Oya, Mototsugu

写真a

Affiliation

School of Medicine, Department of Urology (Shinanomachi)

Position

Professor

Related Websites

External Links

Career 【 Display / hide

  • 1995.01
    -
    1996

    ニューヨーク医科大学泌尿器科留学

  • 1997.01
    -
    1998.09

    デュッセルドルフ大学泌尿器科留学

  • 1998.10
    -
    2001.03

    慶應義塾大学助手(医学部泌尿器科学)

  • 2001.04
    -
    2007.07

    慶應義塾大学専任講師(医学部泌尿器科学)

  • 2004.08
    -
    2006.07

    文部科学省研究振興局学術調査官(併任)

display all >>

Academic Background 【 Display / hide

  • 1987.03

    Keio University, 医学部

    Graduated

Academic Degrees 【 Display / hide

  • 博士(医学), 慶應義塾大学, 1987.09

Licenses and Qualifications 【 Display / hide

  • 医師免許証, 医師免許証, 1987.06

  • 日本泌尿器科学会 泌尿器科専門医, 1992.04

  • 日本泌尿器科学会 泌尿器科指導医 , 1997.04

  • 日本腎臓学会 腎臓専門医, 日本腎臓学会 腎臓専門医

  • 日本がん治療認定医機構 がん治療認定医, 2008.04

display all >>

 

Research Areas 【 Display / hide

  • Life Science / Urology

Research Keywords 【 Display / hide

  • 腎細胞癌

  • 免疫治療

  • 分子標的治療

  • 前立腺癌

  • 膀胱癌

Research Themes 【 Display / hide

  • 腎細胞癌の免疫環境と血管新生阻害後のリモデリングの統合的解析による新規治療の開発, 

    2018.04
    -
    2021.03

  • 腎細胞癌における血管新生阻害薬に対する耐性の機序の解明と新規治療の探索, 

    2015.04
    -
    2018.03

  • 腎細胞癌における上皮間葉転換に着目した新規標的分子の探索, 

    2013.04
    -
    2015.03

 

Books 【 Display / hide

  • 泌尿器科外来マスターバイブル

    「臨床泌尿器科」編集委員会, 大家, 基嗣, 近藤, 幸尋, 小島, 祥敬, 医学書院, 2019.04,  Page: xv, 438p : 挿図

  • New targeted approach to CRPC

    Takeo Kosaka, Mototsugu Oya, Hormone Therapy and Castration Resistance of Prostate Cancer, 2018.05

     View Summary

    © Springer Nature Singapore Pte Ltd. 2018. All rights reserved. Our understanding of the heterogeneity and genetic characteristics of CRPC demonstrates underlying their complexity, which has been thought to be associated with their intractability. Recent advance of integrative next generation sequencing unveiled the extensive mutational landscape of metastatic CRPC, many of which can be a targetable mutation and been linked to ongoing clinical trials. Molecular stratification of patient groups will clearly be critical to successful drug development and clinical trials from the view point of precision medicine. In this review, we discuss the potential of new targeted approach to impact the clinical management of CRPC.

  • Renal Cell Carcinoma-Molecular Features and Treatment Updates-

    Mototsugu Oya, Springer, 2017

Papers 【 Display / hide

  • Health-related quality of life with enzalutamide versus flutamide in castration-resistant prostate cancer from the AFTERCAB study.

    Uemura H, Kobayashi K, Yokomizo A, Hinotsu S, Horie S, Kakehi Y, Nonomura N, Ogawa O, Oya M, Suzuki K, Saito A, Asakawa K, Uno S, Naito S

    International journal of clinical oncology  2022.08

    ISSN  1341-9625

  • Iliopsoas abscess in patients receiving hemodialysis: a case series and a literature survey

    Oshida Takuma, Yoshida Tadashi, Itoh Hiroshi, Oya Mototsugu

    RENAL REPLACEMENT THERAPY 8 ( 1 )  2022.07

  • Functional analysis of GCNT3 for cell migration and EMT of castration-resistant prostate cancer cells.

    Daiki Yamamoto, Katsumasa Sasaki, Takeo Kosaka, Mototsugu Oya, Toshinori Sato

    Glycobiology  2022.07

    ISSN  0959-6658

     View Summary

    Castration-resistant prostate cancer (CRPC) is a malignant tumor that is resistant to androgen deprivation therapy. Treatments for CRPC are limited, and no diagnostic markers are currently available. O-glycans are known to play an important role in cell proliferation, migration, invasion, and metastasis of cancer cells. However, the differences in the O-glycan expression profiles for normal prostate cancer (PCa) cells compared to CRPC cells have not yet been investigated. In this study, the saccharide primer method was employed to analyze the O-glycans expressed in CRPC cells. Expression levels of core 4-type O-glycans were significantly increased in CRPC cells. Furthermore, the expression level of N-Acetylglucosaminyltransferase 3 (GCNT3), a core 4-type O-glycan synthase gene, was increased in CRPC cells. The expression of core 4-type O-glycans and GCNT3 was presumed to be regulated by androgen deprivation. GCNT3 knockdown induced cell migration and epithelial-mesenchymal transition (EMT). These observations elucidate the mechanism of acquisition of castration resistance in PCa and offer new possibilities for the development of diagnostic markers and therapeutic targets in the treatment of PCa.

  • Characterization of aldosterone-producing cell cluster (APCC) at single-cell resolution.

    Norifusa Iwahashi, Hironobu Umakoshi, Tsugio Seki, Celso E Gomez-Sanchez, Kuniaki Mukai, Makoto Suematsu, Yuta Umezawa, Mototsugu Oya, Takeo Kosaka, Masahide Seki, Yutaka Suzuki, Yutaka Horiuchi, Yoshihiro Ogawa, Koshiro Nishimoto

    The Journal of clinical endocrinology and metabolism  2022.07

    ISSN  0021-972X

     View Summary

    CONTEXT: The adrenal cortex consists of zona glomerulosa (ZG), fasciculata (ZF), and reticularis. Aldosterone-producing cell clusters that strongly express aldosterone synthase (CYP11B2) are frequently found in adult adrenals and harbor somatic mutations that are also detected in aldosterone-producing adenomas (APAs). Primary aldosteronism is mainly caused by APAs or idiopathic hyperaldosteronism (IHA). We presume that APCCs are causing IHA and are precursors of APAs. However, the gene expression characteristics and especially the development of APCC are not well understood. OBJECTIVE: This study aimed to analyze the transcriptome of APCC at single-cell resolution and infer the developmental trajectory. METHODS: Single-cell RNA sequencing (scRNA-seq) of two adult adrenals was performed. RESULTS: Immunohistochemical analyses confirmed the two adrenals had APCCs. scRNA-seq data of 2,928 adrenal cells were obtained and 1,765 adrenocortical cells were identified based on unsupervised clustering and the marker gene expression. The adrenocortical cells were divided into 6 clusters, of which three clusters (923 cells) were composed of APCC/ZG cells. By further sub-clustering, the APCC/ZG cells were divided into three clusters (clusters C1, C2, and C3), we finally identified APCC-cluster (C3) and ZG-cluster (C1). Cluster C2 seemed to be ZG-to-ZF transitional cells. RNA velocity analysis inferred the developmental direction from cluster ZG-cluster-C1 to APCC-cluster-C3. The scRNA-seq additionally revealed that many CYP11B2-positive cells were positive for CYP11B1 and/or CYP17A1, which were essential for cortisol but not for aldosterone production. CONCLUSIONS: Our results revealed the gene expression characteristics of APCC at single-cell resolution and show that some ZG cells remodel to APCC.

  • Salvage focal brachytherapy in castration‐resistant prostate cancer with neuroendocrine differentiation after radiation therapy

    Takahiro Komori, Takeo Kosaka, Keitaro Watanabe, Tomoki Tanaka, Yota Yasumizu, Hiroshi Hongo, Shuji Mikami, Toshio Ohashi, Mototsugu Oya

    IJU Case Reports (Wiley)  5 ( 4 ) 233 - 236 2022.07

    ISSN  2577-171X

     View Summary

    Introduction: Treatment strategy for castration-resistant prostate cancer with neuroendocrine differentiation after radiation therapy has not been established. Case presentation: We described a case of castration-resistant prostate cancer with neuroendocrine differentiation after initial external beam radiotherapy followed by salvage androgen deprivation therapy. Magnetic resonance imaging detected recurrence of a suspicious lesion in the left lobe of the prostate, although the prostate-specific antigen level was <0.2 ng/mL. Transperineal prostate saturation needle biopsy detected adenocarcinoma with neuroendocrine differentiation. The patient underwent salvage focal brachytherapy and had a prostate-specific antigen progression-free survival of 20 months with no obvious adverse events. No recurrence has been detected on magnetic resonance imaging for 18 months. Conclusion: Salvage focal brachytherapy for prostate cancer after external beam radiotherapy can be one of the treatment strategies for local recurrence of castration-resistant prostate cancer with neuroendocrine differentiation.

display all >>

Papers, etc., Registered in KOARA 【 Display / hide

display all >>

Reviews, Commentaries, etc. 【 Display / hide

  • COVID-19感染を契機に勃起不全を来したと考えられる1例

    茂田 啓介, 森田 伸也, 荘所 一典, 安水 洋太, 田中 伸之, 武田 利和, 松本 一宏, 小坂 威雄, 水野 隆一, 浅沼 宏, 大家 基嗣

    日本性機能学会雑誌 ((一社)日本性機能学会)  37 ( 1 ) 21 - 22 2022.06

    ISSN  1345-8361

  • 腎機能障害症例に対する泌尿器がん薬物療法

    水野 隆一, 吉田 理, 大家 基嗣

    泌尿器科 ((有)科学評論社)  15 ( 5 ) 572 - 578 2022.05

    ISSN  2435-192X

  • 専門性と多様性を両立させる!泌尿器科外来ベストNAVI 【企画にあたって】

    大家基嗣

    臨床泌尿器科 ((株)医学書院)  76 ( 4 ) 7 - 7 2022.04

    Other, Single Work

  • 前立腺癌を対象にした最新の基礎研究ートランスレーショナルリサーチによる未来予想図ー

    大家基嗣

    Prostate Journal (医学図書出版(株))  9 ( 1 ) 9 - 9 2022.04

    Other, Single Work,  ISSN  2188-4978

  • 【前立腺癌を対象にした最新の基礎研究-トランスレーショナルリサーチによる未来予想図-】神経内分泌がんにおける脱分化制御機構

    安水 洋太, 小坂 威雄, 大家 基嗣

    Prostate Journal (医学図書出版(株))  9 ( 1 ) 80 - 86 2022.04

    ISSN  2188-4978

     View Summary

    神経内分泌がんは多臓器に発生する癌で、共通する遺伝子背景と組織型を有する。De-novoの神経内分泌がんと治療誘導型の神経内分泌がんがあり、治療誘導型はドライバー経路の抑制によって発生する。TP53・RB1の変異を有する前立腺癌はAR axis抑制に伴うエピジェネティックリプログラミングによって神経内分泌前立腺癌に脱分化する。神経内分泌前立腺癌は不均一な集団であり、ARの有無やbHLH(basic helix-loop-helix)転写因子であるASCL1とNEUROD1によって分類される。(著者抄録)

display all >>

Presentations 【 Display / hide

  • 炭酸カルシウムを主成分とする反復性尿路結石の一例

    渡邊 雅斗,高松 公晴,松井 善一,荒川 孝,大東 貴志,大家 基嗣

    第639回日本泌尿器科学会東京地方会, 

    2022.12

  • 希少型前立腺導管癌における遺伝子変異プロファイル解析

    小林 裕章,小坂 威雄,中村 康平,安水 洋太,武田 利和,木村 徳宏,森田 伸也,松本 一宏,西原 広司,大家 基嗣

    第37回前立腺シンポジウム, 

    2022.12

  • 若年女性に発生した腹膣外発生デスモイド型線維腫の一例

    横田 広太朗,松本 一宏,藤原 信之介,山中 健嗣,安水 洋太,田中 伸之,武田 利和,森田 伸也,小坂 威雄,水野 隆一,浅沼 宏,大家 基嗣,秋田 大宇,陣崎 雅弘,牧内 里美,大喜多 肇

    第639回日本泌尿器科学会東京地方会, 

    2022.12

  • シングルセル解析によるタキサン系抗癌剤耐性前立腺癌の病態解明と新規治療

    本郷 周,小坂 威雄,西原 広司,植田 幸嗣,大家 基嗣

    第37回前立腺シンポジウム, 

    2022.12

  • バイオインフォマティクスを用いた難治性前立腺癌リプログラミング薬剤のスクリーニング

    本郷 周,小坂 威雄,安水 洋太,田中 伸之,武田 利和,森田 伸也,松本 一宏,西原 広司,上田 幸嗣,大家 基嗣

    第37回前立腺シンポジウム, 

    2022.12

display all >>

Research Projects of Competitive Funds, etc. 【 Display / hide

  • 腎細胞癌の免疫環境と血管新生阻害後のリモデリングの統合的解析による新規治療の開発

    2018.04
    -
    2021.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), Principal investigator

  • Elucidation of refractory mechanism to the molecular targeted therapy for renal cell carcinoma

    2015.04
    -
    2018.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), Principal investigator

  • 腎細胞癌における上皮間葉転換に着目した新規標的分子の探索

    2013.04
    -
    2015.03

    文部科学省, 科学研究費助成事業, 基盤研究(B), Principal investigator

  • 泌尿器がんのクローン進化と腫瘍間質の空間解析による免疫治療耐性メカニズムの解明

    2024.04
    -
    2028.03

    基盤研究(A), Principal investigator

  • 腎癌におけるlong non-coding RNAの臨床的意義の解明

    2021.04
    -
    2024.03

    Keio University, Grant-in-Aid for Scientific Research (C), No Setting

     View Summary

    Long non-coding RNA (lncRNA)と癌の関連は様々な癌種で報告され始めているが、その機能解析は未だ不十分である。今回我々は、分子標的療法が治療軸を担っている進行性腎癌に着目し、lncRNAとの関連を明らかにすべきと考えた。ハイスループットな新規RNA detection systemと膨張顕微鏡法(expansion microscopy)を組み合わせることで、lncRNAの細胞内局在を定量的に可視化して機能解析を進める。

display all >>

Intellectual Property Rights, etc. 【 Display / hide

  • 前立腺がんの予防又は治療剤

    Date applied: 特願2018-091237  2018.05 

    Patent, Joint

  • カバジタキセル耐性前立腺がんの予防または治療剤

    Date applied: 特願2018-007668  2018.01 

    Patent, Joint

  • 前立腺がんの予防又は治療剤

    Date applied: 特願2018-003169  2018.01 

    Patent, Joint

  • 腎癌の再発リスクの予測に用いるための診断薬及びキット、並びに予測方法

    Date applied: 特願2013-148969  2013.07 

    Patent, Joint

  • 抗がん剤の効果増強剤

    Date applied: 特願20120127405  2012.06 

    Date issued: 5947623  2016.07

    Patent, Joint

Awards 【 Display / hide

  • 第12回日本泌尿器科学会賞

    OYA MOTOTSUGU, 2005.04, 社団法人日本泌尿器科学会, Increased activation of nuclear factor-kappaB is related to the tumor development of renal cell carcinonma. Carcinogenesis 24: 377-384, 2003

    Type of Award: Award from Japanese society, conference, symposium, etc.

     View Description

    腎細胞癌における腫瘍随伴症状のメカニズムとしてnuclear factor-kappaB の活性化を明らかにした。

  • 第6回オレガノン泌尿器科研究奨励賞

    2006.06

  • 第20回日本泌尿器科学会 研究助成金

    2011.04, 分子標的薬に対する耐性機序の解明を目的とした腎細胞癌における上皮-間質転換の意義

 

Courses Taught 【 Display / hide

  • UROLOGY: SEMINAR

    2024

  • UROLOGY: PRACTICE

    2024

  • UROLOGY

    2024

  • LECTURE SERIES, UROLOGY

    2024

  • ADVANCED UROLOGY

    2024

display all >>

Courses Previously Taught 【 Display / hide

  • Renal cell carcinoma: biological features and rationale for molecular targeted therapy

    Keio University

    2015.04
    -
    2016.03

  • 泌尿器がんⅠ

    Keio University

    2015.04
    -
    2016.03

  • 腎腫瘍

    Keio University

    2015.04
    -
    2016.03

  • 腎・泌尿器系の診断と治療(泌尿器科学概論)

    Keio University

    2015.04
    -
    2016.03

 

Memberships in Academic Societies 【 Display / hide

  • 日本泌尿器科学会

     
  • 日本腎臓学会

     
  • 日本透析医学会

     
  • 日本癌学会

     
  • 日本癌治療学会

     

display all >>

Committee Experiences 【 Display / hide

  • 2004.08
    -
    2006.07

    学術調査官, 文部科学省研究振興局