Loss of heterozygosity analysis of microsatellites on multiple chromosome regions in dysplasia and squamous cell carcinoma of the esophagus

Liu,Ming; Zhang,Feng; Liu,Shen; Zhao,Wen; Zhu,Jing; Zhang,Xiaoli

doi:10.3892/etm.2011.297

Loss of heterozygosity analysis of microsatellites on multiple chromosome regions in dysplasia and squamous cell carcinoma of the esophagus

Authors:
- Ming Liu
- Feng Zhang
- Shen Liu
- Wen Zhao
- Jing Zhu
- Xiaoli Zhang
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Affiliations: Department of Cardiothoracic Surgery, Affiliated South-West Hospital, Third Military Medical University, Chongqing 400038, P.R. China, Beijing Institute of Genomics of the Chinese Academy of Sciences, Beijing Genomics Institute, Beijing Proteomics Institute, Beijing 100029, P.R. China, Department of Clinical Laboratory Sciences, Affiliated South-West Hospital, Third Military Medical University, Chongqing 400038, P.R. China, Department of Pathology, Affiliated South-West Hospital, Third Military Medical University, Chongqing 400038, P.R. China
Published online on: June 27, 2011 https://doi.org/10.3892/etm.2011.297
Pages: 997-1001

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Abstract

The objective of this study was to characterize the molecular events in the carcinogenesis of esophageal squamous cell carcinoma (ESCC) and to identify biomarkers for early detection of the disease. Matched precancerous and cancerous tissues resected from 34 esophageal cancer patients from Chongqing, southern China, were compared to evaluate the extent of loss of heterozygosity (LOH). Sixteen microsatellite markers on chromosome regions 3p, 4p, 5q, 8p, 9p, 9q, 11p, 13q and 17p were used for PCR-based LOH analysis. The overall frequency of LOH at the 16 microsatellite loci was significantly increased as the pathological status of the resection specimens changed from low-grade dysplasia (LGD) to high-grade dysplasia (HGD) and SCC (P<0.001). A total of 8 markers showed LOH in the LGD samples. In addition, heterozygosity was regained at 4 loci in the SCC samples of 4 patients, respectively, in comparison to the results for these loci in the HGD samples. The overall rate of LOH increased significantly with the deterioration of the lesions, indicating that tumorigenesis of the esophageal squamous epithelia is a progressive process involving accumulative changes in LOH. The 8 loci showing allelic loss in the LGD samples may be involved in the early-stage tumorigenesis of ESCC, and LOH analysis at these loci may help improve the early detection of this disease. Regain of heterozygosity found in certain patients suggests the possibility of genetic heterogeneity in the tumorigenesis of esophageal cancer.

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