Inactivation of DNA repair gene and their associations with development and progression of pancreatic cancer

2010 Fiscal Year Final Research Report

• Project/Area Number: 20591619
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Gunma University
• Principal Investigator: SUZUKI Hideki Gunma University, 医学部, 講師 (20322018)
• Co-Investigator(Kenkyū-buntansha): SASAKI Shigeru 群馬大学, 医学部, 助教 (50451711) ; MOGI Akira 群馬大学, 大学院・医学系研究科, 助教 (10323362) ; MIYAZAKI Tatsuya 群馬大学, 医学部, 助教 (70372349) ; ASAO Takayuki 群馬大学, 大学院・医学系研究科, 准教授 (40212469) ; KUWANO Hiroyuki 群馬大学, 大学院・医学系研究科, 教授 (90186560)
• Project Period (FY): 2008 – 2010
• Keywords: pancreatic cancer / DNA repair gene / H2AX / MSH2 / ATM

Research Abstract

We already reported that DNA double-strand break(s) (DSBs) repair are related to chromosomal deletions / aberrations. And this result suggested that aberrations of DSBs repair are reflected to some parts of tumorgenesis and developments in pancreatic cancer. In this study, we examined that the relationship of tumorgenesis in pancreatic cancer and aberrations of DSB repair genes. At first, we selected three DSBs repair genes, H2AX, MSH2 and ATM, and examined amount of expressions of these genes at surgical specimens. At the same time, we examined localizations of these genes at surgical specimens. At last, we will compare some clinical or pathological information and the expressions of these genes (on going).