p53 abnormalities are not a significant prognostic factor in primary, resected NSCLC when all histologic subtypes are combined, but may be a useful prognosticator for adenocarcinomas. Additional studies are warranted for further evaluation, specifically of adenocarcinomas.
Background: Cyclin D1 is essential for G 1 progression through the cell cycle phase. It is a possible proto-oncogene whose aberrant expression may be responsible for the occurrence of some types of human neoplasms. The objective of the present study was to demonstrate immunohistochemically cyclin D1 expression in bladder cancer tissues and establish any relationship with the histologic findings and the clinical course.
Methods:Tissue from 102 patients with bladder cancers and bladder tissue from five normal subjects were used for an immunohistochemical study of cyclin D1 using the avidin-biotin complex method. Results: Nuclear staining of cyclin D1 was found in 79 (77%) out of the 102 cases of bladder cancer. The five cases of normal epithelium had no immunostaining for cyclin D1. All grade 1 tumors were positive for cyclin D1. With the advance of tumor grade the incidence of cyclin D1 decreased. All pTa tumors stained positively for cyclin D1, whereas the positive staining rates of invasive tumors were 47% in pT1, 73% in pT2, 31% in pT3 and 0% in pT4 tumors. Although a univariate analysis revealed patients with lesions positive to cyclin D1 had more favorable survival rates than those with negative findings, a multivariate analysis showed that positivity for cyclin D1 is not an independent prognostic factor. No relationship was discovered between positivity for cyclin D1 and tumor recurrence in patients with superficial bladder cancers. Conclusions: These findings suggest that cyclin D1 demonstrated immunohistochemically could be used as an inverse indicator for the level of invasiveness of bladder cancer, but not as an independent prognostic factor.
Summary Accumulating evidence suggests that the p53 gene is a good target for molecular epidemiological studies. We previously reported an association between the presence of p53 mutations and lifetime cigarette consumption. Although over 675 p53 mutations have been reported in lung cancers in the literature thus far, very little is known about the nature of such changes in lung cancers in the absence of a smoking background. In the present study, we therefore analysed 69 non-small-cell lung cancer specimens from individuals without any history of active smoking and identified p53 mutations in 26% of the cases. Statistical analysis of the present cohort of non-smokers also showed absence of significant relationship between p53 mutations and age, sex, histological type or disease stage. Comparison of mutational spectra between the present results in non-smokers and previously reported mutations in smokers clearly demonstrated G:C to T:A transversions to be significantly less frequent in non-smokers than in smokers (OR 5.35, 95% Cl 1.77-16.12). Interestingly, G:C to C:G and G:C to A:T mutations were also observed in tumours of non-smokers at similar frequencies to G:C to T:A mutations, suggesting that these mutations can occur relatively frequently in the absence of active smoking. This study is, to our knowledge, the largest so far analysing a welldefined cohort of non-smokers in a single laboratory.
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