Microsatellite instability and oncogene expression in gastric cancer

Research Project

Project/Area Number	07671417
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Digestive surgery
Research Institution	Nara Medical University
Principal Investigator	YAMADA Yukishige Nara Medical University, Faculty of Medicine, Assistant, 医学部, 助手 (50254496)
Co-Investigator(Kenkyū-buntansha)	WATANABE Akihiko Nara Medical University, Faculty of Medicine, Associate-Professor, 医学部, 講師 (80211671)
Project Period (FY)	1995 – 1997
Project Status	Completed (Fiscal Year 1997)
Budget Amount *help	¥2,200,000 (Direct Cost: ¥2,200,000) Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000) Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000) Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
Keywords	gastric cancer / oncogene / Microsatellite instability / c-erbB-2 / c-met / cyclin E / Replication error / がん抑制遺伝子 / マイコロサテライトインスタビリティー / マイクロサテライトインスタビリティー
Research Abstract	Overexpression of cyclin E was obserbed in 22.4% of gastric cancer cases. Those were significantly corraleted with depth of invasion and lymph node metastasis. The survival rate of the patients with cyclin E overexpression was significantly poorer than that of the patients without cyclin E overexpression. Overexpression of c-met and c-erbB-2 was obserbed in 46.1% cases and 16.4% cases, respectively. Gene amplification of c-met and c-erbB-2 was detected in 10.2% and 11.7% of gastric cancer cases, respectively. Amplification and overexpression of c-met was significantly correlated with depth of invasion and lymph node metastasis, while amplification and overexpression of c-erbB-2 was significantly correlated with histologic differentiation. The survival rate of the patients with c-met or c-erbB-2 amplification and/or overexpression was significantly poorer than that of the patients without amplification or overexpression. We examined DNA from 42 surgical specimens of gastric cancers for genetic instability at three microsatellite marker loci on chromosomes 2 and 3. We detected differences between tumor and normal DNA banding patterns in 12 of the 42 tumors examined (28.6%). There was no correlation between microsatellite instability and clinicopathological features.