Significance of Loss of Heterozygosity at Chromosome 7q31.1 in Human Gastric Carcinoma and Precancerous Lesions
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Graphical Abstract
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Abstract
Objective To analyze loss of heterozygosity (LOH) at chromosome 7q31.1 in human gastric carcinomas and precancerous lesions by microdissection，to construct allelic loss mappings and define the minimally lost regions (MLR) at chromosome 7q31.1，further to explore the molecular genetic alteration during the malignant progression of human gastric mucosa. Methods The gastric carcinoma and atypical hyperplasia lesions cells were microdissected from paraffin sections.Seven high dense microsatellite markers were used，combined with polymerase chain reaction (PCR)，to detect the frequencies of LOH of every selected microsatellite site at chromosome 7q31.1 in gastric carcinoma and precancerous lesions，then to map detailed alleic losses and define the minimally lost regions on chromosome 7q31.1. Results requency of LOH at chromosome 7q31.1 in gastric carcinoma tissues achieved 70% (21/30).Seven microsatellite markers' frequencies of LOH in loci D7S2459，D7S523，D7S2502，D7S486，D7S480，D7S650 and D7S2486 were 10.0%，6.7%，23.3%，43.3%，26.7%，26.7% and 20.0%，respectively.Through analyzing allelic loss mapping on chromosome 7q31.1，we have found that the MLR was between D7S2502 and D7S480.Additionally，the 7q31.1 LOH was confirmed to be existed in the precancerous lesions of human gastric mucosa，but the frequency of LOH was lower.In the atypical hyperplasia of gastric mucosa，frequency of LOH reached 36.7% (11/30)，and the microsatellite marker with the highest loss frequency was D7S480 (23.3%，7/30).Frequencies of 7q31.1 LOH were significantly different with different degrees of atypical hyperplasia of gastric mucosa (P<0.01). Conclusion The MLR at chromosome 7q31.1 in gastric carcinoma is at the region from D7S2502 to D7S480，which suggests that the region probably harbors a candidate TSG associated with human gastric carcinoma.Gastric precancerous lesionsexists allelic loss at 7q31.1，which is one of the molecular incidences happened early during the development of gastric carcinoma.
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