増幅といった特徴を有する細胞では、T-DXdの効果が減弱することが明らかとなった。

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  • ネラチニブ耐性乳がんモデル動物におけるダサチニブ併用療法の有用性の検討

    研究課題/領域番号:19H00408  2019年 - 2020年

    日本学術振興会  科学研究費助成事業 奨励研究  奨励研究

    武田 達明

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    配分額:540000円 ( 直接経費:540000円 )

    ネラチニブは、現在海外で乳がんの治療に使用されている、新規の分子標的治療薬である。臨床において分子標的治療に対する耐性化が問題となっており、ネラチニブに対しても耐性の出現が予想される。そこで申請者は、ネラチニブ耐性乳がん細胞株を樹立し、耐性克服方法の検討を行ってきた。その結果、慢性骨髄性白血病の治療薬として使用されているダサチニブをネラチニブと併用した場合、抗腫瘍効果が著しく増大することを明らかにした。本研究では、ネラチニブ耐性乳がんモデルマウスを用いて、臨床に近づけた環境で抗腫瘍効果の評価を行い、ダサチニブとネラチニブの併用療法の有効性を明らかにした。

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担当授業科目

  • 実務実習事前教育III (2023年度) 特別  - その他

  • 早期体験学習A (2023年度) 1・2学期  - 金5~8

  • 早期体験学習I (2023年度) 1・2学期  - 金5~8

  • 臨床医薬品治療学1 (2023年度) 第1学期  - 月7~8

  • 臨床医薬品治療学1 (2023年度) 第1学期  - 月7~8

  • 臨床医薬品治療学2 (2023年度) 第2学期  - 月7~8

  • 臨床医薬品治療学2 (2023年度) 第2学期  - 月7~8

  • 臨床準備教育5 (2023年度) 特別  - その他

  • 臨床準備教育III (2023年度) 特別  - その他

  • 薬剤師倫理学 (2023年度) 第1学期  - 火1~2

  • 薬剤師倫理学 (2023年度) 第1学期  - 火1~2

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