title: [Alteration of p53 gene during tree shrews' hepatocarcinogenesis].
abstract: OBJECTIVE
  To detect the expression and variation of p53 gene during tree shrews' hepatocarcinogenesis induced by hepatitis B virus (HBV) and aflatoxin B1 (AFB1).
  
  
  METHODS
  Tree shrews were divided into four groups: the tree shrews were infected with HBV and fed with AFB1 in group A, only infected with HBV in group B, fed with AFB1 alone in group C, and normal control in group D. All the tree shrews were performed liver biopsy every 15 weeks. The tissues of liver and tumor were detected by immunohistochemistry and molecular biotechnologies.
  
  
  RESULTS
  (1) The incidence of hepatocellular carcinoma (HCC) in group A (66.7%) was higher than that in Group B and C (30%). HCC appearance in group A was earlier than that in group C (120.0 weeks +/-16.6 weeks vs 153.3 weeks +/-5.8 weeks, t = 3.336, P<0.01). (2) Mutated p53 protein was not found before the 75th week of the experiment in each group. (3) At the 105th week, the expression rates of mutated p53 protein were 78.6%, 60% and 71.4% in group A, B and C respectively, which were much higher than that (10%) in group D (x2 > or = 5.03, P<0.05). An abnormal band of p53 gene was detected in both group A and C. (4) The mutation points of p53 gene in liver cancer of tree shrew were at codon 275, 78 and 13. The nucleotide sequence and amino acids sequence of tree shrew's wild-type p53 showed 91.7% and 93.4% homology with those of human p53 respectively.
  
  
  CONCLUSIONS
  There is a remarkable synergistic effect between HBV and AFB1 on HCC. Mutated p53 protein is expressed before HCC occurrence, which promotes the development and progress of HCC. HBV and AFB1 may synergistically induce p53 gene mutation.
authors.affiliation: Guangxi Cancer Institute, Nanning 530021, China.
authors.forename: Jian-jia
authors.initials: JJ
authors.lastname: Su
authors.forename: Yuan
authors.initials: Y
authors.lastname: Li
authors.forename: Ke-chen
authors.initials: KC
authors.lastname: Ban
authors.forename: Liu-liang
authors.initials: LL
authors.lastname: Qin
authors.forename: Hui-yun
authors.initials: HY
authors.lastname: Wang
authors.forename: Chun
authors.initials: C
authors.lastname: Yang
authors.forename: Chao
authors.initials: C
authors.lastname: Ou
authors.forename: Xiao-xian
authors.initials: XX
authors.lastname: Duan
authors.forename: Yong-yi
authors.initials: YY
authors.lastname: Li
authors.forename: Rui-qi
authors.initials: RQ
authors.lastname: Yan
mesh_terms: D016604:Aflatoxin B1 / Q000633:toxicity; D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000235:genetics*; D003043:Cocarcinogenesis; D015972:Gene Expression Regulation, Neoplastic; D014644:Genetic Variation; D006509:Hepatitis B / Q000821:virology; D006515:Hepatitis B virus; D008114:Liver Neoplasms, Experimental / Q000235:genetics*; D017354:Point Mutation; D012334:RNA, Neoplasm / Q000032:analysis; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D014418:Tupaiidae
chemical_list: D012334:RNA, Neoplasm; D016159:Tumor Suppressor Protein p53; D016604:Aflatoxin B1