Abstract
p53 gene function and tumor cell proliferation are thought to be important parameters for tumor progression in bladder cancer. In this study immunohistochemistry and fluorescence in situ hybridization were used to determine the relationship between p53 alterations, tumor proliferation (Ki-67 Labeling Index), and numerical chromosomal aberrations in formalin fixed bladder tumors. p53 expression was associated with Ki-67 LI (p = 0.0014), polysomy 17 (p = 0.001) and polysomy 7 (p = 0.0241). This is further evidence for a significant role of the p53 gene in proliferation control and preservation of genomic stability.
MeSH terms
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Carcinoma, Transitional Cell / genetics
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Carcinoma, Transitional Cell / pathology
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Chromosome Aberrations*
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Chromosomes, Human, Pair 17*
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Chromosomes, Human, Pair 7*
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Formaldehyde
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Gene Expression
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Genes, p53*
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Humans
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Immunohistochemistry
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In Situ Hybridization, Fluorescence
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Ki-67 Antigen
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Mitotic Index
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Neoplasm Proteins / analysis*
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Nuclear Proteins / analysis*
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Tumor Suppressor Protein p53 / analysis
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Tumor Suppressor Protein p53 / biosynthesis
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Urinary Bladder Neoplasms / genetics*
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Urinary Bladder Neoplasms / pathology*
Substances
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Ki-67 Antigen
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Neoplasm Proteins
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Nuclear Proteins
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Tumor Suppressor Protein p53
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Formaldehyde