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

Eastern Austrian regional mortality patterns of oral cancer (oral cavity, pharynx and larynx) and oesophageal, lung and urinary bladder cancer were compared to smoker rates and to liver cirrhosis mortality by type of residence: Vienna (1.7 x 10(6) inhabitants), middle towns (50,000-100,000 and 10,000-50,000 inhabitants), small towns (2000-10,000 inhabitants) and rural areas categorized by agrarian quota less than or equal to 10%, 10%-20% and greater than 20%. The study area (Vienna, Lower Austria and Burgenland) covers 23,600 km2 with 3.23 x 10(6) inhabitants. In men, liver cirrhosis correlated negatively with smoker rates (r = 0.74, P = 0.1). Deaths from oral cancer and oesophageal cancer correlated significantly with deaths from liver cirrhosis (r = 0.81, P = 0.03; r = 0.78, P = 0.04, respectively) but not with smoker rates; lung cancer and bladder cancer correlated significantly with smoker rates (r = 0.91, P = 0.01; r0.83, P = 0.04, respectively), but not with liver cirrhosis. In women, similar urban-rural gradients for all parameters resulted in a positive correlation between liver cirrhosis and smoker rates (r = 0.59, P = 0.22) and a significant correlation of lung cancer with liver cirrhosis (r = 0.75, P = 0.05). Oral cancer correlated significantly with liver cirrhosis (r = 0.83, P = 0.02), but not with smoker rates; lung cancer correlated more significantly with smoker rates (r = 0.92, P = 0.01) than with liver cirrhosis; bladder cancer correlated positively with smoker rates (r = 0.70, P = 0.12). Geographical distribution of oral and oesophageal cancer in Eastern Austria seems thus to be highly subject to the prevalence of heavy drinking. Sociocultural influences upon the occurrence of these cancers seem to be mediated through drinking habits rather than through smoking habits alone.
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PMID:Tobacco-related cancer in relation to prevalence of drinking and smoking in eastern Austria. 151 83

A 1:1 pair matched case-control study was conducted in 1988 to investigate the risk factors for bladder cancer. Cases were inpatients suffering from bladder cancer, while controls were those admitted to hospitals not due to urinary diseases and smoking-related diseases such as lung cancer, oral cancer, or throat cancer. A total of 101 pairs of cases and controls from five major hospitals in Wuhan city, matched on sex, age, and hospital, were interviewed regarding their health history, lifestyle, occupational exposures, and familial history of cancer. Bivariate analysis revealed 10 factors significantly associated with bladder cancer. Conditional logistic regression analysis showed that 5 out of the 10 factors were risk factors for bladder cancer. Cigarette smoking, history of urinary diseases, working at the unit with more than one person ever suffering from bladder cancer, and eating mo than 1.5 kilograms of meat monthly were involved highest significant risks, whereas drinking milk appeared to have negative significant association with bladder cancer.
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PMID:[1:1 pair matched case-control study on bladder cancer]. 227 86

Snuff taking produces a white to yellowish, wrinkled lesion of the oral mucosa at the site where the quid is placed. The lesion is reversible, and only rarely exhibits dysplasia. Gingival recession and loss of attachment may occur in conjunction with the mucosal lesion. The risk of oral cancer varies greatly among the different published studies, from a relative risk of 48 to no increase in risk at all. Case control studies have found no association between oral tobacco and bladder cancer, whereas cigarette smoking carries a relative risk of about two. There appears to be no evidence for an association between oral snuff and cancer in general when the analysis takes into account confounders such as occupation, smoking and alcohol. The epidemiological evidence for an association with cardiovascular disease is contradictory. Snuff may probably cause hypertension, and one large study has reported a relative risk of 2 for dying of ischaemic heart disease. Biochemical evidence disfavors the hypothesis that snuff is atherogenic. In conclusion, the health hazards of oral moist snuff seem modest, and very much smaller than those of cigarette smoking.
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PMID:[Health hazards when using snuff]. 865 57

The CDKN2A gene encodes p16 (CDKN2A), a cell-cycle inhibitor protein which prevents inappropriate cell cycling and, hence, proliferation. Germ-line mutations in CDKN2A predispose to the familial atypical multiple-mole melanoma (FAMMM) syndrome but also have been seen in rare families in which only 1 or 2 individuals are affected by cutaneous malignant melanoma (CMM). We therefore sequenced exons 1alpha and 2 of CDKN2A using lymphocyte DNA isolated from index cases from 67 families with cancers at multiple sites, where the patterns of cancer did not resemble those attributable to known genes such as hMLH1, hMLH2, BRCA1, BRCA2, TP53 or other cancer susceptibility genes. We found one mutation, a mis-sense mutation resulting in a methionine to isoleucine change at codon 53 (M531) of exon 2. The individual tested had developed 2 CMMs but had no dysplastic nevi and lacked a family history of dysplastic nevi or CMM. Other family members had been diagnosed with oral cancer (2 persons), bladder cancer (1 person) and possibly gall-bladder cancer. While this mutation has been reported in Australian and North American melanoma kindreds, we did not observe it in 618 chromosomes from Scottish and Canadian controls. Functional studies revealed that the CDKN2A variant carrying the M531 change was unable to bind effectively to CDK4, showing that this mutation is of pathological significance. Our results have confirmed that CDKN2A mutations are not limited to FAMMM kindreds but also demonstrate that multi-site cancer families without melanoma are very unlikely to contain CDKN2A mutations.
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PMID:CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein. 938 68

Persons who use chewing tobacco and snuff experience an increased risk of oral cancer. Because of the pharmacologic properties of nicotine and other constituents of smokeless tobacco, there is also concern that smokeless tobacco products may lead to cardiovascular diseases as well. The relatively few human population studies to date conflict with respect to whether smokeless tobacco use elevates cardiovascular risk factors or leads to cardiovascular disease or death from cardiovascular causes. Hemoglobin adducts to carcinogens present in smokeless tobacco products are measurable in the blood of smokeless tobacco users, indicating that smokeless-tobacco-related carcinogens circulate throughout the body. This prompts a concern that smokeless tobacco may increase risks of other cancers as well. The evidence to date from epidemiologic studies indicates no relationship between smokeless tobacco and bladder cancer, but there is suggestive evidence linking smokeless tobacco use to prostate cancer risk. Only single studies have been conducted of some cancers, and inconsistencies among studies of the same cancer site have been reported. Molecular epidemiologic studies may help identify markers of malignant transformation in smokeless tobacco users that may help in early intervention to prevent or ameliorate the consequences of oral cancer. Further studies are needed to determine more clearly the cardiovascular and non-oral cancer risks potentially associated with smokeless tobacco use.
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PMID:Epidemiology of cancer and other systemic effects associated with the use of smokeless tobacco. 952 31

Using data from the 1960 and 1970 Swedish censuses and the Swedish Cancer Register for 1971 to 1989, this study investigated variations in cancer risk by gender associated with employment in painting trades and paint manufacturing. Among men, standardized incidence ratios were significantly increased for lung cancer among painters and lacquerers; bladder cancer among artists; and pancreas cancer, lung cancer, and nonlymphocytic leukemia among paint and varnish plant workers. Risks for women were elevated for cancers of the esophagus, larynx, and oral cavity among lacquerers and for oral cancer among glaziers. These findings are consistent with the report of the International Agency for Research on Cancer that classified painting as an occupationally related cause of cancer and provide further evidence that the risk of certain cancers is increased by exposures in the paint manufacturing process.
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PMID:Exposures in the painting trades and paint manufacturing industry and risk of cancer among men and women in Sweden. 1191 Oct 27

Amplification of chromosomal band 11q13 is a common event in human cancer. It has been reported in about 45% of head and neck carcinomas and in other cancers including esophageal, breast, liver, lung, and bladder cancer. To understand the mechanism of 11q13 amplification and to identify the potential oncogene(s) driving it, we have fine-mapped the structure of the amplicon in oral squamous cell carcinoma cell lines and localized the proximal and distal breakpoints. A 5-Mb physical map of the region has been prepared from which sequence is available. We quantified copy number of sequence-tagged site markers at 42-550 kb intervals along the length of the amplicon and defined the amplicon core and breakpoints by using TaqMan-based quantitative microsatellite analysis. The core of the amplicon maps to a 1.5-Mb region. The proximal breakpoint localizes to two intervals between sequence-tagged site markers, 550 kb and 160 kb in size, and the distal breakpoint maps to a 250 kb interval. The cyclin D1 gene maps to the amplicon core, as do two new expressed sequence tag clusters. We have analyzed one of these expressed sequence tag clusters and now report that it contains a previously uncharacterized gene, TAOS1 (tumor amplified and overexpressed sequence 1), which is both amplified and overexpressed in oral cancer cells. The data suggest that TAOS1 may be an amplification-dependent candidate oncogene with a role in the development and/or progression of human tumors, including oral squamous cell carcinomas. The approach described here should be useful for characterizing amplified genomic regions in a wide variety of tumors.
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PMID:High-resolution mapping of the 11q13 amplicon and identification of a gene, TAOS1, that is amplified and overexpressed in oral cancer cells. 1217 9

We present a meta-analysis to test the hypothesis that the presence of a high level of bulky DNA adducts in tissues is associated with an increased risk of cancer in humans. Seven articles were selected that matched the selection criteria, for a total of 691 cancer patients and 632 control subjects. In five studies the cases had lung cancer, in one oral cancer, and in one bladder cancer. Six studies measured adducts in WBCs and one in normal lung tissue around tumor tissue. Six were case-control investigations, and one was a case-control study on lung cancer nested within a cohort. Current smokers showed a statistically significant difference between cases and controls, with cases having 83% higher levels of adducts than controls (95% confidence interval, 0.44-1.22). Results were negative or contradictory in ex-smokers and nonsmokers. This observation was confirmed by sensitivity analyses. Publication bias does not seem to be a problem. Despite some methodological limitations, our meta-analysis shows that current smokers with high levels of adducts have an increased risk of lung and bladder cancers. This conclusion also suggests that similar (aromatic) compounds may be involved in the etiology of both types of cancer.
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PMID:Bulky DNA adducts and risk of cancer: a meta-analysis. 1258 26

Overexpression of the HER-2/neu oncogene, a frequent molecular event in a variety of cancers including bladder cancer, is associated with tumor progression and poor prognosis. Therapeutic strategies to targeting HER-2/neu-overexpressing cancer cells have shown promise. Pseudorabies virus (PrV), a herpesvirus of swine, may be exploited as an oncolytic agent for human cancer. Herein, we generated a conditionally replicating glycoprotein E-defective PrV mutant carrying glycoprotein D and herpes simplex virus type 1 thymidine kinase genes, which are essential for viral entry and replication, under the transcriptional control of the HER-2/neu promoter. The recombinant PrV, designated YP2, selectively replicated in and lysed HER-2/neu-overexpressing human bladder, mouse bladder, and hamster oral cancer cells in vitro. Notably, YP2 retarded MBT-2 bladder tumor growth in mice by more than 50% and more than half of the mice survived for over 50 days, whereas all the control mice survived less than 30 days. Taken together, our results suggest that YP2 may have therapeutic potential for the treatment of invasive bladder cancer. Furthermore, because HER-2/neu is overexpressed in a broad spectrum of cancers, this conditionally replicating PrV may be broadly applicable.
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PMID:Development of a conditionally replicating pseudorabies virus for HER-2/neu-overexpressing bladder cancer therapy. 1716 84

Through a prospective clinical sequencing program for advanced cancers, four index cases were identified which harbor gene rearrangements of FGFR2, including patients with cholangiocarcinoma, breast cancer, and prostate cancer. After extending our assessment of FGFR rearrangements across multiple tumor cohorts, we identified additional FGFR fusions with intact kinase domains in lung squamous cell cancer, bladder cancer, thyroid cancer, oral cancer, glioblastoma, and head and neck squamous cell cancer. All FGFR fusion partners tested exhibit oligomerization capability, suggesting a shared mode of kinase activation. Overexpression of FGFR fusion proteins induced cell proliferation. Two bladder cancer cell lines that harbor FGFR3 fusion proteins exhibited enhanced susceptibility to pharmacologic inhibition in vitro and in vivo. Because of the combinatorial possibilities of FGFR family fusion to a variety of oligomerization partners, clinical sequencing efforts, which incorporate transcriptome analysis for gene fusions, are poised to identify rare, targetable FGFR fusions across diverse cancer types.
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PMID:Identification of targetable FGFR gene fusions in diverse cancers. 2355 53


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