Objective: To investigate whether deletion of chromosome 17 is involved in the carcinogenesis of primary glioblastoma multiforme and to localize the possible common deletion region in the aforementioned chromosome. Me...Objective: To investigate whether deletion of chromosome 17 is involved in the carcinogenesis of primary glioblastoma multiforme and to localize the possible common deletion region in the aforementioned chromosome. Methods: Polymerase chain reaction-based microsatellite analysis was used to assess loss of heterozygosity (LOH) on chromosome 17 in 20 primary glioblastoma multiforme (GBM). Fifteen fluorescent dye-labeled polymorphic markers were used. Results: Thirteen of twenty (65%) GBM displayed LOH on at least one marker of chromosome 17p. Two tumors showed either LOH or non-informativeness on all markers tested. The most frequent LOH was observed at loci including D17s799 (53.3%), D17s1852 (53.8%), D17s938 (63.20/o), D17s831 (55.6%). The loci D17s831 (on 17p13) and D17s799–D17s1852 (17p11.2–p12) are distal and proximal to p53 respectively. The frequencies of LOH at all loci examined on chromosome 17q were relatively low (<30%). None of informative loci exhibited microsatellite instability in this study. Conclusion: Loss of genetic material on chromosome 17p may play an important role in the pathogenesis of GBM. Besides the well-known TSG p53 on 17p, other unknown TSCs associated with GBM may be present on the chromosomal regions 17p13 and 17p11.2–p12, which are distal and proximal to p53 respectively.展开更多
Aim:The herpes simplex virus(HSV),one of the most common viruses infecting humans,is featured by a high infection rate and usually causes complex disorders difficult to diagnose and treat.Disease progression is always...Aim:The herpes simplex virus(HSV),one of the most common viruses infecting humans,is featured by a high infection rate and usually causes complex disorders difficult to diagnose and treat.Disease progression is always combined with the specific interaction between organism and environment,but genetic factors play a decisive role in most pathogenic processes.Like most human disorders,individual difference has also been involved in the pathogenesis of HSV infection.The present study aimed to screen the potential gene loci that regulates human predisposition to HSV infection.Methods:With reference to previous studies,inbred mouse lines with significantly distinct predisposition to HSV infection were chosen for gene loci screening.Gene sites on mouse chromosome 17 associated with susceptibility to HSV infection were then identified by correlation analysis and genome-wide scanning technique.Results:Genes affecting the vulnerability of mice to HSV infection were mapped to three regions on the 17th mouse chromosome,D17MIT51.1,D17MIT39.1 and the region between D17MIT180.1 and D17MIT184.Conclusion:The results suggest that the mouse genetic background plays an important role in its susceptibility to HSV-1 infection,which might be regulated by multiple predisposing quantitative trait loci.展开更多
文摘Objective: To investigate whether deletion of chromosome 17 is involved in the carcinogenesis of primary glioblastoma multiforme and to localize the possible common deletion region in the aforementioned chromosome. Methods: Polymerase chain reaction-based microsatellite analysis was used to assess loss of heterozygosity (LOH) on chromosome 17 in 20 primary glioblastoma multiforme (GBM). Fifteen fluorescent dye-labeled polymorphic markers were used. Results: Thirteen of twenty (65%) GBM displayed LOH on at least one marker of chromosome 17p. Two tumors showed either LOH or non-informativeness on all markers tested. The most frequent LOH was observed at loci including D17s799 (53.3%), D17s1852 (53.8%), D17s938 (63.20/o), D17s831 (55.6%). The loci D17s831 (on 17p13) and D17s799–D17s1852 (17p11.2–p12) are distal and proximal to p53 respectively. The frequencies of LOH at all loci examined on chromosome 17q were relatively low (<30%). None of informative loci exhibited microsatellite instability in this study. Conclusion: Loss of genetic material on chromosome 17p may play an important role in the pathogenesis of GBM. Besides the well-known TSG p53 on 17p, other unknown TSCs associated with GBM may be present on the chromosomal regions 17p13 and 17p11.2–p12, which are distal and proximal to p53 respectively.
文摘Aim:The herpes simplex virus(HSV),one of the most common viruses infecting humans,is featured by a high infection rate and usually causes complex disorders difficult to diagnose and treat.Disease progression is always combined with the specific interaction between organism and environment,but genetic factors play a decisive role in most pathogenic processes.Like most human disorders,individual difference has also been involved in the pathogenesis of HSV infection.The present study aimed to screen the potential gene loci that regulates human predisposition to HSV infection.Methods:With reference to previous studies,inbred mouse lines with significantly distinct predisposition to HSV infection were chosen for gene loci screening.Gene sites on mouse chromosome 17 associated with susceptibility to HSV infection were then identified by correlation analysis and genome-wide scanning technique.Results:Genes affecting the vulnerability of mice to HSV infection were mapped to three regions on the 17th mouse chromosome,D17MIT51.1,D17MIT39.1 and the region between D17MIT180.1 and D17MIT184.Conclusion:The results suggest that the mouse genetic background plays an important role in its susceptibility to HSV-1 infection,which might be regulated by multiple predisposing quantitative trait loci.
