Development of anti-tumor therapy model using MCM2 function

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590476
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: KITAGAWA Masanobu 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (10177834)
• Co-Investigator(Renkei-kenkyūsha): 倉田 盛人 東京医科歯科大学, 医歯(薬)学総合研究科, 講師 (40451926) ; 阿部 晋也 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (70596725)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: MCM2 / アポトーシス / 腫瘍 / 治療モデル

Outline of Final Research Achievements

The interaction of viral proteins with host-cellular proteins elicits the activation of cellular signal transduction pathways. Previously, we have clarified that an infection with Friend leukemia virus (FLV) markedly enhanced the IR-induced apoptosis of hematopoietic cells in C3H mice in association with P53, ATM, and DNA-PK. The host specificity of this phenomenon was caused by the up-regulated expression of minichromosome maintenance (MCM) 2 in C3H mice. Furthermore, combined FLV and doxorubicin treatment extended the survival of SCID mice bearing MCM2-highly expressing 8047 leukemia cells.

Free Research Field

病理学