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平成 26 年 4 月 8 日 April/08/2014 大学院学生各位 To All Graduate Students 平成 26 年度 基盤医学特論 特徴あるプログラム 開講通知 Cancer Science Course Information on Special Lecture Tokuron 2013 Toku Pro2013 題目:腫瘍の不均一性と微小環境:Akt/giridn シグナル経路からの 理解 Title:Tumor heterogeneity and microenvironment: a view from the Akt/girdin signaling pathway 講師:榎本 篤 先生 (名古屋大学大学院医学系研究科 Teaching Staff : Atsushi Enomoto 腫瘍病理学・准教授) (Department of Pathology, Nagoya University Graduate School of Medicine・Associate Professor) 日時:平成 26 年 5 月 22 日(木) 17 時 00 分~18 時 30 分 Time and Date:. May 22(Thur) , 2014 17:00-18:30 場所: 基礎研究棟 会議室2 Room : Building for Medical Research, Meeting Room2 言語: 英語 Language: English ※ 関係講座・部門等の連絡担当者 分子腫瘍学 荒川 (内線 2454) Contact : Division of Molecular Carcinogenesis, Arakawa (ext 2454) 事前の申込みは不要です。No registration required 医学部学務課大学院掛 Student Affairs Division, School of Medicine Tumor heterogeneity and microenvironment: a view from the Akt/girdin signaling pathway 腫瘍の不均一性と微小環境:Akt/giridn シグナル経路からの理解 Atsushi Enomoto Department of Pathology, Nagoya University Graduate School of Medicine [email protected] The understanding of the heterogeneity and microenvironment of human cancer is critical for the development of new strategies for treating the disease. Increasingly,it is becoming relevant to cancer research with the concept that a minor population called cancer stem cells (CSC) maintains cancer tissues, the property of which is distinct from that of more differentiated and diverse cancer cells. In the seminar, we talk about the role of girdin, which we found is a substrate for the serine/threonine kinase Akt, in the regulation of CSC maintenance and the migratory response of differentiated cancer cells. The involvement of the Akt/girdin pathway in the development of tumor microenvironment is also discussed in terms of the recruitment of cancer-associated fibroblasts. Finally, we discuss another feature of intratumor heterogeneity, which is the presence of leading and following cells that constitute cancer cell collectives, with reference to our recent findings suggesting a distinct mechanism for the formation of leading cells.