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1. Tyagi AK, Agarwal C, Singh RP, Shroyer KR, Glode LM, Agarwal R: Silibinin down-regulates survivin protein and mRNA expression and causes caspases activation and apoptosis in human bladder transitional-cell papilloma RT4 cells. Biochem Biophys Res Commun; 2003 Dec 26;312(4):1178-84
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  • [Title] Silibinin down-regulates survivin protein and mRNA expression and causes caspases activation and apoptosis in human bladder transitional-cell papilloma RT4 cells.
  • Bladder cancer is the fourth and eighth most common cancer in men and women in the United States, respectively.
  • Survivin, a member of inhibitor of apoptosis protein (IAP) gene family, is deregulated in a wide range of malignancies, including carcinoma of the bladder urothelium.
  • Recent advances have identified survivin as a novel intervention target to induce apoptosis in cancer cells by phytochemicals or synthetic agents.
  • Human bladder transitional-cell papilloma RT4 cells were treated with silibinin and analyzed for survivin protein and mRNA levels by Western blotting and real-time RT-PCR, respectively.
  • Together, these findings suggest that more studies are needed to investigate in vivo effect of silibinin on survivin expression and associated biological effects in bladder cancer that could provide useful information for silibinin efficacy in the prevention/intervention of human bladder cancer.
  • [MeSH-major] Caspases / metabolism. Microtubule-Associated Proteins / metabolism. RNA, Messenger / metabolism. Silymarin / pharmacology. Urinary Bladder Neoplasms / metabolism. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Apoptosis / drug effects. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / pathology. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Activation / drug effects. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins. Papilloma / metabolism. Papilloma / pathology

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  • (PMID = 14651997.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R03 CA99079
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Silymarin; 4RKY41TBTF / silybin; EC 3.4.22.- / Caspases
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2. Waalkes MP, Liu J, Diwan BA: Transplacental arsenic carcinogenesis in mice. Toxicol Appl Pharmacol; 2007 Aug 1;222(3):271-80
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  • Additional postnatal treatment with diethylstilbestrol or tamoxifen after prenatal arsenic in CD1 mice induces urinary bladder transitional cell proliferative lesions, including carcinoma and papilloma, and enhances the carcinogenic response in the liver of both sexes.
  • Overall this model has provided convincing evidence that arsenic is a transplacental carcinogen in mice with the ability to target tissues of potential human relevance, such as the urinary bladder, lung and liver.
  • Transplacental carcinogenesis clearly occurs with other agents in humans and investigating a potential transplacental component of the human carcinogenic response to arsenic should be a research priority.

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  • (PMID = 17306315.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / Z01 BC005488-21; United States / Intramural NIH HHS / / Z99 ES999999; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Arsenicals; 0 / Carcinogens; 0 / Estrogens; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS28781; NLM/ PMC1995036
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3. Reitmair A, Shurland DL, Tsang KY, Chandraratna RA, Brown G: Retinoid-related molecule AGN193198 potently induces G2M arrest and apoptosis in bladder cancer cells. Int J Cancer; 2005 Jul 20;115(6):917-23
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  • [Title] Retinoid-related molecule AGN193198 potently induces G2M arrest and apoptosis in bladder cancer cells.
  • Here, we extend these findings to show that AGN193198 potently and rapidly induces apoptosis in bladder carcinoma cell lines.
  • One micromolar of AGN193198 completely abolished the growth of the transitional cell carcinoma lines UM-UC-3 and J82, and the squamous cell carcinoma line SCaBER; the transitional cell papilloma line RT-4 was slightly less sensitive to the growth inhibitory effect of AGN193198.
  • Treated cells accumulated in the G2M phase of the cell cycle.
  • As reported for prostate cancer cells, AGN193198 provoked rapid activation of caspases-3 (by 6 hr), -8 (by 16 hr) and -9 (by 6 hr) in bladder cancer cells.
  • These findings suggest that AGN193198 and related compounds, whose mechanism of action does not appear to involve RARs and RXRs, may be useful in the treatment of bladder cancer.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Transitional Cell / pathology. Papilloma / pathology. Quinolines / pharmacology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Division / drug effects. Humans. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors / metabolism. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15729717.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AGN193198; 0 / Antineoplastic Agents; 0 / Quinolines; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors
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4. Damaraju S, Damaraju VL, Mowles D, Sawyer MB, Damaraju S, Cass CE: Cytotoxic activity of gemcitabine in cultured cell lines derived from histologically different types of bladder cancer: role of thymidine kinase 2. Biochem Pharmacol; 2010 Jan 1;79(1):21-9
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  • [Title] Cytotoxic activity of gemcitabine in cultured cell lines derived from histologically different types of bladder cancer: role of thymidine kinase 2.
  • World wide incidence of bladder cancer is rising with nearly 13,760 deaths attributed to bladder cancer in 2007 in the USA.
  • Tumor types of the urothelium include transitional cell carcinomas, squamous cell carcinomas, and adenocarcinomas.
  • This study was undertaken to determine gemcitabine's efficacy against bladder cancer cell lines of different origins (HTB2, a papilloma; HTB3, a squamous cell carcinoma; and HTB4, a transitional cell carcinoma).
  • Roles of nucleoside transporters and key enzymes in gemcitabine pharmacology were examined on the premise that cells originating from different types of bladder cancer exhibit different levels and/or types of nucleoside transporters and enzymes and thus may respond differently to gemcitabine.
  • Sequencing experiments revealed no mutations either in coding exons or intron-exon boundaries of the hENT1 genes of the three cell lines.
  • Elevated TK expression in squamous cell carcinomas warrants further study and offers new insights into rational treatment strategies based on bladder cancer phenotype.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Thymidine Kinase / physiology. Urinary Bladder Neoplasms / enzymology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Dose-Response Relationship, Drug. Humans. Tumor Cells, Cultured

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  • (PMID = 19660438.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.1.- / thymidine kinase 2; EC 2.7.1.21 / Thymidine Kinase
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5. Tada Y, Fujitani T, Yano N, Yuzawa K, Nagasawa A, Aoki N, Ogata A, Yoneyama M: Chronic toxicity of thiabendazole (TBZ) in CD-1 mice. Toxicology; 2001 Dec 28;169(3):163-76
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  • The bladder weights of male and female mice of the 0.5% group were significantly higher than those of the control mice.
  • Gross findings in treated mice included the renal atrophy, hydronephrosis, calculi in renal pelvis and/or bladder and ovarian atrophy.
  • Microscopic findings in the kidneys of treated mice included the nephrosis, hydronephrosis or hyperplasia of transitional epithelium of renal pelvis or papilla.
  • In the bladder of treated mice, hyperplasia or squamous metaplasia of transitional epithelium and one transitional cell papilloma were observed.
  • [MeSH-major] Kidney Diseases / chemically induced. Neoplasms / chemically induced. Thiabendazole / toxicity. Urinary Tract / drug effects
  • [MeSH-minor] Administration, Oral. Animals. Animals, Outbred Strains. Blood Platelets / drug effects. Body Weight / drug effects. Carcinogenicity Tests. Dermatitis. Dose-Response Relationship, Drug. Eating / drug effects. Female. Hair / drug effects. Kidney / drug effects. Kidney / pathology. Male. Mice. Motor Activity / drug effects. Organ Size / drug effects. Platelet Count. Sex Factors. Survival Rate. Time

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  • (PMID = 11718957.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] N1Q45E87DT / Thiabendazole
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6. Swaminathan S, Torino JL, Burger MS: Human urinary bladder epithelial cells lacking wild-type p53 function are deficient in the repair of 4-aminobiphenyl-DNA adducts in genomic DNA. Mutat Res; 2002 Jan 29;499(1):103-17
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  • [Title] Human urinary bladder epithelial cells lacking wild-type p53 function are deficient in the repair of 4-aminobiphenyl-DNA adducts in genomic DNA.
  • The effect of the tumor suppressor gene TP53 on repair of genomic DNA damage was examined in human urinary bladder transitional cell carcinoma (TCC) cell lines.
  • Utilizing TCC10 containing wild-type p53 (wt-p53) as the parental line, an isogenic set of cell lines was derived by retroviral infection that expressed a transdominant mutant p53 (Arg --> His at codon 273, TDM273-TCC10), or the human papilloma virus 16-E6 oncoprotein (E6-TCC10).
  • The amount of adducts in urothelial DNA ranged between 0.1 and 20 per 10(6) nucleotides, N-OAc-AABP yielding the highest levels, followed by N-OH-ABP and N-OH-AABP.
  • At the dose used for DNA repair studies, N-OH-AABP or N-OAc-AABP did not induce apoptosis in TCC10.
  • These results suggest that p53 might modulate the repair of DNA adducts generated from the human bladder carcinogen ABP in its target human uroepithelial cells.
  • [MeSH-major] Aminobiphenyl Compounds / chemistry. DNA Adducts / physiology. Deoxyguanosine / analogs & derivatives. Repressor Proteins. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Urinary Bladder / physiology
  • [MeSH-minor] Apoptosis / drug effects. Carcinogens / pharmacology. Cells, Cultured. Codon. DNA Repair / drug effects. DNA Repair / physiology. Epithelial Cells / drug effects. Epithelial Cells / pathology. Epithelial Cells / physiology. Humans. Mutation. Oncogene Proteins, Viral / genetics. Oncogene Proteins, Viral / metabolism

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  • (PMID = 11804609.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-82035; United States / NIEHS NIH HHS / ES / ES-09090
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aminobiphenyl Compounds; 0 / Carcinogens; 0 / Codon; 0 / DNA Adducts; 0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 16054949HJ / 4-biphenylamine; 26541-56-0 / N-acetoxy-4-acetylaminobiphenyl; 4463-22-3 / N-hydroxy-4-acetylaminobiphenyl; 6810-26-0 / N-hydroxy-4-aminobiphenyl; 86408-34-6 / N-(deoxyguanosin-8-yl)-4-aminobiphenyl; G9481N71RO / Deoxyguanosine
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7. Tannehill-Gregg SH, Sanderson TP, Minnema D, Voelker R, Ulland B, Cohen SM, Arnold LL, Schilling BE, Waites CR, Dominick MA: Rodent carcinogenicity profile of the antidiabetic dual PPAR alpha and gamma agonist muraglitazar. Toxicol Sci; 2007 Jul;98(1):258-70
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  • Benign gallbladder adenomas occurred at low incidences in male mice at 20 and 40 mg/kg (area under the curve [AUC] exposures > or = 62 times human exposure at 5 mg/day) and were considered drug related due to an increased incidence of gallbladder mucosal hyperplasia at these doses.
  • There was a dose-related increased incidence of transitional cell papilloma and carcinoma of the urinary bladder in male rats at 5, 30, and 50 mg/kg (AUC exposures > or = 8 times human exposure at 5 mg/day).
  • At 30 and 50 mg/kg, the urinary bladder tumors were accompanied by evidence of increased urine solids.
  • Subsequent investigative studies established that the urinary bladder carcinogenic effect was mediated by urolithiasis rather than a direct pharmacologic effect on urothelium.
  • Incidences of subcutaneous liposarcoma in male rats and subcutaneous lipoma in female rats were increased at 50 mg/kg (AUC exposures > or = 48 times human exposure at 5 mg/day) and attributed, in part, to persistent pharmacologic stimulation of preadipocytes.
  • Considering that muraglitazar is nongenotoxic, the observed tumorigenic effects in mice and rats have no established clinical relevance since they occurred at either clinically nonrelevant exposures (gallbladder and adipose tumors) or by a species-specific mechanism (urinary bladder tumors).
  • [MeSH-major] Carcinogens. Glycine / analogs & derivatives. Hypoglycemic Agents / toxicity. Oxazoles / toxicity. PPAR alpha / agonists. PPAR gamma / agonists
  • [MeSH-minor] Animals. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Male. Mice. Mice, Inbred ICR. Neoplasms / chemically induced. Neoplasms / epidemiology. Neoplasms / pathology. Rats. Rats, Sprague-Dawley. Survival Analysis. Urinalysis

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  • (PMID = 17426106.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Hypoglycemic Agents; 0 / Oxazoles; 0 / PPAR alpha; 0 / PPAR gamma; TE7660XO1C / Glycine; W1MKM70WQI / muraglitazar
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8. Sejima T, Isoyama T, Miyagawa I: Comparative study of apoptotic antitumor effect between angiogenesis inhibitor AGM-1470 and MVAC chemotherapy on rat urinary bladder cancer. Urol Int; 2004;73(3):226-33
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  • [Title] Comparative study of apoptotic antitumor effect between angiogenesis inhibitor AGM-1470 and MVAC chemotherapy on rat urinary bladder cancer.
  • OBJECTIVES: To investigate the antitumor apoptotic effect of AGM-1470 by comparing it to that induced by methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) therapy, currently the standard chemotherapy for bladder cancer, in a rat bladder cancer model.
  • RESULTS: Our experimental protocol succeeded in producing invasive bladder tumors in the majority of rats.
  • CONCLUSIONS: AGM-1470 and MVAC appear to exert a prominent mass reduction effect via tumor cell apoptosis in cases of invasive bladder tumor, although these therapies did not demonstrate any obvious modulation of bcl-2 protein expression status.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Cisplatin / therapeutic use. Doxorubicin / therapeutic use. Methotrexate / therapeutic use. Sesquiterpenes / therapeutic use. Urinary Bladder Neoplasms / drug therapy. Vinblastine / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carcinoma, Squamous Cell / drug therapy. Cyclohexanes. Female. Gene Expression. Genes, bcl-2. Hyperplasia. Models, Animal. Papilloma / drug therapy. Rats. Rats, Wistar. Treatment Outcome. Urinary Bladder / pathology

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  • [Copyright] copyright 2004 S. Karger AG, Basel
  • (PMID = 15539841.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; YL5FZ2Y5U1 / Methotrexate; M-VAC protocol
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9. Vinh PQ, Sugie S, Tanaka T, Hara A, Yamada Y, Katayama M, Deguchi T, Mori H: Chemopreventive effects of a flavonoid antioxidant silymarin on N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis in male ICR mice. Jpn J Cancer Res; 2002 Jan;93(1):42-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemopreventive effects of a flavonoid antioxidant silymarin on N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis in male ICR mice.
  • The modifying effects of dietary administration of a flavonoid antioxidant, silymarin, a mixture of three flavonoids isolated from milk thistle seeds, on N-butyl-N-(4-hydroxybutyl)nitrosamine (OH-BBN)-induced urinary bladder carcinogenesis were examined in male ICR mice.
  • Animals were divided into 5 groups, and groups 1 to 3 were given OH-BBN (500 ppm) in drinking water for 6 weeks.
  • Animals in group 4 were given only the test compound, and those in group 5 were given the basal diet alone throughout the experiment.
  • Animals were sacrificed at the end of week 32.
  • The frequency of bladder lesions, cell proliferation and cell cycle progression activity estimated in terms of the 5-bromodeoxyuridine (BrdU) labeling index or cyclin D1-positive cell ratio were compared among the groups.
  • Administration of silymarin in the initiation or postinitiation phase significantly decreased the incidences of bladder neoplasms and preneoplastic lesions.
  • Dietary exposure to this agent significantly reduced the labeling index for BrdU and the cyclin D1-positive cell ratio in various bladder lesions.
  • These findings suggest that silymarin is effective in preventing OH-BBN-induced bladder carcinogenesis in mice.
  • [MeSH-major] Antioxidants / pharmacology. Butylhydroxybutylnitrosamine / toxicity. Carcinogens / toxicity. Carcinoma, Transitional Cell / prevention & control. Papilloma / prevention & control. Silymarin / pharmacology. Urinary Bladder Neoplasms / prevention & control
  • [MeSH-minor] Administration, Oral. Animals. Anticarcinogenic Agents / pharmacology. Bromodeoxyuridine / metabolism. Cell Cycle / drug effects. Cyclin D1 / metabolism. Male. Mice. Mice, Inbred ICR. Precancerous Conditions / chemically induced. Precancerous Conditions / pathology. Precancerous Conditions / prevention & control


10. Singh RP, Tyagi A, Sharma G, Mohan S, Agarwal R: Oral silibinin inhibits in vivo human bladder tumor xenograft growth involving down-regulation of survivin. Clin Cancer Res; 2008 Jan 1;14(1):300-8
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  • [Title] Oral silibinin inhibits in vivo human bladder tumor xenograft growth involving down-regulation of survivin.
  • PURPOSE: Chemoprevention is an upcoming approach to control bladder cancer, which is one of the commonly diagnosed malignancies showing recurrence rate of 70% or even higher.
  • Recently, we observed the in vitro efficacy of silibinin, a flavanolignan, in human bladder transitional cell papilloma RT4 cells.
  • EXPERIMENTAL DESIGN: RT4 tumor xenograft was implanted s.c. in athymic nude mice, and then animals were oral gavaged with silibinin at 100 and 200 mg/kg doses, 5 days/week for 12 weeks.
  • Tumor growth, body weight, and diet consumption were recorded, and tumors were analyzed for proliferation, apoptosis, and angiogenesis biomarkers and molecular alterations by immunohistochemistry, immunoblot analysis, and ELISA. p53 small interfering RNA was used in cell culture to examine the role of p53 in survivin expression.
  • Silibinin moderately (P < 0.001) decreased cell proliferation and microvessel density and strongly (P < 0.001) increased apoptosis in tumors.
  • CONCLUSION: These findings identified in vivo antitumor efficacy of silibinin against human bladder tumor cells involving down-regulation of survivin and an increase in p53 expression together with enhanced apoptosis.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Transitional Cell / drug therapy. Microtubule-Associated Proteins / drug effects. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis / drug effects. Blotting, Western. Cell Proliferation / drug effects. Down-Regulation. Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Repressor Proteins. Silymarin / administration & dosage. Tumor Suppressor Protein p53 / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 18172282.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R03 CA99079
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Birc5 protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Repressor Proteins; 0 / Silymarin; 0 / Tumor Suppressor Protein p53; 4RKY41TBTF / silybin
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11. Waalkes MP, Liu J, Ward JM, Diwan BA: Enhanced urinary bladder and liver carcinogenesis in male CD1 mice exposed to transplacental inorganic arsenic and postnatal diethylstilbestrol or tamoxifen. Toxicol Appl Pharmacol; 2006 Sep 15;215(3):295-305
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  • [Title] Enhanced urinary bladder and liver carcinogenesis in male CD1 mice exposed to transplacental inorganic arsenic and postnatal diethylstilbestrol or tamoxifen.
  • The treatments alone did not impact urinary bladder carcinogenesis, but arsenic plus TAM significantly increased formation of urinary bladder transitional cell tumors (papilloma and carcinoma; 13%) compared to control (0%).
  • Urinary bladder proliferative lesions (combined tumors and hyperplasia) were also increased by arsenic plus TAM (40%) or arsenic plus DES (43%) compared to control (0%) or the treatments alone.
  • Urinary bladder proliferative lesions occurred in the absence of any evidence of uroepithelial cytotoxic lesions.
  • Urinary bladder lesions and hepatocellular carcinoma induced by arsenic plus TAM and/or DES overexpressed estrogen receptor-alpha, indicating that aberrant estrogen signaling may have been a factor in the enhanced carcinogenic response.
  • In utero arsenic also initiated urinary bladder tumor formation when followed by postnatal TAM and uroepithelial proliferative lesions when followed by TAM or DES.
  • [MeSH-major] Arsenic / toxicity. Diethylstilbestrol / toxicity. Liver Neoplasms / etiology. Tamoxifen / toxicity. Urinary Bladder Neoplasms / etiology
  • [MeSH-minor] Animals. Drug Synergism. Estrogen Receptor alpha / metabolism. Estrogens, Non-Steroidal / toxicity. Female. Male. Maternal-Fetal Exchange. Mice. Mice, Inbred Strains. Pregnancy. Prenatal Exposure Delayed Effects. Selective Estrogen Receptor Modulators / toxicity

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  • (PMID = 16712894.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens, Non-Steroidal; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic
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12. Jiménez Pacheco A, Martínez Torres JI, Pareja Vilchez M, Arrabal Martín M, Valle Díaz de la Guardia F, López León V, Zuluaga Gómez A: [Statistical analysis of the influence of the virus of papilloma human in the development of the vesical carcinoma]. Actas Urol Esp; 2007 May;31(5):469-76
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  • [Title] [Statistical analysis of the influence of the virus of papilloma human in the development of the vesical carcinoma].
  • [Transliterated title] Análisis estadístico de la influencia del virus del papiloma humano en el desarrollo del carcinoma vesical.
  • INTRODUCTION: The bladder cancer is an important disease by its morbi-mortality and its multifactorialidad.
  • At the moment, between the possible aetiology agents that they have been indicated is the infection by the virus of papilloma human (VPH).
  • The objective study is to analyse, by meta-analysis, the relationship between bladder cancer and infection by human papillomavirus.
  • MATERIAL AND METHODS: We made a search in the electronic data base MEDLINE of the articles published until September of the 2004 that relate the infection of the VPH to the bladder tumors.
  • This demonstrated to association between VPH and the bladder cancer.
  • [MeSH-major] Carcinoma, Squamous Cell / virology. Carcinoma, Transitional Cell / virology. Papillomavirus Infections / complications. Urinary Bladder Neoplasms / virology

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  • (PMID = 17711164.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas espanolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 44
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13. Shi Y, Cui L, Dai G, Chen J, Pan H, Song L, Cheng S, Wang X: Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats. Prostaglandins Leukot Essent Fatty Acids; 2006 May;74(5):309-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats.
  • To investigate the prostaglandin E2 (PGE2) biosynthetic mechanism in bladder carcinogenesis, we established Wistar rat model of bladder papilloma and transitional cell carcinoma (TCC) induced by 5% terephthalic acid (TPA) treatment.
  • Proliferating cell nuclear antigen (PCNA) was determined by immunohistochemistry.
  • Bladder papilloma (100%, 8/8) was examined in rats after 24-week treatment, and bladder TCC (80%, 16/20) was found after 48-week treatment.
  • The incidence of bladder papilloma and TCC in test group was significantly higher than that in control group (P<0.01).
  • The mRNA levels of cPLA2, COX-2 and mPGES-1 in the bladder papilloma and TCC were significantly higher than those in normal bladder (P<0.01), while the mRNA levels of COX-1 and mPGES-2 in TCC were unchanged compared with normal bladder.
  • Bladder TCC exhibited a substantial expression of COX-2 protein.
  • On the contrary, normal bladder tissue barely expresses COX-2 protein.
  • PCNA labeling index (LI) and the level of PGE2 in bladder papilloma are much higher than those in normal bladder (P<0.01), but lower than those in bladder TCC (P<0.05).
  • In conclusion, increasing PGE2 level via cPLA2--COX-2--mPGES-1 pathway may play an important role in rat bladder carcinogenesis.
  • PGE2 may be a biomarker for the development of bladder TCC. cPLA2 and mPGES-1 may be targets for development of novel chemoprevention strategies for bladder TCC.
  • [MeSH-major] Cyclooxygenase 2 / metabolism. Dinoprostone / metabolism. Intramolecular Oxidoreductases / metabolism. Phospholipases A / metabolism. Phthalic Acids / toxicity. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Animals. Base Sequence. Blotting, Western. Carcinoma, Transitional Cell / chemically induced. Carcinoma, Transitional Cell / genetics. Carcinoma, Transitional Cell / metabolism. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Group IV Phospholipases A2. Immunohistochemistry. Isoenzymes / genetics. Isoenzymes / metabolism. Male. Molecular Sequence Data. Papilloma / chemically induced. Papilloma / genetics. Papilloma / metabolism. Phospholipases A2. Random Allocation. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Urinary Bladder Calculi / chemically induced. Urinary Bladder Calculi / genetics. Urinary Bladder Calculi / metabolism

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  • (PMID = 16621493.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Phthalic Acids; 6S7NKZ40BQ / terephthalic acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group IV Phospholipases A2; EC 3.1.1.4 / Phospholipases A2; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; K7Q1JQR04M / Dinoprostone
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