Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The post-initiation enhancing activities of the non-genotoxic agent NaHCO3 and the genotoxic agent N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN) in combination with uracil-induced urolithiasis were investigated in a rat bladder carcinogenesis model. Animals were treated with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 4 weeks, and then 3% uracil was given for 3 weeks in the early (weeks 4-7), middle (weeks 8-11) or late (weeks 12-15) post-initiation phase. In addition, administration of 3% NaHCO3, 20 ppm EHBN or no chemical supplement was performed for the 13 weeks when the rats were not receiving BBN or uracil. NaHCO3 in sequential combination with early and middle stages uracil treatment strongly enhanced tumorigenesis in the urinary bladder, while EHBN treatment amplified lesion development at the middle stage only of uracil treatment. DNA synthesis and associated epithelial surface alterations observed by scanning electron microscopy tended to be increased in the NaHCO3 and EHBN groups without BBN initiation, independently of uracil treatment timing. The present results demonstrated that uracil-induced urolithiasis during the middle post-initiation phase is highly active in enhancing bladder tumor development under the influence of a promoter or carcinogen.
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PMID:Timing effects of uracil-induced urolithiasis on amplification of second-stage promotion in rat bladder carcinogenesis. 165 69

A considerable amount of experimental, clinical and epidemiological data indicate that dietary fats play a role in urinary tract tumorigenesis. In rodents, chronic essential fatty acid (EFA) deficiency seems to induce both urolithiasis and transitional hyperplasias, followed by a tendency for tumorigenesis of the urinary passages. High intake of saturated fats or non-EFAs, conditions that may induce EFA deficiency (EFAD) increase the risk of bladder cancer in case-control studies. In other cell populations, EFAs are beneficial as preventive and therapeutic nutrients for the treatment of cancer. Thus, it is reasonable to assume that abnormal metabolism and/or nutritional deprivation of EFA, by inducing a chronic or a subclinical EFA deficiency, may enhance the risk of urothelial tumorigenesis.
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PMID:Is the risk of urinary tract tumorigenesis enhanced by a marginal chronic essential fatty acid deficiency (EFAD)? 953 Jun 54