摘要
AIM: To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3, 4 and 11), chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC).METHODS: PCR and PCR-based microsatellite polymorphism analysis techniques were used.RESULTS: LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%), at D22S421 (22q11.2-22q12.1) in 3 of 20(15%), at TP53.A (p53gene exon 2-3) in 4 of 20 (20%), at TP53.B (p53gene exon 4) in 6 of 20(30%), and at TP53.G (p53gene exon 11)in 0 of 20(0%). Homozygous deletion was detected at 10q22-10q23(8/20; 40%), 22q11.2-22q12.1(8/20; 40%), p53 gene exon 2-3(0/20;0%), p53gene exon 4(6/20; 30%), and p53gene exon 11(2/20; 10%).CONCLUSION: There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis and development of HCC.
AIM:To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3,4 and 11),chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC). METHODS:PCR and PCR-based microsatellite polymorphism analysis techniques were used. RESULTS:LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%),at D22S421 (22q11.2-22q12.1) in 3 of 20(15%),at TP53.A (pE3gene exon 2-3) in 4 of 20 (20%),at TP53.B (p53gene exon 4) in 6 of 20(30%),and at TP53.G (p53gene exon 11) in 0 of 20(0%).Homozygous deletion was detected at 10q22-10q23(8/20;40%),22q11.2- 22q12.1(8/20;40%),p53 gene exon 2-3(0/20,0%),p53 gene exon 4(6/20,30%),and p53gene exon 11(2/20;10%). CONCLUSION:There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11. 2-22q12.1 that contribute to the pathogenesis and development of HCC.
基金
Supported by the Natural Science Foundation of Anhui Province,No.99044312(YW),No.01043716(SYG)and Natural Science Foundation of Anhui Educational Commission,No.JL-97-077(YW)
