Y Wang1, Y Ke, T Ning, L Feng, G Lu, W Liu, Z E. 1. Department of Cancer Genetics, Beijing Institute for Cancer Research, Beijing Medical University, Beijing, 100034 P.R.China.
Abstract
OBJECTIVE: To identify the microsatellite instability(MSI) rates in Chinese gastric cancer samples. METHODS: 29 microsatellite markers were selected to examine 42 paired gastric cancer tissues for MSI on all chromosomes except Y. RESULTS: The total frequency of MSI in all 42 gastric cancers was 33.9% with higher rates at loci of D3S1577, D3S1067,D8S279,D9S257, D1S248, D7S520 and D2S147,and the highest rate at D3S1577 and D3S1067(51.35%). MSI varied with different pathological types. The frequencies of MSI were signi- ficantly higher in poorly differentiated tumors and signet cell types, compared with well differentiated tumors(P=0.0026 and 0.0013 by chi-square test),and no difference was noted between poorly differentiated and signet cell types. CONCLUSION: MSI may play an important role in Chinese gastric cancer, particularly the poorly differentiated adenocarcinomas. The data presented here further support the previous hypothesis that pathologically distinct subtypes of gastric cancer undergo different genetic pathways during tumorigenesis.
OBJECTIVE: To identify the microsatellite instability(MSI) rates in Chinese gastric cancer samples. METHODS: 29 microsatellite markers were selected to examine 42 paired gastric cancer tissues for MSI on all chromosomes except Y. RESULTS: The total frequency of MSI in all 42 gastric cancers was 33.9% with higher rates at loci of D3S1577, D3S1067,D8S279,D9S257, D1S248, D7S520 and D2S147,and the highest rate at D3S1577 and D3S1067(51.35%). MSI varied with different pathological types. The frequencies of MSI were signi- ficantly higher in poorly differentiated tumors and signet cell types, compared with well differentiated tumors(P=0.0026 and 0.0013 by chi-square test),and no difference was noted between poorly differentiated and signet cell types. CONCLUSION: MSI may play an important role in Chinese gastric cancer, particularly the poorly differentiated adenocarcinomas. The data presented here further support the previous hypothesis that pathologically distinct subtypes of gastric cancer undergo different genetic pathways during tumorigenesis.