BACKGROUND: p53 is the most highly mutated tumor suppressor gene in human cancers. Recently, p73, a first homologue of p53, was identified and considered to be an imprinted tumor suppressor gene. Thus, we analyzed the possible role of p73 in human prostate cancers. METHODS: We investigated the expression levels and expressed allelotypes and searched for mutations in the p73 gene in 27 primary prostate cancers with matched normal tissues as well as in four prostate cell lines. RESULTS: Allelic expression analysis using polymorphisms in exons 2 and 5 revealed that p73 is biallelically expressed in both normal and tumor tissues, suggesting that p73 is not imprinted in prostate tissues. Quantitative PCR demonstrated that p73 expression is the same in both normal and tumor prostate tissues. Denaturing high-performance liquid chromatography and DNA sequencing revealed that there were no tumor-specific mutations in the p73 gene at the genomic level. CONCLUSIONS: These data indicate that alterations of p73, including mutations, changes in message abundance, and changes in allelic expression, are likely to be rare in early-stage prostate cancer, and that p73 could be a tissue-specific imprinting gene.
BACKGROUND:p53 is the most highly mutated tumor suppressor gene in humancancers. Recently, p73, a first homologue of p53, was identified and considered to be an imprinted tumor suppressor gene. Thus, we analyzed the possible role of p73 in humanprostate cancers. METHODS: We investigated the expression levels and expressed allelotypes and searched for mutations in the p73 gene in 27 primary prostate cancers with matched normal tissues as well as in four prostate cell lines. RESULTS: Allelic expression analysis using polymorphisms in exons 2 and 5 revealed that p73 is biallelically expressed in both normal and tumor tissues, suggesting that p73 is not imprinted in prostate tissues. Quantitative PCR demonstrated that p73 expression is the same in both normal and tumor prostate tissues. Denaturing high-performance liquid chromatography and DNA sequencing revealed that there were no tumor-specific mutations in the p73 gene at the genomic level. CONCLUSIONS: These data indicate that alterations of p73, including mutations, changes in message abundance, and changes in allelic expression, are likely to be rare in early-stage prostate cancer, and that p73 could be a tissue-specific imprinting gene.
Authors: A R M Ruhul Amin; Phillip A Karpowicz; Thomas E Carey; Jack Arbiser; Rita Nahta; Zhuo G Chen; Jin-Tang Dong; Omer Kucuk; Gazala N Khan; Gloria S Huang; Shijun Mi; Ho-Young Lee; Joerg Reichrath; Kanya Honoki; Alexandros G Georgakilas; Amedeo Amedei; Amr Amin; Bill Helferich; Chandra S Boosani; Maria Rosa Ciriolo; Sophie Chen; Sulma I Mohammed; Asfar S Azmi; W Nicol Keith; Dipita Bhakta; Dorota Halicka; Elena Niccolai; Hiromasa Fujii; Katia Aquilano; S Salman Ashraf; Somaira Nowsheen; Xujuan Yang; Alan Bilsland; Dong M Shin Journal: Semin Cancer Biol Date: 2015-03-06 Impact factor: 15.707
Authors: Alessandro Rufini; Massimiliano Agostini; Francesca Grespi; Richard Tomasini; Berna S Sayan; Maria Victoria Niklison-Chirou; Franco Conforti; Tania Velletri; Antonio Mastino; Tak W Mak; Gerry Melino; Richard A Knight Journal: Genes Cancer Date: 2011-04