title: [Expression of phosphatase and tensin homology deleted on chromosome ten(PTEN) and p53 protein and their significance in human hepatocellular carcinomas].
abstract: OBJECTIVE
  Tumor suppressor gene phosphatase and tensin homology deleted on chromosome ten (PTEN) was first reported in 1997 and has become a hot spot shortly after discovery. Mutations of PTEN gene in human hepatocellular carcinomas (HCCs) have been examined by several groups abroad, while little is known about expression of PTEN in HCCs. It has been believed that p53 mutation plays a role in the oncogenesis of HCCs. However, divergence exist as regards the relationship between p53 mutation and some biological behaviors of HCCs. The current study was designed to investigate the correlations of expression of PTEN and mutant p53 with carcinogenesis and tumor progression of HCCs.
  
  
  METHODS
  Sixty-two paraffin-embedded hepatocellular carcinoma samples were composed and all the tissue sections included both HCC and surrounding non-tumor liver tissues. Expression of PTEN and mutant p53 was examined using SP immunohistochemical technique.
  
  
  RESULTS
  All sixty-two samples showed decidedly positive staining of PTEN in surrounding non-tumor liver tissues (plasma). While, only twenty-nine tumors were detected positive staining of PTEN (46.8%). The expression level of PTEN in HCC samples without invasiveness or with complete capsule was higher than that in HCC samples with invasiveness or without complete capsule. No positive staining of p53 was detected in surrounding non-tumor liver tissues for all sixty-two samples. However, twenty-one tumors showed positive staining of p53 (nucleon). The expression level of p53 protein was not related with invasion or differentiation of HCCs.
  
  
  CONCLUSIONS
  Loss of PTEN expression and mutation of p53 may play a role in occurrence of HCCs. Loss of PTEN expression may be pertinent to deterioration of HCCs.
authors.affiliation: Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P. R. China. chengliming2002@hotmail.com
authors.forename: Li-Ming
authors.initials: LM
authors.lastname: Cheng
authors.forename: Si-Yuan
authors.initials: SY
authors.lastname: Wang
authors.forename: Ju-Sheng
authors.initials: JS
authors.lastname: Lin
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000378:metabolism* / Q000473:pathology; D016147:Genes, Tumor Suppressor; D016158:Genes, p53; D006801:Humans; D008099:Liver / Q000378:metabolism; D008113:Liver Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009154:Mutation; D009361:Neoplasm Invasiveness; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases / Q000096:biosynthesis* / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human