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AIM:To analyze loss of heterozygosity (LOH) and homozygousdeletion on p53 gene (exon2-3,4 and 11),chromosome10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellularcarcinoma (HCC).METHODS:PCR and PCR-based microsatellite polymorphismanalysis techniques were used.RESULTS:LOH was observed at D10S579 (10q22-10q23)in 4 of 20 tumors (20%),at D22S421 (22q11.2-22q12.1) in3 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%),andat TP53.G (p53gene exon 11) in 0 of 20(0%).Homozygousdeletion 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 tumorsuppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis anddevelopment 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 Results: LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%), at D22S421 (22q11.2-22q12.1) in3 of 20 (15%) at TP53. Microsatellite polymorphism analysis techniques were used. A (pE3gene exon 2-3) in 4 of 20 (20%) at TP53.B (p53 gene exon 4) in 6 of 20 (30%), andat TP53.G (p53 gene exon 11) %). Homozygous deletion was detected at 10q22-10q23 (8/20; 40%), 22q11.2-22q12.1 (8/20; 40%), p53 gene exon 2-3 CONCLUSION: There might be unidentified tumors uppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the p53 gene exon 4 (6/20, 30%), and p53 gene exon 11 (2/20; 10% pathogenesis and development of HCC