Abstract
Objective To investigate the loss of heterozygosity at 17 microsatellites of 10 chromosome arms in 68 resected specimens of esophageal cancer, and the relationship to the clinicopathological phenotypes of patients. Methods 68 tumor specimens (20 well-differentiated squamous carcinomas, 30 moderately differentiated carcinomas and 18 poorly differentiated carcinomas) and their matched blood samples were analyzed for LOH at 17 microsatellites by using PCR and fluorescence-based DNA sequencing technology, and the association of LOH with the clinicopathological phenotypes of patients was compared statistically. Results The lowest detection frequency of LOH in our subjects was observed at D8S261 with 33. 3%, and the highest frequency was at D9S125 with 85. 2%. There were 12 markers with the frequency of LOH higher than 50.0%, and 3 markers (D3S1597, D3S1285 and D9S125) with the frequency higher than 75. 0%. There was a significant difference in the frequency of LOH at D9S111 and D13S153 between tumors with different histological grades. LOH at D9S111 was observed in 2 of 12 tumors with well differentiation in 14 of 20 tumors with moderate differentiation, and in 14 of 16 tumors with poor differentiation. LOH at DI3S153 was observed in 2 of 8 tumors with well differentiation, in 12 of 28 tumors with moderate differentiation, and in 11 of 12 tumors with poor differentiation. There was a significant difference in the frequency of LOH at D8S261 between tumors with lymph node metastasis and without lymph node metastasis. LOH at D8S261 was found in 1 of 14 tumors with lymph node metastasis, and in 12 of 22 tumors without lymph node metastasis. Conclusions The widespread and frequent loss of heterozygosity may exist in esophageal cancer, and the candidate genes located in the site of frequent LOH may be involved in the development of this cancer; LOH at D9S11 and D13S153 are more commonly observed in the patients with higher histological grades, the tumors with LOH at D8S261 may have a low tendency to lymph node involvement. Key words: Esophageal neoplasms; Microsatellite repeats; Loss of heterozygosity
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