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

In a comparative study of tryptophan metabolism and urinary excretion of nucleic acid derivatives (including beta-aminoisobutyric acid, 7-methylguanine, pseudouridine, and urate) in 12 male bladder cancer patients, the excretion of pseudouridine and 7-methylguanine decreased significantly after an oral dose of 2 g L-tryptophan. A similar decrease occurred after an oral nicotinamide load of 50 mg four times a day, which indicated a possible common mode of action of tryptophan and nicotinamide. No definite resolution could be made as to the causal mechanism for the observed descrase in RNA turnover.
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PMID:Effect of tryptophan and nicotinamide loads on urinary excretion of RNA metabolites by bladder cancer patients. 14 44

The incidence of urinary bladder cancer differs markedly among the different ethnic and national groups in the Pacific Basin. Because of these differences, the following colaborative studies can be done to identify and characterize factors associated with bladder cancer: 1) study population groups with different levels of bladder cancer risk who reside in the same geographic setting; 2) study ethnically similar groups who differ in risk and reside in different locations; and 3) study population groups who differ in risks and reside in different geographical regions. Factors possibly related to bladder cancer that have been identified and studied by others include occupational exposure to certain chemicals, cigarette smoking, coffee drinking, artificial sweeteners, certain viruses, radiation exposure, phenacetin, bracken fern, Schistosoma haematobium, tryptophan metabolites, nitrosamines, estrogens, hair dyes, vitamin A, and ascorbic acid. In collaborative studies, the pathologic interpretation of histologic material and the content of the questionnaire should be well standardized, and the laboratory tests should be done at one laboratory. Among the population groups in the Pacific Basin, the Japanese in Hawaii and in Japan provide a unique resource for further investigation with respect to bladder cancer.
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PMID:Cancer of the urinary bladder in the Pacific Basin. 39 42

Animal studies have shown that metabolites of tryptophan can cause bladder cancer, and human observations reveal an appreciable incidence of abnormalities of tryptophan metabolism in patients with bladder cancer. It has been suggested that pyridoxine (vitamin B6) may correct this abnormality and prevent recurrences of superficial bladder cancers. Intravesical instillation of thiotepa has been used for more than fifteen years in the treatment of superficial bladder cancer, but no controlled trials have been done. We report here a prospective clinical trial of 121 patients with Stage I bladder cancer randomized to placebo, pyridoxine, or intravesical thiotepa. The percentages of patients with recurrences over the period of study were 60.4, 46.9, and 47.4 for the three groups, respectively, and did not differ significantly. However, if patients having recurrences during the first ten months or followed up less than ten months were excluded, pyridoxine was significantly better than placebo (P = 0.03). Thiotepa significantly reduced the recurrence rate compared with placebo (P = 0.016) or pyridoxine (P = 0.015). These results suggest that a new trial of pyridoxine should be undertaken in which the tryptophan metabolites are measured and that further study of intravesical instillation of chemotherapeutic agents is warranted.
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PMID:Comparisons of placebo, pyridoxine, and topical thiotepa in preventing recurrence of stage I bladder cancer. 41 2

The existence of at least two stages in bladder carcinogenesis was evaluated in male Fischer rats using N-[14-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) fed for six weeks at a level of 0.2% of the diet as the initiator. Sodium saccharin and DL-tryptophan were fed at levels of 5 and 2% of the diet, respectively, as possible promoting chemicals, and they were fed either immediately after FANFT administration or after six weeks of FANFT plus six weeks of control diet. All surviving rats were killed at the end of two years. Both chemicals significantly increased the incidence of bladder tumors following FANFT feeding compared to six weeks of FANFT feeding followed by control diet, and the results were similar whether saccharin or tryptophan feeding was started immediately after FANFT feeding was concluded or after a six-week delay. Saccharin was considerably more potent as a promoting agent than was tryptophan, inducing higher incidences of bladder tumors and having a shorter latent period. Long-term administration of FANFT induced a 100% incidence of bladder cancer. Sequential epithelial changes were observed by scanning and transmission electron microscopy as well as by light microscopy. Pleomorphic microvilli were present on the superficial cells of all tumors examined and on the surface cells of hyperplastic bladder epithelium after six weeks of FANFT plus six weeks of saccharin, but not after six weeks of FANFT and six weeks of control diet. Rats fed only saccharin tryptophan, or control diet did not have bladder tumors or pleomorphic microvilli on bladder epithelium. These data suggest that saccharin and tryptophan might act as tumor-promoting agents during bladder carcinogenesis.
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PMID:Promoting effect of saccharin and DL-tryptophan in urinary bladder carcinogenesis. 42 Dec 4

Urinary excretion before and after a loading dose of tryptophan, plasma pyridoxal phosphate concentration and urinary excretion of 4-pyridoxic acid was studied in 44 male bladder cancer patients from Copenhagen. Six patients (14%) had abnormal tryptophan metabolism, decreased plasma pyridoxal phosphate concentration and in most cases low urinary excretion of 4-pyridoxic acid indicating decreased availability of vitamin B6 or decreased formation of pyridoxal phosphate from vitamin B6. It is concluded that abnormal tryptophan metabolism only plays a minor role for bladder cancer carcinogenesis in Copenhagen. It is, however, stressed that such studies do not rule out the possibility that the aromatic degradation products of tryptophan may be cocarcinogens or promotors as other studies have indicated.
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PMID:Tryptophan metabolism in bladder cancer patients from Copenhagen. 48 65

A nonhuman primate species infected with Schistosoma haematobium provided a model system for controlled studies on biharzial bladder cancer. Urinary excretion of tryptophan metabolites by capuchin monkeys (Cebus apella) was similar to that of humans when expressed per g creatinine. Liver tryptophan oxygenase activity of the capuchin monkeys was comparable to that of humans. Excretion of 3-hydroxykynurenine and 3-hydroxyanthranilic acid was elevated above control levels in capuchin monkeys infected experimentally with S. haematobium. The capuchin-S. haematobium system closely resembles the human biharziasis system and offers a reproducible laboratory model system for the controlled study of the parasitology, pathogenesis, and biochemistry of biharzial bladder cancer.
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PMID:Experimental biharzial bladder cancer: tryptophan metabolism in nonhuman primates experimentally infected with Schistosoma haematobium. 81 56

Administration of a dietary supplement of 6 g D,L tryptophan/day for 4 1/2 years following the administration of a single dose of 50 mg 4-aminobiphenyl/kg produced a bladder tumor in 1 of 4 beagle dogs. No tumors were observed in 6 dogs given the same dose of 4-aminobiphenyl without supplemental tryptophan. In a second experiment, administration of a supplement of 6 g D,L-tryptophan/day for 3 years following the administration of 5 mg 2-naphthylamine/kg/day for 30 days produced bladder tumors in 2 of 4 dogs. No tumors or other bladder pathology was produced by treatment of 4 dogs with this dose of 2-naphthylamine alone. Dogs given D,L-tryptophan alone developed no bladder tumors, but in most dogs receiving tryptophan the "tryptophan effect", i.e., a darkly stained mucosa with white areas of focal hyperplasia, was observed. Both experiments suggest a role of D,L-tryptophan as a cocarcinogen or promotor in the induction of bladder cancer.
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PMID:Cocarcinogenic interaction between D,L-tryptophan and 4-aminobiphenyl or 2-naphthylamine in dogs. 86 60

Tryptophan metabolism was studied in a family in which a sister and brother had bladder cancer. Urinary tryptophan metabolites after administration of 2 g L-tryptophan were measured in 4 sisters and 1 brother, all free of disease when studied. One sister with and 2 without histories of bladder cancer had significantly elevated levels of kynurenine, acetylkynurenine, and 3-hydroxykynurenine. Administration of 100 mg pyridoxine hydrochloride returned the tryptophan metabolism to normal in these 3 individuals. One brother with a 1 sister without bladder cancer had normal metabolism. A repeat study 2 years later confirmed the abnormal metabolism in the 3 sisters. Two sisters with abnormal tryptophan metabolism were given 200 mg L-kynurenine sulfate orally to bypass the effects of tryptophan oxygenase activity. Both excreted elevated levels of kynurenine and 1 excreted elevated levels of 3-hydroxykynurenine.
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PMID:Abnormal tryptophan metabolism in a family with a history of bladder cancer. 99 12

A retrospective study of medical records from 13 veterinary university hospital clinics yielded 114 dogs with microscopically confirmed primary malignancy of the bladder. When matched to controls, there was no increased frequency to suggest an association of urogenital tumors or anomalies with neoplasms of the bladder. The majority of tumors seen in this study were transitional cell carcinomas. Four breeds were identified with excessive risk for bladder cancer and may serve as models for further research into genetic determinants, such as abnormal tryptophan metabolism. The epidemiologic features of canine bladder cancer were compared with the disease in man. An excess among female dogs may be the result of less frequent urination as compared to male dogs. Assuming an etiology from urine-borne carcinogens applies to spontaneously occurring bladder cancer in dogs, then monitoring the frequency of occurrence of canine bladder cancer may provide an early warning of emerging environmental hazards to man.
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PMID:Canine bladder cancer: epidemiologic features. 99 13

The Authors describe the various anomalies of the metabolism of tryptophan that are observed in various diseases. The oxidative pathway is most important of the metabolic pathway of the amino acid; the degredation of tryptophan is particularly influenced by steroid hormones and vitamins' want. The metabolic anomalies are demonstrable both in malignant tumors (mostly in bladder cancer and Hodgkin's disease), both during psychiatric diseases (such as depression and schizophrenia) and in the diseases of connective tissue in addition to congenital errors of the degradation of tryptophan (such as Hartnup's disease, tryptophanuria and 3-hydroxychinureninuria). The metabolic pictures are manifest after amino acid's in the diseases of connective tissue but are independent for clinical seriousness and, in any case, less significant than those observed in other pathological pictures, mostly in Hodgkin's disease. The existence of anomalies of tryptophan's metabolism is certainly shown in many diseases, however the true physiopathogenetic meaning of these metabolic alterations is not yet specified. Particularly it is not definite if these alterations are the cause of diseases, which they appear in, or if they are secondary alterations.
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PMID:[Clinical significance of changes in tryptophan metabolism]. 109 26


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