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World J Gastroenterol. Jul 7, 2008; 14(25): 4070-4076
Published online Jul 7, 2008. doi: 10.3748/wjg.14.4070
Microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence
Jian-Chun Cai, Di Liu, Kai-Hua Liu, Hai-Ping Zhang, Shan Zhong, Ning-Sao Xia
Jian-Chun Cai, Di Liu, Kai-Hua Liu, Hai-Ping Zhang, Shan Zhong, Department of Oncology Surgery, Xiamen Cancer Center, Affiliated Xiamen First Hospital, Fujian Medical University, Xiamen 361003, Fujian Province, China
Jian-Chun Cai, Department of Material Science and Engineering, Chemistry and Chemical Engineering College, Xiamen University, Xiamen 361005, Fujian Province, China
Ning-Sao Xia, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, Xiamen University, Xiamen 361005, Fujian Province, China
Author contributions: Cai JC designed the research; Cai JC, Liu D, Liu KH, and Zhong S performed the research; Cai JC, Zhang HP and Xia NS analyzed the data; Cai JC and Liu D wrote the paper.
Correspondence to: Dr. Jian-Chun Cai, Department of Oncology Surgery, Xiamen Cancer Center, Affiliated Xiamen First Hospital, Fujian Medical University, Xiamen 361003, Fujian Province, China. jianchunfh2@sina.com
Telephone: +86-592-2137271
Fax: +86-592-2137189
Received: April 1, 2008
Revised: June 10, 2008
Accepted: June 17, 2008
Published online: July 7, 2008
Abstract

AIM: To investigate the microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence.

METHODS: Forty-one specimens were obtained from esophageal cancer (EC) patients. Histopathological assessment identified 23 squamous cell carcinomas (SCC) and 18 adenocarcinomas (ADC), including only 8 ADC with Barrett esophageal columnar epithelium (metaplasia) and dysplasia adjacent to ADC. Paraffin-embedded normal squamous epithelium, Barrett esophageal columnar epithelium (metaplasia), dysplasia and esophageal tumor tissues were dissected from the surrounding tissues under microscopic guidance. DNA was extracted using proteinase K digestion buffer, and DNA was diluted at 1:100, 1:1000, 1:5000, 1:10 000 and 1:50 000, respectively. Seven microsatellite markers (D2S123, D3S1616, D3S1300, D5S346, D17S787, D18S58 and BATRII loci) were used in this study. Un-dilution and dilution polymerase chain reactions (PCR) were performed, and microsatellite analysis was carried out.

RESULTS: No statistically significant difference was found in microsatellite instability (MSI) and loss of heterozygosity (LOH) of un-diluted DNA between SCC and ADC. The levels of MSI and LOH were high in the metaplasia-dysplasia-adenocarcinoma sequence of diluted DNA. The more the diluted DNA was, the higher the rates of MSI and LOH were at the above 7 loci, especially at D3S1616, D5S346, D2S123, D3S1300 and D18S58 loci.

CONCLUSION: The sequence of metaplasia-dysplasia-adenocarcinoma is associated with microsatellite alterations, including MSI and LOH. The MSI and LOH may be the early genetic events during esophageal carcinogenesis, and genetic alterations at the D3S1616, D5S346 and D3S123 loci may play a role in the progress of microsatellite alterations.

Keywords: Microsatellite alteration; Dilution PCR; Metaplasia-dysplasia-adenocarcinoma sequence; Esophageal squamous epithelium; Squamous cell carcinoma