GOTO Akiteru

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Bioregulatory Medicine  Department of Cellular and Organ Pathology

Laboratory Address

Hondo 1-1-1, Akita City, 010-8543, Japan

Mail Address

E-mail address

Research Interests 【 display / non-display

  • Human Pathology

Graduating School 【 display / non-display

  •  
    -
    1995.03

    The University of Tokyo   Faculty of Medicine   Graduated

Graduate School 【 display / non-display

  •  
    -
    1999.03

    The University of Tokyo  Graduate School, Division of Medicine  Doctor's Course  Completed

Campus Career 【 display / non-display

  • 2011.10
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Bioregulatory Medicine   Professor  

Research Areas 【 display / non-display

  • Life Science / Human pathology

Qualification acquired 【 display / non-display

  • Doctor

 

Research Achievements 【 display / non-display

    ◆Original paper【 display / non-display

  • Macrophage numbers in the marginal area of sarcomas predict clinical prognosis

    Umakoshi M.

    Scientific Reports ( Scientific Reports )  13 ( 1 )   2023.12  [Refereed]

    Research paper (journal)  

    DOI Repository

  • A New Chemotactic Mechanism Governs Long-Range Angiogenesis Induced by Patching an Arterial Graft into a Vein

    Minerva D, Othman NL, Nakazawa T, Ito Y, Yoshida M, Goto A, Suzuki T.

    International Journal of Molecular Sciences ( International Journal of Molecular Sciences )  23 ( 19 ) 11208 - 11208   2022.09  [Refereed]

    Research paper (journal)   International Co-author

    DOI PubMed CiNii Research

  • The prognostic role of M2 tumor-associated macrophages in non-small-cell lung cancer

    Li Z, Wang YJ, Zhou J, Umakoshi M, Goto A.

    Histology and Histopathology ( Histology and Histopathology )  37 ( 12 ) 1167 - 1175   2022.05  [Refereed]  [Invited]

    Research paper (journal)   International Co-author

    DOI

  • Soft tissue round cell sarcoma of the abdominal wall, with EWSR1-non-ETS fusion (EWSR1-NFATC2 sarcoma): A case report and literature review emphasizing its clinical features

    Tsuchie H, Umakoshi M, Hasegawa T, Nagasawa H, Okada K, Nanjyo H, Goto A, Miyakoshi N.

    Journal of Orthopaedic Sciences ( Journal of Orthopaedic Science )  29 ( 1 ) 374 - 378   2022.04  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI CiNii Research

  • SKAP2 suppresses inflammation-mediated tumorigenesis by regulating SHP-1 and SHP-2

    Takagane K.

    Oncogene ( Oncogene )  41 ( 8 ) 1087 - 1099   2022.02  [Refereed]

    Research paper (journal)  

    DOI

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    ◆Other【 display / non-display

  • Identification of telomere maintenance gene variations related to lung adenocarcinoma risk by genome‐wide association and whole genome sequencing analyses

    白石 航也, 高橋 篤, 桃沢 幸秀, 醍醐 弥太郎, 金子 修三, 川口 喬久, 國頭 英夫, 松本 慎吾, 堀之内 秀仁, 後藤 明輝, 本多 隆行, 清水 公裕, 虎澤 匡洋, 高柳 大輔, 齋藤 元伸, 斎藤 聡, 大江 裕一郎, 渡辺 俊一, 後藤 功一, 坪井 正博, 土原 一哉, 髙田 定暁, 碧井 智美, 高野 淳, 小林 正嗣, 宮城 洋平, 田中 和美, 鈴木 弘行, 前田 大地, 山浦 匠, 松田 麻衣子, 島田 陽子, 水野 孝昭, 坂本 裕美, 吉田 輝彦, 後藤 悌, 吉田 達哉, 山地 太樹, 園部 誠, 豊岡 伸一, 米田 和恵, 真砂 勝泰, 田中 文啓, 原 めぐみ, 布施 昇男, 西塚 哲, 元井 紀子, 澤田 典絵, 西田 裕一郎, 熊田 和貴, 竹内 研時, 丹野 高三, 谷田部 恭, 角南 久仁子, 菱田 智之, 宮崎 泰成, 伊藤 秀美, 雨宮 光宏, 戸塚 裕彦, 中山 治彦, 横瀬 智之, 石垣 和慶, 永島 宗晃, 大瀧 容一, 今井 一博, 高澤 建, 南谷 佳弘, 小林 和馬, 大久保 憲一, 若井 建志, 清水 厚志, 山本 雅之, 岩崎 基, 松田 浩一, 稲澤 譲治, 白石 友一, 西川 博嘉, 村上 善則, 久保 充明, 松田 文彦, 鎌谷 洋一郎, 浜本 隆二, 松尾 恵太郎, 河野 隆志

    Cancer Communications ( Wiley )  44 ( 2 ) 287 - 293   2024.02  [Refereed]

    非喫煙者に多いEGFR変異肺腺がんへのかかりやすさを解明 肺腺がんの予防・早期発見にむけた手がかりとして期待. 京都大学プレスリリース. 2023-11-09.

    CiNii Research

  • Association between NLRP3 Inflammasome and Tumor-Node-Metastasis Staging in Prostate Cancer: Immunohistochemical Studies of Prostate Needle Biopsy and Radical Prostatectomy Specimens

    Miyauchi Toshiya, Narita Shintaro, Saiki Yuriko, Kudo-Asabe Yukitsugu, Horii Akira, Fukushige Shinichi, Habuchi Tomonori, Nanjo Hiroshi, Goto Akiteru

    The Tohoku Journal of Experimental Medicine ( 東北ジャーナル刊行会 )  264 ( 4 ) 203 - 213   2024

    <p>The pathological role of NLRP3 inflammasome in prostate cancer (PCa) remains unclear. This study aimed to elucidate the expression of its major components in PCa by immunohistochemistry and its clinicopathological significance. An immunohistochemical analysis of 184 prostate needle biopsy and 38 radical prostatectomy specimens from PCa revealed the expression status of NLRP3, PYCARD, and caspase-1, which form NLRP3 inflammasome. Furthermore, the association between the expression of these 3 proteins and the clinical parameters at diagnosis and operation was analyzed. In biopsy specimens, the Cochran-Armitage test demonstrated that the proportion of the high expression of NLRP3 (P < 0.001) and PYCARD (P < 0.001) in cancerous tissue tended to increase as the value of the Gleason Grade Group increased, and immunohistochemistry of NLRP3 and PYCARD helped to distinguish cancerous tissue from adjacent noncancerous tissue in some cases. Furthermore, a univariable logistic regression analysis revealed the high expression of NLRP3 to be associated with clinical T3–4 (P = 0.0056) and distant metastasis at diagnosis (P = 0.011), while the high expression of PYCARD was associated with clinical T3–4 (P < 0.001), regional lymph node metastasis (P < 0.001), and distant metastasis at diagnosis (P < 0.001). However, a multivariable logistic regression analysis showed no significant association. In prostatectomy specimens, no significant association existed between the expression of NLRP3 inflammasome and the clinical parameters at operation, partly due to the influence of neoadjuvant chemohormonal or hormone therapy. In conclusion, these results suggest that NLRP3 inflammasome may promote disease progression and metastasis in PCa, therefore immunohistochemistry of NLRP3 and PYCARD could be useful for diagnosing PCa accurately.</p>

    DOI PubMed CiNii Research

  • Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population

    Shi J.

    Nature Communications ( Nature Communications )  14 ( 1 )   2023.12  [Refereed]

    DOI

  • A Case of Papillary Lung Adenocarcinoma Derived from Malignant Transformation of Papillary Adenoma

    Takahashi Shugo, Saito Yoshitaro, Murakami Masayo, Goto Akiteru, Matsuzaki Ikuo

    Haigan ( The Japan Lung Cancer Society )  63 ( 4 ) 314 - 318   2023.08

    <p><b><i>Background. </i></b>Pulmonary papillary adenoma may malignantly transform into lung adenocarcinoma, although this is very rare. We herein report a case of papillary lung adenocarcinoma derived from malignant transformation of papillary adenoma. <b><i>Case. </i></b>A 45-year-old man was referred to our department for the examination and treatment of a nodular shadow in the right lower lobe on computed tomography (CT) performed by a primary care physician because of right back pain. Eight years previously, a nodular shadow was incidentally found in the right lower lung lobe on CT, and surgical biopsy was considered. However, the patient had refused to address it. Bronchoscopy raised the suspicion of lung adenocarcinoma, and right lower lung lobe resection and mediastinal lymph node dissection were performed. Grossly, the tumor was well-defined, round, and 20 mm in diameter. A pathological examination revealed papillary proliferation and lepidic growth at the tumor margin. Although the clinical course, imaging and gross findings were suggestive of papillary adenoma, the diagnosis of papillary lung adenocarcinoma was made based on the relatively high degree of nuclear atypia and the presence of lepidic growth. In addition, CTNNB1 mutation was detected, which suggested malignant transformation. <b><i>Conclusion. </i></b>We report a very rare case of papillary adenoma with malignant transformation into lung adenocarcinoma.</p>

    DOI CiNii Research

  • CCDC85A is regulated by miR-224-3p and augments cancer cell resistance to endoplasmic reticulum stress

    Takahashi S.

    Frontiers in Oncology ( Frontiers in Oncology )  13   2023  [Refereed]

    DOI

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Grant-in-Aid for Scientific Research 【 display / non-display

  • Grant-in-Aid for Scientific Research(C)

    Project Year: 2024.04  -  2027.03 

  • Grant-in-Aid for Scientific Research(B)

    Project Year: 2023.04  -  2027.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year: 2022.04  -  2025.03