Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007138 (transitional cell carcinoma)
 3,949 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and five patients with renal pelvic and ureteral tumor entered our treatment program between 1982 and 1991. Of 105 patients, 81 had resectable transitional cell carcinoma and were treated with radical or total nephroureterectomy (57 vs. 24) and/or lymph node dissection (66). Adjuvant chemotherapy was added in 26 patients with high stage disease and with lymph node disease. There were 61 male and 20 female patients. Their ages ranged from 36 to 86 years, with a mean of 62 years. The follow-up period was 3 to 114 months, with a mean of 31 months. The estimated 5-year survival was 67% in all 81 patients. Classified according to the pathological stage, 5-year survival was 70% in pTis + pTa disease group, 91% in pT1 group, 88% in pT2 group, 53% in pT3 group, and 27% in pT4 group. Under the grading system, 5-year survival was 100% in grade 1 disease, 74% in grade 2, and 26% in grade 3. It was 78% in 52 patients with negative node disease and 26% in 15 with positive node disease. There were 51 patients (61%) with no recurrent disease. Seventeen patients (21%) had recurrence in the bladder after a median latent period of 8-month, and 15 (19%) patients had recurrence in the retroperitoneum, liver, lung and (or) other site after a median latent period of 8 months. The results of this series were quite similar to those of previous reports. The efficacy of lymph node dissection and adjuvant chemotherapy could not be confirmed.
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PMID:[Clinical results in the treatment for primary carcinoma of the renal pelvis and ureter]. 849 12

A deletion analysis of chromosome 3 was conducted in 72 cases of transitional cell carcinoma of the urinary bladder using seven microsatellites spanning the 3p arm and two additional microsatellites in 3q. Results showed that 19 of 72 (26.4%) cases had deletions in one or more 3p regions. Two regions of frequent deletion were identified: 3p12-14 and 3p21-23. Less frequent deletions at 3p24.2-25 were also observed. Deletions at 3p were weakly correlated with tumor grade, but strongly with pathological stage. Among 70 cases with histological grade available, 4 of 29 (13.8%) grade 1 and 2 tumors, and 15 of 41 (36.6%) grade 3 tumors showed allelic losses in one or more of the 3p regions studied (P = 0.055). Among 69 cases with pathological stage available, none of 27 superficial carcinomas (pTa, pTis, and pT1) showed 3p deletions, whereas 18 of 42 (42.9%) muscle invasive lesions (pT2, pT3, and pT4) displayed allelic losses at 3p (P < 0.001). In addition, 12 cases showed microsatellite instability, but there was no correlation between abnormalities and tumor grade or stage. No correlation was found between deletions at 3p21-23 and microsatellite instability. In conclusion, deletions at three discrete regions of 3p were identified in bladder carcinoma, suggesting the involvement of candidate tumor suppressor genes residing in these regions. Moreover, detection of allelic losses in these regions was associated with higher tumor grade and more advanced stage, suggesting their potential involvement in bladder tumor progression.
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PMID:Chromosome 3 allelic losses and microsatellite alterations in transitional cell carcinoma of the urinary bladder. 868 47

To elucidate whether a significant difference in malignant potential between ureteropelvic transitional cell carcinoma (TCC) and bladder TCC is present, the argyrophilic nucleolar organizer region (AgNOR), nuclear DNA content and mean nuclear area (MNA) were evaluated in 32 ureteropelvic TCCs and 60 bladder TCCs, and were also compared with histological grade and stage. The parameters used were the mean AgNOR count (C-AgNOR), the percentage of cells exhibiting more than 3 AgNOR dots within nuclei (P-AgNOR), 2c deviation index (2cDI), 5c exceeding rate (5cER) and MNA. No significant difference in these 5 parameters was found between ureteropelvic and bladder TCCs. In addition, within each histological grade of tumor, no significant difference in each parameter between ureteropelvic and bladder TCCs was noted. Similarly, within pTa or pT1 TCCs, there was no significant difference in the parameters between ureteropelvic and bladder TCCs. On the other hand, invasive TCCs (pT2 and higher), the C-AgNOR and P-AgNOR were significantly higher in ureteropelvic than in bladder TCC (p < 0.05), while no significant difference in 2cDI, 5cFR and MNA was noted. These findings suggest that: (i) as a whole, the difference in malignant potential between ureteropelvic and bladder TCCs appears to be less significant, and (ii) factors other than the malignant potential of a tumor might contribute to the unfavorable clinical outcome in patients with ureteropelvic TCC.
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PMID:Comparison of ureteropelvic transitional cell carcinoma with bladder transitional cell carcinoma using an image analyzer. 886 Jul 37

The identification of new prognostic parameters in Superficial Transitional Cell Carcinoma of the Bladder (STCCB) is important since conventional methods are often insufficient for prognostic purposes. We studied the proliferation activity and the DNA ploidy status of 60 pTa and pT1 Superficial Transitional Cell Carcinoma of the Bladder in relation to grade and recurrence rate. The proliferative activity was investigated by measuring the PCNA expression in paraffin embedded tissue sections. The DNA content was studied in Feulgen stained imprints by image analysis technique using a SAMBA 2005 analyser. According to our measurements a statistically significant difference was found in PCNA expression among tumors grade I, grade II, grade III (F = 5.43, p < 0.001), between tumors of the same grade with, and without recurrence (p < 0.001); and between recurrent and non-recurrent tumors (T58 = -6.03, p < 0.001). A statistically significant difference was also observed concerning the DNA-index among grade I, grade II and grade III (F = 4.81, p < 0.01), and between recurrent and non-recurrent tumors concerning the DNA DNA ploidy status (DNA-euploid vs. DNA-aneuploid tumors) (X2 = 24.96, p < 0.001). The recurrence status is also strongly influenced by the proliferation rate and the DNA ploidy status of tumors (X23 = 41.19, p < 0.001). No cases recurrence were found in the group of DNA-euploid tumors with PCNA. expression lower than 30%, in contrast a very high percentage of recurrence in patients with DNA-aneuploid tumors with PCNA expression higher than 30%. Although a small proportion of cases could not be included in me previous categories, STCCB may be classified in to main groups concerning the risk of recurrence. In keeping with this view of proliferation rate and DNA ploidy status could provide useful information, on the potential malignancy of Superficial Transitional Cell Carcinoma of the Bladder. However further studies are required to establish the clinical utility of these parameters.
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PMID:DNA content and proliferation activity in superficial transitional cell carcinoma of the bladder. 906 20

Since 1985 a special work group involved in the coordination of hospital cancer registries in Germany (AKKK) has been collecting, storing and analysing data on tumour patients, received from cancer centres, oncological departments and specialised practices. The documentation of tumour patients is based, among other things, on information concerning localisation, histological findings and tumour spread. The data are stored in a central database administered by the work group. At present it contains data on approximately 500,000 oncological patients. In the period from 1987 to 1992, 56,013 initial entries were made concerning patients with urological tumours. Of these cases, tumours of the kidney (n = 11,424) constituted 20.4%. In 94.6% of the cases, histological investigation revealed a renal cell carcinoma-pT1: 5.8%; pT2: 53.6%, pT3: 37.2% and pT4: 3.4%. Tumours of the urinary bladder (n = 16,246) constituted 29.0% of all urological tumours. In 93.8% of the cases a transitional cell carcinoma was detected-pTis: 1.0%; pTa: 36.9%; pT1: 29.6%; pT2: 16.9%; pT3: 11.4%; pT4: 4.4%. Transitional cell carcinomas of the ureter or of the collecting system (n = 1,846) constituted 3.3% of the cases. The proportion of testicular tumours (n = 6,594) amounted to 11.8%; 53.6% of these germ-cell tumours (n = 6,281) were seminomas and 46.6% were non-seminomas. In all, 66.3% of the cases were lymph-node negative. Tumours of the prostate (n = 19,903) constituted 35.5% of the cases. In the period from 1987 to 1992, the proportion of lymph-node-positive prostate carcinomas decreased from 39.8% to 16.2%. The detailed analysis of these data shows how the hospital cancer registries can support the discussion regarding diagnosis and therapy of urological tumours.
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PMID:[Urologic tumors in Germany. Initial data of 56,013 cases from clinical cancer registers]. 919 42

Bladder tumors were induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in five Beagles and four mongrel dogs. The tumors were observed for long periods and the tumor progression was traced using histopathological mapping. The results indicated (1) that low-dose BBN over a long period induced multiple low-grade (G1-2) and low-stage (pTa-1) papillary tumors, resembling superficial bladder cancer in humans; (2) that high-dose BBN over a short period induced high-grade (G2-3) and high-stage (pT3b) nonpapillary tumors and carcinoma in situ (CIS) resembling invasive cancer and CIS in humans; (3) that beagle dogs required longer periods and higher total doses of BBN as compared with mongrel dogs; (4) that the tumors induced by low-dose BBN in beagles were observed without BBN as long as the animals lived, and neither increasing numbers of tumors nor malignant features such as deep infiltration and metastasis was observed; and (5) that low-dose BBN seems to induce mild dysplasia, which is followed by Brunn's nest-like proliferation in the lamina propria and nodular change, eventually leading to the development of papillary noninvasive transitional cell carcinoma (TCC); and that high-dose BBN seems to induce severe dysplasia which leads to CIS and nonpapillary invasive TCC. These results may contribute to clarifying the natural history of human bladder cancer.
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PMID:A histopathological mapping study of the urinary bladder tumors induced by N-butyl-N-(4-hydroxybutyl)nitrosamine in dogs. 937 11

Mutations of p53 gene have been found in a variety of human malignancies; however, the impact of immunohistological detection of p53 expression in the development and progression of TCC of the bladder is still uncertain. In the present study, we investigated the p53 oncoprotein expression and compared the findings to DNA ploidy and pathohistological stage and grade. The study included 147 patients with transitional cell carcinoma of the bladder investigated between February 1981 and September 1994. The average age of the 55 women and 92 men was 67 years (range: 20-71 years). A total of 76 patients (52%) had stage pTa to pT1, 35 (24%) stage pT2, 25 (17%) stage pT3, and 11 (7%) stage pT4 disease. Frozen sections of tumor biopsies obtained by transurethral resection were immunohistochemically stained using the monoclonal antibody clone D0-7 (DAKO), which recognized two different epitopes for mutant and wild-type p53 protein. Tumors expressing p53 in more than 10% of the tumor nuclei were regarded as positive. The DNA ploidy was determined by image analysis. Immunohistochemical detection of p53 expression was found in 84 (57%) of the 147 tumors examined. Positive p53 staining was seen in grade I tumors in 10 to 25%, in grade II tumors 25 to 75%, and in grade III up to 58% of the tumor nuclei. There was a positive correlation between p53 expression and pathological stage (28% in pTa, 73% in pT1-2, and 68% in pT3-4 tumors). There was no appreciable relationship between DNA Ploidy and p53. Although carcinomas with p53 expression had a slight tendency to be more prevalent among higher disease stages and poorly differentiated transitional cell carcinoma, immunohistochemical detection of p53 is not a valuable tool for predicting the outcome of patients with TCC or for identifying subgroups of patients that may be at a higher risk for tumor progression.
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PMID:Immunohistochemical detection of p53 protein in transitional cell carcinoma of the bladder in correlation to DNA ploidy and pathohistological stage and grade. 946 48

Cancer registration statistics of economically advanced countries indicate that bladder carcinoma incidence ranks fourth in men and eighth in women, but a reliable tumor marker for predicting the disease course is still lacking. We designed an immunohistochemical study to comprehensively assess the trophoblastic hormone production profile of transitional cell carcinoma (TCC) of the bladder. Moreover, we correlated histological differentiation and tumor stages with marker expression and, finally, evaluated a potential tumor origin of hCGbeta core-fragment (hCGbetacf). To this end, formalin-fixed, paraffin-embedded tumor tissues from 104 patients with urothelial neoplasms of various histological grades (23 GI, 24 GII, and 38 GIII) and stage (19pTis, 21pTa, 29pT1, and 35pT2-T4) were analyzed by the immunoperoxidase technique using our own well-characterized monoclonal antibodies against the glycoprotein hormones human chorionic gonadotropin (hCG) and its derivatives hCGalpha, hCGbeta, hCGbetacf, luteinizing hormone (LH, LHbeta), follicle-stimulating hormone (FSH, FSHbeta), and the protein hormones placental lactogen (hPL) and growth hormone (hGH-V/N). Overall, trophoblastic hormone immunoreactivity was found in 36% of TCC. Detailed analysis showed 35% hCGbeta, 17% hCGbetacf, 9% hCGalpha, 4% hCG, and 2% hPL-positive cases. The tumors produced neither GH-N, placental GH-V, nor the pituitary gonadotropins FSH/FSHbeta and LH/LHbeta. Marker positivity significantly increased with high-grade lesions (26% GI- v 55% GIII-TCC) and advanced tumor stages (24% pTa v 63% > or = pT2). Hormone immunoreactivity was frequently observed in highly proliferating areas. Our findings, together with recent structural and clinical studies, strongly suggest that these hormones, or derivates thereof, might act as local tumor growth factors. Normal urothelium, urothelial papillomas, and carcinoma in situ showed no positive reactions. All tumors producing hCG-derived molecules were negative for the concommitantly analyzed neuroendocrine markers chromogranin A, synaptophysin, and neuron-specific enolase (NSE). In summary, one third of TCC ectopically produce trophoblastic hormones, which is specifically correlated with stage and grade. Apart from hCGbeta (97% of the marker-positive cases), the intracellular occurrence of hCGbetacf, apparently the second most frequently produced marker, was surprising, and there was also a lesser degree free hCGalpha and intact holo-hormone expression. The placental protein hormones PL and GH-V are not appropriate tumor marker candidates. Finally, our histogenetic findings support a metaplastic origin of the hCG producing choriocarcinomatous phenotype of some TCC.
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PMID:Production of trophoblastic hormones by transitional cell carcinoma of the bladder: association to tumor stage and grade. 956 88

We report a case of transitional cell carcinoma arising in the fossa navicularis of the male urethra. The patient was 87-years-old and noticed intermittent urethral bleeding. We could see a tumor protruding from the urethral meatus, removed it successfully, and irradiated the base of the tumor with Nd:YAG laser. The histologic finding was grade 2 transitional cell carcinoma, pTa. There was no other tumor in the urinary bladder or upper urinary tract. The postoperative course was uneventful and the patient showed no evidence of disease for 4 months after treatment but died from other causes.
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PMID:Transitional cell carcinoma in the fossa navicularis of the male urethra: a case report. 962 65

The cascade of genetic alterations leading to malignant transformation has been described for adenocarcinoma of the colon but is not established for other common tumor entities. In the present study, different stages of transitional cell carcinoma (TCC) of the bladder are analyzed by comparative genomic hybridization. A dynamic pattern of the chromosomal changes during tumor progression is described. Deletion of chromosome arm 9q is the earliest genetic alteration in pTa tumors. In stage pT1 carcinomas, losses of 9q, 9p, and 11p and gain of 1q and 8q are the most common. In addition to the changes specific for earlier stages, gain of 5p and 20q becomes prominent in carcinomas stage > or =pT2. Association analysis reveals a remarkable cooccurrence of 9p deletion with gain of 5p and 20q in > or =pT2 tumors. In order to determine more precisely the size of the amplified segment and the degree of amplification on chromosome arm 8q in stage pT1 tumors, this region was analyzed by semiquantitative PCR using polymorphic microsatellite markers. These studies revealed an up to 13-fold amplification. The common region of amplification could be narrowed down to 8q22.3 and between GAAT1A4 and D8S1834 (about 7 cM).
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PMID:Chromosomal changes during progression of transitional cell carcinoma of the bladder and delineation of the amplified interval on chromosome arm 8q. 973 20


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