p53 mutations and prognosis in bladder tumors

T Uchida, C Wada, H Ishida, C Wang… - The Journal of …, 1995 - auajournals.org
T Uchida, C Wada, H Ishida, C Wang, S Egawa, E Yokoyama, T Kameya, K Koshiba
The Journal of urology, 1995auajournals.org
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 percent) showed
loss of heterozygosity of 17p13, including 9 (90.0 percent) with disease beyond stage pT2.
The p53 mutations were detected in 20 of 43 patients (46.5 percent), including 9 (95.0 …
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 percent) showed loss of heterozygosity of 17p13, including 9 (90.0 percent) with disease beyond stage pT2. The p53 mutations were detected in 20 of 43 patients (46.5 percent), including 9 (95.0 percent) with disease beyond grade 2 and 17 (85.0 percent) with cancer beyond stage pT2. The incidence of p53 gene mutations was not significantly influenced by habitual smoking but G:C to T:A substitutions, often observed in lung cancers, were detected only in mutations from smokers (5 of 10 or 50 percent, p less than 0.05). Groups with and without loss of heterozygosity showed essentially the same results, while significant differences were found for groups with grades 1 and 2 to 3 (p less than 0.05) cancer, stages pT1 and pT2 to 4 (p less than 0.01) disease, and with and without p53 gene mutations (p less than 0.01, Cox-Mantel test). Genetic alternation chromosome 17p and p53 mutations would, thus, appear to occur more frequently in high grade and invasive bladder tumors. Cigarette smoking may possibly be a determining factor of mutations of the p53 gene in bladder tumors.
Our results indicate that an unfavorable prognostic factor may possibly be linked not only to histopathological findings but the presence of a p53 mutation in bladder tumors as well. Accordingly, mutations of the p53 gene may be deeply involved in late events of tumorigenesis and possibly useful as ideal molecular markers for prognosis in bladder tumors.
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