title: [Correlation of c-myc gene amplification, MTS1/p16 gene alternation, and HBV infection in human hepatocellular carcinoma].
abstract: OBJECTIVE
  To observe the roles of c-myc gene amplification, MTS1/p16 gene alternation, and HBV infection in the pathogenesis and progression of hepatocellular carcinoma (HCC).
  
  
  METHODS
  A d-PCR-PAGE-laser scanning technique was used to define amplifications of c-myc oncogene. Alternations of MTS1/p16 gene exon1 and exon2 were analysed by PCR and single-strand conformation polymorphism (SSCP) silver stain method. HBV-DNA was assayed by PCR.
  
  
  RESULTS
  (1)The positive rates of c-myc gene amplification of HCCs and their paired non-cancerous liver tissues were 44.83% (13/29) and 51.72% (15/29). The discrepancies between them were not significant (P>0.05), but they were both significantly higher than that of cirrhotic liver tissues (8.33%, 1/12, P<0.05). (2)A total of 3 homozygous deletions and no mutations of MTS1/p16 gene exon1 and exon2 in HCCs were found in the subset of HCCs. (3)The discrepancies of the positive rates of HBV-DNA among normal liver (14.29%, 2/14), cirrhotic liver (66.67%, 8/12) and HCCs (96.55%, 28/29) were significant (P<0.001). Moreover, the HBV-DNA positive rates increased according to the development of liver lesions (b=0.3986, P<0.001).
  
  
  CONCLUSIONS
  (1)C-myc gene amplification and HBV infection are closely related to the development and progression in a subset of HCCs. However, c-myc gene amplification does not correlate with the HBV infection in HCCs. (2)The homozygous deletions and mutations of MTS1/p16 gene are infrequently encountered in the subset of HCCs.
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing 100083, China.
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: K
authors.initials: K
authors.lastname: Wang
authors.forename: S
authors.initials: S
authors.lastname: Cong
authors.forename: F
authors.initials: F
authors.lastname: Qiu
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: P
authors.initials: P
authors.lastname: Wang
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000473:pathology / Q000821:virology*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics*; D004279:DNA, Viral / Q000032:analysis; D018450:Disease Progression; D005260:Female; D005784:Gene Amplification; D006515:Hepatitis B virus / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000473:pathology / Q000821:virology*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics*; D013223:Statistics as Topic
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D004279:DNA, Viral; D016271:Proto-Oncogene Proteins c-myc