1995
DOI: 10.1097/00005392-199504000-00004
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p53 Mutations and Prognosis in Bladder Tumors

Abstract: The incidence of loss of heterozygosity on chromosome 17p and p53 gene mutations was assessed in 43 bladder tumor patients. Histological findings, cigarette smoking and prognosis were examined for possible correlation with the presence or absence of loss of heterozygosity on 17p and p53 mutations. Of 20 informative cases 10 (50.0%) showed loss of heterozygosity of 17p13, including 9 (90.0%) with disease beyond stage pT2. The p53 mutations were detected in 20 of 43 patients (46.5%), including 9 (95.0%) with dis… Show more

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Cited by 32 publications
(37 citation statements)
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“…The few nonsmoker cases reported at this time show an overall level of mutations comparable to, but a base substitution pattern deviant from, that in smokers (21). Nuclear overexpression or mutations have been found in 40 to 45% of bladder tumors from smokers and at a lower level (30-35%) among ex-smokers and nonsmokers in many (12,22) but not all (23) studies.…”
Section: Discussionmentioning
confidence: 59%
“…The few nonsmoker cases reported at this time show an overall level of mutations comparable to, but a base substitution pattern deviant from, that in smokers (21). Nuclear overexpression or mutations have been found in 40 to 45% of bladder tumors from smokers and at a lower level (30-35%) among ex-smokers and nonsmokers in many (12,22) but not all (23) studies.…”
Section: Discussionmentioning
confidence: 59%
“…Accordingly, when averaged across all tumour stages, increased p21 expression did not correlate with either the presence or the absence of p53 accumulation (Table 3). In urothelial carcinoma accumulation of p53 protein, particularly in advanced tumours, is usually due to mutations in the gene (Cordon-Cardo et al, 1994;Williamson et al, 1994;Grimm et al, 1995;Uchida et al, 1995;Vet et al, 1995). This suggests that in the majority of tumours staining positive for both proteins, p21 was not induced by p53.…”
Section: Discussionmentioning
confidence: 99%
“…Genes involved in cell cycle control and affected in urothelial carcinoma comprise MTSJ/p16 and MTS2/p15 encoding inhibitors of cyclin-dependent kinases (CDKs) (Orlow et al, 1995), cyclin Dl (Bringuier et al, 1994), RB (Xu et al, 1993) and MYC (Lipponen, 1995;Schmitz-Drager et al, 1996). In addition, depending on stage and grade, a considerable fraction of urothelial carcinomas display accumulation of p53 protein usually due to point mutations in the gene (Wright et al, 1991;Cordon-Cardo et al, 1994;Esrig et al, 1994;Schmitz-Drager et al, 1994;Williamson et al, 1994;Uchida et al, 1995;Vet et al, 1995).…”
mentioning
confidence: 99%
“…TP53 sequences in exons 5, 7 and 8 were amplified by hot-start PCR using the primers listed in Table 1. 18,19 TP53 sequences were amplified using 3 ml of genomic DNA, 2.3 mM MgCl 2 , 10 mM Tris-HCl (pH 8.3), 50 mM KCl, 0.2 mM deoxynucleotide triphosphates, 0.8 mCi a-32 PdATP, 0.33 mM of each primer and 1 unit of Taq DNA polymerase (Bio-Rad, Hercules, CA, USA) with a final volume of 25 ml. Each PCR protocol had an initial denaturing step of 951C for 5 min, followed by 35 cycles at 951C for 30 s, 551C for 30 s and 721C for 30 s, which was then followed by a single final extension step at 721C for 7 min.…”
Section: Sscp Analysismentioning
confidence: 99%