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Query: UMLS:C0005684 (bladder cancer)
 16,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the relationships between the mutant p53 gene and human bladder cancer, the authors used in situ hybridization to detect 30 of bladder cancer and 4 of normal bladder samples. The results showed that p53 gene positive rate of mRNA was 23.3% in cancer patient, and all negative in normal-bladder. The positive rate was significantly different in pathological grading and clinical stages of carcinoma (P < 0.05). It suggests that the mutant p53 gene participats in transformation of carcinoma and may be used as a tumor marker for determinating invasiveness and prognosis of bladder carcinoma.
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PMID:[Abnormal expression and clinical significance of mutation p53 gene on human bladder cancer]. 758 77

A loss of chromosome-9 material is one of the most frequent genomic aberrations known in bladder cancer. In order to better understand the role of chromosome-9 losses in bladder cancer, 125 formalin-fixed and 37 unfixed bladder tumors were examined using fluorescence in situ hybridization (FISH). A repetitive probe for a pericentromeric region on 9q12 (pHUR98) was applied for chromosome-9 copy-number enumeration. Under-representation of chromosome 9 was found in 74 of 162 cases. There was no association between loss of chromosome 9 and increased grade or stage, papillary growth pattern, p53 protein expression, or tumor-cell proliferation (Ki-67). These data show that chromosome-9 loss is an early event in bladder-cancer development, occurring independently of p53 alterations. In order to determine the prevalence of large sub-regional chromosome-9 deletions, dual hybridizations with pHUR98 and cosmid probes for 9q34, 9q22, and 9p21 were performed. Partial deletion was detected in only 1 of 36 cases for 9q34 and in 1 of 24 cases for 9p21. Surprisingly, amplification of the interferon alpha locus on 9p21 was seen in 1 of 24 tumors. The finding of 9p amplification may indicate the site of an oncogene relevant for bladder cancer.
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PMID:Chromosome-9 loss detected by fluorescence in situ hybridization in bladder cancer. 761 60

The p53 gene product has been detected frequently in various human malignancies. We have studied the expression of p53 protein in urothelial transitional cell cancers (TCCs) and examined its correlation with pathologic grade, stage(pT) and patient survival. Specimens from 69 surgically-resected TCCs (38 cases of urinary bladder cancer, 17 cases of ureteral cancer and 14 cases of renal pelvic cancer) were examined by immunohistochemical staining, using two anti-p53 monoclonal antibodies, PAb1801 and PAb240, and a polyclonal antibody, CM-1. Twenty-six TCCs (37.6%) were positively stained by at least one of the three antibodies. Statistical analysis showed a significant correlation between p53 expression and high pathologic grade (p < 0.05, p < 0.001) or progressive pathologic stage (p < 0.01). In addition, in 51 of the patients who were available for follow-up (23 cases of urinary bladder cancer, 13 cases of ureteral cancer, and 15 cases of renal pelvic cancer), the correlation between p53 protein expression and prognosis was examined. The survival of patients exhibiting positive p53 protein expression was significantly worse than those with p53-negative tumors (p < 0.05). These results suggest that an immunohistochemical test for p53 protein may be a useful method of evaluating the malignant potential of TCCs. Additionally, expression of p53 protein in TCCs is an indicator of a poor prognosis which should be considered in drawing up treatment strategies.
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PMID:Correlation of p53 protein expression in human urothelial transitional cell cancers with malignant potential and patient survival. 762 37

To examine the significance of Y chromosome losses in bladder cancer, fluorescence in situ hybridization (FISH) was used to determine its prevalence and associations with known parameters of malignancy. Cells were dissociated from formalin-fixed paraffin-embedded bladder tumors from 68 male patients and from 11 post-mortem bladder washes of male patients with a negative bladder cancer history, and were examined by FISH using centromeric probes for chromosomes X, Y, 7, 9, and 17. Nullisomy for chromosome Y was seen in 23 of 68 tumors (34%), monosomy in 28 of 68 tumors (41%), and polysomy in 17 of 68 tumors (25%). There was no association between chromosome Y loss and tumor grade, stage, tumor growth fraction (Ki67 LI), p53 immunostaining, and presence of p53 deletions. Patient age was higher for tumors with a Y loss (73.5 +/- 12.0 years) than for tumors without Y loss (66.6 +/- 10.8 years; p = 0.0207). In one normal bladder wash, a distinct subpopulation (38% of cells) with Y nullisomy was seen. These data suggest that Y loss is a frequent event that can occur early in bladder cancer, although there is no evidence for a role of Y loss in tumor progression.
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PMID:Y chromosome loss detected by FISH in bladder cancer. 766 48

Frequent recurrences and multicentricity of bladder cancer suggest that alterations of the urothelium distant from the tumor may be relevant to prognosis. In this study immunohistochemistry and fluorescence in situ hybridization (FISH) were used to examine expression of p53, erbB-2, and epidermal growth factor receptor (EGF-r), genomic aberrations, and tumor cell proliferation (Ki67 LI) in normal and dysplastic urothelium. Biopsy specimens examined included normal urothelium (n = 40), mild dysplasia (n = 34), moderate dysplasia (n = 18) and carcinoma in situ (CIS; n = 20). Several different oncogene expression patterns were found, only some of which were associated with dysplasia. EGF-r expression was equally frequent in normal and dysplastic urothelium and showed a strong association with Ki67 LI (P < .0001). A purely superficial erbB-2 positivity was present in both normal and dysplastic biopsies. However, diffuse erbB-2 positivity and p53 overexpression were both associated with advanced dysplasia (P < .0001 each). FISH analysis showed erbB-2 gene amplification and p53 deletions in selected CIS, as well as a marked chromosome 17 copy number heterogeneity in all six CIS examined. These findings indicate a considerable genomic instability in bladder CIS. They show that both erbB-2 and p53 are altered during malignant transformation. Detectable oncogene expression alone, however, is not diagnostic of malignancy in bladder urothelium.
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PMID:Patterns of p53, erbB-2, and EGF-r expression in premalignant lesions of the urinary bladder. 767 97

Expression of p53 protein, c-erbB-2 protein, neuron-specific enolase (NSE), Phe 5, chromogranin, laminin and collagen type IV was studied by immunohistochemistry in formalin-fixed and paraffin-embedded specimens from 20 patients with renal pelvic carcinoma. Positive membrane-bound c-erbB-2 staining was not found in any case. Two tumors stained for p53 protein. Focal immunoreactivity for laminin was present in 55% and for collagen type IV in 80%. 25% of the cases were NSE positive. None of the tumors stained for Phe 5 or chromogranin. The results were compared with the clinical outcome and the immunohistological findings of p53 protein and c-erbB-2 protein in 13 cases of bladder carcinoma in the same patient group. Four of the thirteen bladder cancer specimens, but only 2 of the 20 renal pelvic cancer specimens, expressed p53 protein. As for renal pelvic carcinoma, c-erbB-2 protein was not expressed in bladder carcinoma. We conclude that p53 gene abnormalities may be of importance in the development of carcinoma in the renal pelvis and urinary bladder, but c-erbB-2 protein expression does not play a major role.
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PMID:Transitional cell carcinoma of the renal pelvis and its expression of p53 protein, c-erbB-2 protein, neuron-specific enolase, Phe 5, chromogranin, laminin and collagen type IV. 771 33

Surgical specimens from 30 patients with transitional cell carcinoma of the bladder were examined for the presence of mutation of the p53 tumor suppressor gene using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. All of the specimens were superficial, low grade cancer, and 10 patients had recurrences during an observation period of 24 months following the initial surgical treatment. Among the 30 patients with superficial bladder cancer, 4 were found to have the mutated p53 gene and 3 of them had recurrences, which involved either invasive or high grade tumors. Two of these recurrent tumors with the p53 gene mutation showed identical mutations with those primary tumors, whereas the other one did not have the same mutation. The data suggest that bladder cancers with a mutation of the p53 gene have a greater probability of poor prognosis than those which do not, even if the primary lesion was a superficial, low grade tumor. Therefore, the presence of the p53 gene mutation may provide important clues to the factors involved in bladder cancer.
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PMID:p53 gene mutation in recurrent superficial bladder cancer. 771 16

Archival biopsy specimens from transitional cell bladder tumours (n = 185) were analysed immunohistochemically for expression of c-myc protein. The results were compared with histopathological and clinical parameters and survival. Forty-three per cent of the tumours were negative for c-myc protein and weak, moderate, or strong cytoplasmic expression was found in 34, 14, and 9 per cent of cases, respectively. Nuclear positivity for c-myc protein was detected in 35 per cent of tumours and nuclear positivity was related to overexpression of c-erb B-2 (P = 0.01) and a high proportion of nuclei were also positive for p53 oncoprotein (p < 0.05). Cytoplasmic expression of c-myc protein was related to histological grade (P = 0.005), papillary status (P = 0.007), the S-phase fraction (P = 0.008), the mitotic index (P = 0.021), overexpression of epidermal growth factor receptor (P = 0.045), and c-erb B-2 (P = 0.17). Expression of c-myc protein was not significantly related to the progression of tumours and it had no prognostic value in survival analysis. Independent predictors were the T-category (P < 0.001), papillary status. (P = 0.001), and S-phase fraction (P = 0.061). The results show that while c-myc gene product participates in growth regulation of human bladder cancer cells, it has no independent prognostic significance.
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PMID:Expression of c-myc protein is related to cell proliferation and expression of growth factor receptors in transitional cell bladder cancer. 773 16

Amplification and overexpression of c-myc have been suggested as prognostic markers in human cancer. To assess the role of c-myc gene copy number alterations in bladder cancer, 87 bladder tumors were examined for c-myc aberrations by fluorescence in situ hybridization. Dual labeling hybridization with a repetitive pericentromeric probe specific for chromosome 8 and a probe for the c-myc locus (at 8q24) was performed to analyze c-myc copy number in relation to chromosome 8 copy number on a cell by cell basis. A clear-cut c-myc amplification (up to 40 to 150 copies per cell) was found in 3 tumors. There was a low level c-myc copy number increase in 32 of the remaining 84 tumors. There was no association of low level c-myc copy number increase with c-myc protein overexpression. This suggests that a c-myc gene copy number gain as detected by fluorescence in situ hybridization does not necessarily reflect a disturbed c-myc gene function but may indicate a structural chromosome 8 abnormality including gain of distal 8q. The strong association of low level c-myc (8q) gains with tumor grade (P < 0.0001), stage (P < 0.0001), chromosome polysomy (P < 0.0001), p53 protein expression (P = 0.0019), p53 deletion (P = 0.0403), and tumor cell proliferation (Ki67 labeling index; P = 0.0021) is consistent with a role of chromosome 8 alterations in bladder cancer progression.
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PMID:c-myc copy number gains in bladder cancer detected by fluorescence in situ hybridization. 774 7

Although patients with superficial bladder cancer (Ta, T1) have a generally good prognosis, those of them who have tumours invading muscle or metastatic disease will have a poor clinical prognosis. In the current study, 41 patients undergoing complete transurethral resection for superficial transitional cell cancer of the bladder were investigated for different clinical and biological characteristics as possible prognostic factors: age, sex, previous instillation therapy, immunohistochemical determination of mutational inactivation of p53 tumour suppressor gene (monoclonal antibody pAb 1801) and proliferation rate determined immunohistochemically by staining for PCNA (proliferating cell nuclear antigen; monoclonal antibody PC 10). After a median follow-up of 54 months 7 of 8 patients (87.5%) with more than 20% of cells positive for p53 had disease recurrence, as against only 1 of 33 patients (3%) negative for p53 detection (P < 0.01; Chi-square test). During univariate analysis histological grade (G1 vs G2; P = 0.007), positivity for PCNA (> 60% of cells; P = 0.003) and positivity for p53 (P = 0.001) were significant prognostic factors for disease progression (log rank test), while during multivariate analysis only positivity for p53 was a significant predictor for relapse of bladder cancer (P = 0.0035; multivariate Cox regression analysis).
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PMID:[Value of the proliferation status (PCNA) and p53 immunohistochemistry as a prognostic factor for the clinical course of superficial cancer of the urinary bladder]. 775 87


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