title: Mutation analysis of the p51 gene and correlation between p53, p73, and p51 expressions in prostatic carcinoma.
abstract: BACKGROUND
  p73 and p51 are genes possessing amino-acid similarities to p53. We previously found no mutation in p73 in prostatic carcinoma, but did find abnormal expression of the gene. Involvement of these genes in prostatic carcinogenesis is still poorly understood.
  
  
  METHODS
  Mutation analysis of the p51 gene and allelotyping of 3q28, on which p51 lies, were performed. Expression of p53, p73, and p51 was examined using reverse transcription-polymerase chain reaction, and expression levels were compared.
  
  
  RESULTS
  No mutation in p51 was found (0/55 cases). Loss of heterozygosity at 3q28 was detected in 6 of 28 cases (21.8%). By expression analysis we found that in p53, 4 of 38 cases (10.5%) showed downregulation. No cases showed upregulation of p53. In contrast, p73 and p51 were downregulated in 42.1 and 39.5% of cases, respectively, and upregulated in 31.5 and 34.2% of cases, respectively. Expression levels of p51 corresponded with those of p73 in 25 of 38 cases (65.8%).
  
  
  CONCLUSIONS
  Somatic mutations in p73 and p51 are not important in prostatic carcinogenesis. These genes may be associated with tumors by expression levels and may have roles in addition to tumor suppression.
authors.affiliation: Department of Pathology, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: K
authors.initials: K
authors.lastname: Fukutome
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Furusato
authors.forename: T
authors.initials: T
authors.lastname: Shiraishi
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: S
authors.initials: S
authors.lastname: Ikawa
authors.forename: H
authors.initials: H
authors.lastname: Hano
mesh_terms: D000368:Aged; D000483:Alleles; D002277:Carcinoma / Q000235:genetics* / Q000378:metabolism; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000737:chemistry; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics*; D004587:Electrophoresis, Agar Gel; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D016147:Genes, Tumor Suppressor; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000096:biosynthesis / Q000235:genetics*; D010750:Phosphoproteins; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000378:metabolism; D017422:Sequence Analysis, DNA; D015534:Trans-Activators; D014157:Transcription Factors; D014407:Tumor Cells, Cultured; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins
chemical_list: D004273:DNA, Neoplasm; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D010750:Phosphoproteins; C115051:TP63 protein, human; C000606460:TP73 protein, human; D015534:Trans-Activators; D014157:Transcription Factors; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins