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

The new continuous cell line HOK-1 derived from a grade-III transitional-cell bladder carcinoma with foci of squamous and glandular differentiation was shown to retain this phenotypical heterogeneity for more than 45 passages in vitro. Electron microscopy revealed transitional as well as a considerable proportion of squamous carcinoma and adenocarcinoma cells. PAS-positive mucus was detected in numerous cells. These features were principally maintained when grown as multicellular spheroids and in nude mice. More pronounced signs of differentiation (i.e., expression of cytokeratins 10 and 11, formation of glandular structures) were found in xenograft tumours. Independently, cytokeratins 13, 18 and 19 were detected in vitro and in vivo, reflecting the urothelial origin. The line forms distinct colonies in soft agar, expresses Lewis-x and Lewis-y antigens and reacts with monoclonal antibodies (MAbs) against CEA, beta-HCG and URO-5. Cytogenetic analysis revealed several related clones with a rearrangement at chromosome 1 and loss of one X chromosome as common karyotypic changes in all clones. DNA content, as quantified by image analysis, showed a DNA stemline close to 2c. The new cell line HOK-1 can be used as an in vitro model to study the mechanisms of heterogeneous differentiation patterns in bladder cancer.
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PMID:Characterization of the new bladder cancer cell line HOK-1: expression of transitional, squamous and glandular differentiation patterns. 171 84

Tumour markers are often circulating tumour-associated indicators of tumour development. As such they are not suitable for tumour screening and localization, but valuable as adjuncts for medical follow-up care of tumour patients, where their serum level alterations may anticipate the clinical detection of tumour behaviour by a lead time of 1 to 6 months before other methods. The following tumour may be controlled by established markers: endocrine tumours by NSE, calcitonin, parathormone, 5-HIAA, catecholamines/metabolites etc.; head-neck tumours: SCC, CEA; thyroid carcinoma: TG, calcitonin; lung cancer: CEA, NSE, SCC; liver cancer: AFP (PLC), CA 19-9 (cholangiocell.), CEA (secondary): biliary tract and pancreatic cancer: CA 19-9; colorectal carcinoma: CEA, CA 19-9; squamous cell carcinoma (ENT, oesophagus, anal): SCC; breast cancer: CEA and CA 15-3; ovarian cancer: CA 125 (epithelial), CA 19-9 (mucinous); germ cell tumours (ovary including trophoblastic tumours/testes): AFP and HCG; prostatic cancer: PAP and PSA; bladder cancer: TPA.
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PMID:[Clinical relevance of tumor markers]. 267 6

Prognostic factors in genitourinary cancers, renal cell carcinoma, bladder cancer, prostatic cancer, and testicular tumor, were discussed from several aspects on the basis of the analysis of own cases and reviews of literatures. The anatomical distribution of disease, particularly beyond the kidney, and degree of tumor differentiation were mostly related to prognosis in renal cell carcinoma. In bladder cancer, macroscopic growth pattern, histopathological intramural mode of spread, lymphatic and venous invasion, played an important role in prognosis, as do tumor grade and stage including metastasis. Hormone dependency and tumor markers were reconfirmed to be important and complementary as prognostic indicators as well as stage and grade in prostatic cancer. In testicular tumors, the most important factors for survival were extent of disease and tumor size, and histological cell type and determination of tumor markers, AFP and HCG, were also important and complementary as prognostic indicators.
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PMID:[Prognostic factors in genitourinary cancer]. 340 56

Serum levels of the peptide hormones, LH, FSH, TSH, prolactin, beta-HCG and PTH are observed to significantly modulate in patients with urogenital tumors, beta-HCG appears elevated in patients with chorioncarcinoma, teratoma and embryonal carcinoma and is shown to increase serum prolactin. TSH and prolactin are measured in pathological range in patients with renal carcinomas. Following nephrectomy serum TSH persists in high levels only in patients with advanced diseases, while PTH is more frequently suppressed in these patients. Serum LH and prolactin show a more distinct change of values in infiltrating bladder cancer, when compared to that of noninvasive bladder carcinomas. Prostate benign hyperplasia and cancer demonstrate similar ranges for peptide hormones, that will be changed by estrogen treatment in its LH, TSH and prolactin pattern. Serum levels of peptide hormones are affected by a complex system of ectopic hormone production, synthesis of peptide analogues, metabolic changes due to age and treatment.
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PMID:[Peptide hormones LH, FSH, TSH, prolactin, beta-HCG and PTH in patients with urogenital tumors]. 679 55

The biopsies from 75 patients with transitional cell carcinoma of the bladder (25 Ta-T1; 45 T2-T4, 5M) were studied immunohistochemically for the expression of beta-human chorionic gonadotrophin (beta-HCG). Only 5 Ta-T1 tumours contained a small number of beta-HCG positive cells but 24 invasive tumours and all patients with metastases showed increased numbers of positive cells. A significant correlation was found between beta-HCG immunoreactivity and tumour category. In 30 patients with muscle-invasive disease (T2-T4,N0,M0) who were treated with radical radiotherapy a significant correlation was observed between response to treatment and beta-HCG expression; beta-HCG positive tumours did not respond to treatment. A difference in survival was found between patients with tumours negative for beta-HCG compared with patients with positive tumours, all treated with radical radiotherapy. The results indicate that beta-HCG expression increases with tumour invasiveness and the use of immunohistochemistry may prove a useful means of identifying radioresistant and aggressive forms of bladder cancer.
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PMID:Is beta-human chorionic gonadotrophin production by transitional cell carcinoma of the bladder a marker of aggressive disease and resistance to radiotherapy? 750 30

Detectable levels of HCG have been reported in conditions other than normal pregnancy, including threatened abortion, ectopic pregnancy, trophoblastic tumors, carcinomas of the stomach, liver, pancreas and breast as well as multiple myeloma and melanoma. The present study was conducted to estimate urinary beta-HCG in bladder cancer and benign urinary tract disorders. 163 individuals were included, 68 with bladder cancer (60 males and 8 females), 64 with benign urinary tract diseases (55 males and 9 females) and 31 normal healthy controls (26 males and 5 females). Urinary beta-HCG was estimated by the ELISA technique using the reagents supplied by DRG International Inc., Germany. Results of the study revealed an overexpression of beta-HCG in malignant and benign urinary tract diseases. 60.3% of the cancer patients and 29.7% of patients with benign diseases showed urinary beta-HCG values above the upper limit of the control group (2mIU/ml).
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PMID:Urinary beta-HCG in benign and malignant urinary tract diseases. 754 89

An 86-year-old man consulted our hospital complaining of gross hematuria. Cystoscopy revealed a nodular broad-based cancer at the dome of the bladder. The patient was initially treated by transurethral resection of bladder tumor. Since histological examination showed grade 3 transitional cell carcinoma containing giant cells that were positive for beta-human chorionic gonadotropin (beta-HCG), we made a diagnosis of beta-HCG-producing bladder cancer. Because of his advanced age and poor general condition, the patient underwent partial cystectomy alone without adjuvant chemotherapy. One month later, a chest X-ray film revealed multiple lung metastases, and he developed paraplegia of the lower extremities suggesting spinal metastases. One month later, he was brought to our hospital with cardiopulmonary arrest. This is, to our best knowledge, the 22nd case report of beta-HCG-producing bladder cancer in Japan.
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PMID:[A case of human chorionic gonadotropin-producing bladder cancer]. 1123 22

The clonality of synchronous and metachronous bladder tumors has been studied for years with controversial results. Some recent studies support the 'polyclonal origin' hypothesis, i.e. that independently transformed different tumor cell clones exist in the same bladder cancer patient and arise from the field cancerogenisation affecting the entire bladder urothelium by environmental mutagens. Others could demonstrate a monoclonal origin of primary bladder tumors and its recurrences due to a single genetically transformed cell clone spread through the urinary system. With increasing understanding of the clonal origin of bladder tumors and recurrences, clonality markers might contribute to an early and accurate prediction of tumor recurrence and progression. We used p53 mutations as an identification marker permitting the prediction of clonality in bladder tumors and its recurrences. Primary tumors (n=33) and recurrences (n=63) were screened by direct genomic sequencing the p53 mutation hot spot region, exons 5-8. P53 mutations occurred in 12% in our cohort, predominantly in higher malignant (>or=G2), invasive (>or=T1) tumor samples. We were able to demonstrate intratumoral heterogeneity regarding the p53 status and that recurrences may occur from genetically unrelated primary tumor sites. Some of our results argue for a polyclonal origin of synchronous and metachronous bladder tumors possibly due to the field effect in bladder carcinogenesis. Evidence for a monoclonal origin was found in two cases: one case with a high malignant primary tumor and 3 metachronous recurrences, all of them harbouring the same exon 8 mutation found in the primary tumor; one case with identical mutations of exon 8 in the primary and one recurrent tumor. For further implications concerning clonality of recurrent bladder tumors, p53 status should be combined with a broader range of markers such as CGH and LOH pattern.
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PMID:P53 mutations as an identification marker for the clonal origin of bladder tumors and its recurrences. 1453 39

The multistep development of malignant tumors with increasing accumulation of genetic alterations from preneoplastic lesions to invasive carcinoma is an accepted model of carcinogenesis. Urothelial carcinoma of the bladder and upper urinary tract is an interesting model system to study tumor development and progression. There is both clinical and molecular evidence that urothelial carcinoma can be divided in two groups with different characteristics: 1) well differentiated genetic stable and mostly superficial papillary tumors with frequent recurrence and low progression risk and 2) poorly differentiated mostly solid and invasive tumors with a high number of genetic alterations. The aim of the studies summarized in this manuscript were: 1) to identify genetic changes with importance for urothelial carcinogenesis by investigation of preneoplastic and early neoplastic urothelial lesions, 2) to define molecular markers for progression of papillary carcinoma, and 3) to investigate the importance of microsatellite instability and mismatch repair defects for development of tumors of the upper urinary tract which are frequently found within the HNPCC syndrome. The investigation of urothelial hyperplasias, dysplasias and carcinoma in situ by deletion mapping (LOH analysis), FISH, CGH and mutation detection revealed that urothelial hyperplasias are precursors of papillary bladder tumors and flat dysplasias can be regarded as precursors of solid bladder cancers. In bladder cancer patients, there are genetic alterations already detectable in histologically inconspicous urothelium. The investigation of papillary bladder cancers for progression-related genetic alterations showed that mutations in the wnt pathway genes APC and beta-Catenin do not play an important role in urothelial carcinogenesis. Instead, the expression of the antagonistic wnt-related genes WIF-1 and sFRPI is strongly reduced in bladder cancer and associated with poor prognosis in papillary tumors. Loss of sFRP1 expression is not due to gene mutation but to epigenetic inactivation by promoter hypermethylation and is related to deletions at chromosome 8p12. In contrast to bladder cancers, tumors of the ureter and renal pelvis develop through a different genetic pathway in 30% of cases. The loss of mismatch repair proteins (hMSH2, hMLH1 or hMSH6) leads to a mutator phenotype with accumulation of genetic alterations in multiple repetitive sequences (microsatellite instability, MSI). MSI-positive tumors were predominantly located in the ureter and showed a lower tumor stage and grade and papillary and frequently inverted growth pattern. They were more frequent in females and younger patients and had a higher incidence of colorectal carcinomas and other tumors in the family. Chromosome 9 deletions, a hallmark of urothelial carcinomas, and the number of chromosomal alterations as detected by CGH analysis were significantly less frequent in these tumors. These data strongly suggest a distinct molecular pathway in the development of upper urinary tract tumors with mutator phenotype.
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PMID:[Molecular changes in development and progression of urothelial carcinoma]. 1688 10

BUBR1, a mitotic checkpoint protein, is a key component of the mitotic spindle checkpoint machinery. Defective BUBR1 has been proposed to contribute to chromosomal instability (CIN). To elucidate the relationship of BUBR1 expression with CIN, expression of BUBR1, numbers of centrosomes, numerical aberrations of chromosomes, and DNA ploidy were examined, and BUBR1 expression status was compared with clinicopathological parameters in 104 human urothelial bladder carcinomas. Expression of BUBR1 and numbers of centrosomes were assessed by immunohistochemistry. Numerical aberrations of chromosomes 7, 9, and 17 were evaluated by fluorescence in situ hybridization. Cancers with a large intercellular variation in centromere copy number were designated as CIN cancers. Tumors with BUBR1 overexpression were associated with CIN, DNA aneuploidy, and centrosome amplification. Array CGH revealed that BUB1B amplification and loss rarely occurred, indicating that the overexpression of BUBR1 in these bladder cancers was independent of BUB1B copy number. Overexpression of BUBR1 significantly correlated with higher histological grade, advanced pathological stage, and high cell proliferation. Overexpression of BUBR1 predicted tumor recurrence and disease progression. These data suggest that overexpression of BUBR1 is potentially a new tumor marker for estimating biological characteristics of bladder cancer.
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PMID:Overexpression of BUBR1 is associated with chromosomal instability in bladder cancer. 1735 Apr 65


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