Elucidation of molecular mechanism of pancreatic cancer showing catastrophic progression

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08413
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: National Institute of Advanced Industrial Science and Technology
• Principal Investigator: IKEHARA YUZURU 国立研究開発法人産業技術総合研究所, 生命工学領域, 上級主任研究員 (10311440)
• Co-Investigator(Renkei-kenkyūsha): YAMAGUCHI Takashi 千葉大学, 大学院医学研究院・腫瘍病理学教室, 講師 (60626563) ; Ikehara Sanae 千葉大学, 大学院医学研究院・腫瘍病理学, 特任助教 (50598779)
• Research Collaborator: HASHIMOTO Mika 国立研究開発法人産業技術総合研究所, 創薬基盤研究部門, テクニカルスタッフ
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 膵管がん / 遺伝子改変モデルマウス / T抗原 / ポリオーマウイルス / PanIN / TGFb / Tube forming Growth

Outline of Final Research Achievements

The aggressive clinical course of pancreatic duct adenocarcinoma (PDAC) relies on the invasive growth of cells showing the histoarchitecture of the tube form growth invading into retroperitoneal tissue and the nerve plexus and metastasizes to lymph nodes. Tube forming growth is an essential histological feature, but the appearance of PDAC is not connected well with the precancerous lesion, pancreatic intraepithelial neoplasia (PanIN). In this study, we demonstrated that the induced expression of SV40 tsA58 large T antigen with KrasG12D developed pancreatic intraepithelial neoplasia to PDAC, and elucidated that the activation of TGF-β signaling plays an important role on the tube forming growth.

Free Research Field

実験病理学