[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 26 of about 26
1. Inoue K, Karashima T, Fukata S, Nomura A, Kawada C, Kurabayashi A, Furihata M, Ohtsuki Y, Shuin T: Effect of combination therapy with a novel bisphosphonate, minodronate (YM529), and docetaxel on a model of bone metastasis by human transitional cell carcinoma. Clin Cancer Res; 2005 Sep 15;11(18):6669-77
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of combination therapy with a novel bisphosphonate, minodronate (YM529), and docetaxel on a model of bone metastasis by human transitional cell carcinoma.
  • PURPOSE: Transitional cell carcinoma (TCC) of the urinary tract is a chemosensitive tumor.
  • Most deaths from TCC of the urinary tract are caused by metastasis, which is resistant to conventional chemotherapy.
  • Of these distant metastases, bone metastasis is consistently resistant to cisplatin-based conventional chemotherapy.
  • Therefore, in this study, we investigated whether or not a newly developed minodronate, YM529, could prevent osteolytic bone metastasis of human TCC and also enhance the effect of docetaxel in a bone tumor model of athymic nude mice.
  • EXPERIMENTAL DESIGN: In the present study, we evaluated the effect of in vitro treatment with minodronate and/or docetaxel on the proliferation by cell count, the induction of apoptosis by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) assay, and the biological activity of osteoclast by pit formation assay in human bladder cancer cell line, UMUC-14, and mouse osteoclast cells.
  • RESULTS: In vitro: In vitro treatment with docetaxel inhibited proliferation and resorption pit-forming activity and induced apoptosis of mouse osteoclast cells and UMUC-14 cells.
  • In vitro treatment with minodronate inhibited proliferation and activity and induced apoptosis of mouse osteoclast cells but not UMUC-14 cells.
  • The treatment with minodronate enhanced the inhibition of proliferation and activity by docetaxel in osteoclasts.
  • In vivo: In vivo combination therapy with docetaxel and minodronate significantly reduced the tumor incidence compared with the control (P < 0.05) and also growth of intraossal TCC in athymic nude mice compared with the control (P < 0.001), single therapy with docetaxel (P < 0.01), and minodronate (P < 0.05).
  • Drug-induced body weight loss was not significantly different in any treatment group.
  • Therapy with minodronate significantly enhanced inhibition of proliferation by docetaxel in osteoclasts of bone tumors compared with the control (P < 0.01), single therapy with docetaxel (P < 0.01), and minodronate (P < 0.05).
  • CONCLUSIONS: These studies indicate that combination therapy with minodronate and docetaxel may be beneficial in patients with bone metastasis of human TCC in the urinary tract.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / prevention & control. Carcinoma, Transitional Cell / drug therapy. Urinary Bladder Neoplasms / drug therapy. Xenograft Model Antitumor Assays
  • [MeSH-minor] Acid Phosphatase / analysis. Animals. Apoptosis / drug effects. Bone Resorption / prevention & control. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. Diphosphonates / administration & dosage. Dose-Response Relationship, Drug. Humans. Imidazoles / administration & dosage. Immunohistochemistry. In Situ Nick-End Labeling. Isoenzymes / analysis. Mice. Mice, Inbred BALB C. Mice, Nude. Osteoblasts / chemistry. Osteoblasts / cytology. Osteoblasts / drug effects. Proliferating Cell Nuclear Antigen / analysis. Taxoids / administration & dosage. Tibia / drug effects. Tibia / pathology

  • Genetic Alliance. consumer health - Transitional cell carcinoma.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16166446.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 0 / Isoenzymes; 0 / Proliferating Cell Nuclear Antigen; 0 / Taxoids; 127657-42-5 / YM 529; 15H5577CQD / docetaxel; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
  •  go-up   go-down


2. Martínez-Torrecuadrada JL, Cheung LH, López-Serra P, Barderas R, Cañamero M, Ferreiro S, Rosenblum MG, Casal JI: Antitumor activity of fibroblast growth factor receptor 3-specific immunotoxins in a xenograft mouse model of bladder carcinoma is mediated by apoptosis. Mol Cancer Ther; 2008 Apr;7(4):862-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of fibroblast growth factor receptor 3-specific immunotoxins in a xenograft mouse model of bladder carcinoma is mediated by apoptosis.
  • Human single-chain Fv directed against fibroblast growth factor receptor 3 (FGFR3) have been shown to block proliferation of RT112 bladder carcinoma cells in vitro.
  • Here, we examined the ability of the recombinant gelonin toxin (rGel) to enhance this inhibitory effect in vitro and in vivo on the bladder cancer cell line RT112 and the corresponding xenografts.
  • The mechanism of immunotoxin-induced cell death was found to be mediated by apoptosis.
  • These results show that FGFR3-driven immunotoxins may be an effective therapeutic agent against human bladder and other tumor types overexpressing FGFR3.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Apoptosis / drug effects. Immunotoxins. Receptor, Fibroblast Growth Factor, Type 3 / metabolism. Ribosome Inactivating Proteins, Type 1 / therapeutic use. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / pathology. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Female. Flow Cytometry. Fluorescent Antibody Technique. Humans. Immunoblotting. Immunoglobulin Fragments. Mice. Mice, Nude. Mice, SCID. Protein Transport. RNA, Small Interfering / pharmacology. Recombinant Fusion Proteins / therapeutic use. Surface Plasmon Resonance. Survival Rate. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18413799.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunoglobulin Fragments; 0 / Immunotoxins; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / Ribosome Inactivating Proteins, Type 1; 75037-46-6 / GEL protein, Gelonium multiflorum; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3
  •  go-up   go-down


3. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • Silibinin robustly decreased survivin protein expression and its nuclear localization, as well as tumor-secreted level in mouse plasma, but increased p53 and cleaved caspase-3 levels 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

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. Liu H, Schwartz MJ, Hwang DH, Scherr DS: Tumour growth inhibition by an imidazoquinoline is associated with c-Myc down-regulation in urothelial cell carcinoma. BJU Int; 2008 Apr;101(7):894-901
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour growth inhibition by an imidazoquinoline is associated with c-Myc down-regulation in urothelial cell carcinoma.
  • OBJECTIVE: To detect and characterize the potential role of c-Myc in the inhibition of proliferation and induction of cell death of urothelial cell carcinoma by imidazoquinolines, Toll-like receptor-7 (TLR7) agonists, that are thought to exert their immunogenic effects through the MyD88/NF-kappaB pathway.
  • MATERIALS AND METHODS: Human (T24) and murine (MBT-2) bladder cancer cell lines were cultured in normal culture medium or medium supplemented with imidazoquinoline.
  • Effects of imidazoquinoline on in vivo bladder tumour growth and gene expression were investigated using a mouse model of orthotopic bladder cancer.
  • RESULTS: There was a dose-dependent decrease in c-Myc expression in bladder cancer cells treated with imidazoquinoline; the transcriptional activity of c-Myc was also significantly reduced.
  • For in vivo experiments, a third of mice with bladder cancer treated with intravesical imidazoquinoline showed evidence of residual bladder tumour, vs all the placebo-treated mice.
  • In vivo expression of c-Myc, cyclin D2 and proliferating cell nuclear antigen in the bladder tumour tissue were also down-regulated.
  • CONCLUSIONS: Imidazoquinolines can inhibit c-Myc expression and directly affect cell growth and tumorigenesis of bladder cancer cells, independent of an immune response.
  • Our findings could broaden the potential application of imidazoquinoline therapy beyond dermatological malignancies, and further clinical studies are warranted.
  • [MeSH-major] Carcinoma, Transitional Cell / drug therapy. Proto-Oncogene Proteins c-myc / metabolism. Toll-Like Receptor 7 / agonists. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation. Gene Expression. Humans. Imidazoles / agonists. Imidazoles / therapeutic use. Immunohistochemistry. Mice. Quinolines / agonists. Quinolines / therapeutic use

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18241249.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Proto-Oncogene Proteins c-myc; 0 / Quinolines; 0 / Toll-Like Receptor 7
  •  go-up   go-down


5. Kawano H, Komaba S, Yamasaki T, Maeda M, Kimura Y, Maeda A, Kaneda Y: New potential therapy for orthotopic bladder carcinoma by combining HVJ envelope with doxorubicin. Cancer Chemother Pharmacol; 2008 May;61(6):973-8
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New potential therapy for orthotopic bladder carcinoma by combining HVJ envelope with doxorubicin.
  • PURPOSE: To establish a new therapeutic method to treat bladder carcinoma, we investigated the therapeutic potential of doxorubicin hydrochloride (DXR) combined with hemagglutinating virus of Japan-envelope vector (HVJ-E) in an orthotropic mouse bladder cancer model.
  • METHODS: DXR and/or HVJ-E were instilled into the bladder after implantation of MB49 cells.
  • Antitumor effects of combination therapy were evaluated by histological analysis of the bladder on day 14 after tumor implantation.
  • The surviving mice were re-challenged with intravesical injection of MB49 cells, and the bladder was observed after 3 weeks.
  • After combination therapy, surviving mice formed no tumors in the bladder following intravesical re-instillation of MB49.
  • [MeSH-major] Antibiotics, Antineoplastic / chemistry. Antibiotics, Antineoplastic / pharmacology. Carcinoma, Transitional Cell / drug therapy. Doxorubicin / chemistry. Doxorubicin / pharmacology. Sendai virus / chemistry. Urinary Bladder Neoplasms / drug therapy. Viral Envelope Proteins / chemistry
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Female. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Survival Analysis. Tetrazolium Salts / pharmacology

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17653716.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H tetrazolium monosodium salt; 0 / Antibiotics, Antineoplastic; 0 / Tetrazolium Salts; 0 / Viral Envelope Proteins; 80168379AG / Doxorubicin
  •  go-up   go-down


6. Luan FL, Hojo M, Maluccio M, Yamaji K, Suthanthiran M: Rapamycin blocks tumor progression: unlinking immunosuppression from antitumor efficacy. Transplantation; 2002 May 27;73(10):1565-72
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Immunosuppressive drug therapy-induced impairment of the organ graft recipient's immune surveillance is considered to be the mechanism for the heightened incidence and metastatic progression.
  • We identified a cell-autonomous and host-immunity independent mechanism for cyclosporine-associated tumor progression.
  • The effect of rapamycin on renal cancer cell phenotype, molecules (E-cadherin, p27 kip1, cyclin D1) implicated in tumor progression, and the effect of rapamycin on in vivo tumor progression were explored in BALB/c mice and in T-cell, B-cell, and natural killer (NK) cell-deficient severe combined immune deficiency (SCID)-beige mice.
  • In the SCID-beige mice, T24 human bladder transitional cell carcinoma also was used as the tumor inoculum.
  • RESULTS: Rapamycin conditioning of renal cancer cells upregulated E-cadherin expression and induced phenotypic transition from invasive spindle, or dome-shaped cells, with exploratory pseudopodia to noninvasive cuboidal cells that formed cell-to-cell adhesions.
  • Rapamycin treatment alone, or with cyclosporine, prolonged the survival of mice inoculated with renal cancer cells or T24 human bladder cancer cells.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antibiotics, Antineoplastic / pharmacology. Carcinoma, Renal Cell / drug therapy. Immunosuppression. Immunosuppressive Agents / pharmacology. Kidney Neoplasms / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Animals. B-Lymphocytes / immunology. Cadherins / genetics. Cell Cycle Proteins / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p27. DNA Primers. Disease Progression. Genes, Tumor Suppressor. Killer Cells, Natural / immunology. Mice. Mice, Inbred BALB C. Mice, SCID. T-Lymphocytes / immunology. Tacrolimus / pharmacology. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12042641.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI 26932
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cadherins; 0 / Cdkn1b protein, mouse; 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / Immunosuppressive Agents; 0 / Tumor Suppressor Proteins; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
  •  go-up   go-down


7. Li CG, Li ML, Shu XH, Liu YJ, Wu WS: Antitumor effects of recombinant human interleukin-6 on mouse bladder carcinoma through Fas-mediated apoptosis. Cancer Chemother Pharmacol; 2010 Oct;66(5):981-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor effects of recombinant human interleukin-6 on mouse bladder carcinoma through Fas-mediated apoptosis.
  • PURPOSE: An apoptosis-inducing therapy is gradually becoming a new strategy for cancer treatment.
  • The aim of this study was to investigate the mechanism of growth-inhibitory effects of recombinant human interleukin-6 (rhIL-6) on bladder tumor-bearing T739 mice in vivo.
  • METHODS: Murine bladder transitional carcinoma cells (BTT739) were inoculated subcutaneously into T739 mice as a tumor model for evaluating the antitumor effects of rhIL-6.
  • Animals were killed by CO(2) inhalation on the 15th day after tumor cell inoculation.
  • The morphological characteristic changes of tumor cells were observed under electron microscope, and cell cycle analysis was determined by flow cytometry.
  • The expressions of Fas, FasL and Bcl-2 protein on tumor cells were qualitatively detected by immunofluorescence cell staining, and their relative contents (rate of positive cells, RPC) were quantitatively determined with flow cytometry.
  • RESULTS: rhIL-6 could inhibit bladder tumor growth in a dose-dependent manner in vivo.
  • CONCLUSIONS: rhIL-6 had obvious antitumor effects on mouse bladder carcinoma in vivo, and the Fas signaling pathway might play an important role in rhIL-6-induced bladder carcinoma cell apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Interleukin-6 / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Fas Ligand Protein / genetics. Fas Ligand Protein / metabolism. Fas-Associated Death Domain Protein / genetics. Fas-Associated Death Domain Protein / metabolism. Female. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Mice, Inbred Strains. Proto-Oncogene Proteins c-bcl-2 / genetics. Recombinant Proteins

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20499068.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fas Ligand Protein; 0 / Fas-Associated Death Domain Protein; 0 / Interleukin-6; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins
  •  go-up   go-down


8. Karam JA, Fan J, Stanfield J, Richer E, Benaim EA, Frenkel E, Antich P, Sagalowsky AI, Mason RP, Hsieh JT: The use of histone deacetylase inhibitor FK228 and DNA hypomethylation agent 5-azacytidine in human bladder cancer therapy. Int J Cancer; 2007 Apr 15;120(8):1795-802
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of histone deacetylase inhibitor FK228 and DNA hypomethylation agent 5-azacytidine in human bladder cancer therapy.
  • The long-term disease-free survival in patients with metastatic transitional cell carcinoma (TCC) is still considerably low.
  • In this study, we have evaluated several epigenetic modifiers for their therapeutic application in bladder cancer.
  • Both histone deacetylase inhibitors (FK228, TSA) and DNA hypomethylating agent (5-Azacytidine) were tested using in vitro assays such as cell viability, cell cycle analysis and western blot to determine their mechanisms of action.
  • Drug combination experiments were also designed to study any additive or synergistic effects of these agents.
  • In addition, two bladder cancer xenograft models (one subcutaneous and one orthotopic) were employed to assess the therapeutic efficacy of these agents in vivo.
  • Three agents exhibited various growth inhibitory effects on 5 different TCC cell lines in a dose- and time-dependent manner.
  • In addition to G2/M cell cycle arrest, FK228 is more potent in inducting apoptosis than the two other single agents, and combination of both FK228 and 5-Aza further enhances this effect. p21 induction is closely associated with FK228 or TSA but not 5-Aza, which is mediated via p53-independent pathway.

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17230511.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA086354; United States / NCI NIH HHS / CA / CA086354-03; United States / NCI NIH HHS / CA / U24 CA126608; United States / NCI NIH HHS / CA / CA95730; United States / NCI NIH HHS / CA / P20 CA086354-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Depsipeptides; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Tumor Suppressor Protein p53; CX3T89XQBK / romidepsin; M801H13NRU / Azacitidine
  •  go-up   go-down


9. Zhao P, Luo CL, Wu XH, Hu HB, Lv CF, Ji HY: [Proliferation apoptotic influence of crocin on human bladder cancer T24 cell line]. Zhongguo Zhong Yao Za Zhi; 2008 Aug;33(15):1869-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Proliferation apoptotic influence of crocin on human bladder cancer T24 cell line].
  • OBJECTIVE: To investigate the proliferation, apoptosis and mechanisms on T24 cell of transitional cell carcinoma of bladder (TCCB) by crocin.
  • The changes of cell cycle and cell apoptotic percentage were measured by flow cytometry.
  • T24 cells were inoculated into BALB/c nude mice to establish model of carcinoma of bladder.
  • After treatment with 50 mmol x L(-1) crocin, the inhibited growth of tumor was observed.
  • RESULT: The growth of T24 cells was remarkably inhibited after treatment of crocin.
  • Flow cytometric profiles revealed that crocin led to the increase of the cells in G0/G1 phase, the percentage of cell apoptosis was also increased.
  • The morphology changes of cell apoptosis were observed.
  • Bcl-2, Cyclin D1 and survivin expressions determined by immunohistochemical staining were down-regulated after treatment with Bax expression up-regulated.
  • CONCLUSION: Crocin exerts both in vitro and in vivo anti-cancer effect on TCCB T24 cell line.
  • The mechanisms may change tumour cell cycle and induce tumour cell apoptosis by down-regulating the expression of Bcl-2, Survivin, Cyclin D1 and up-regulating the expression of Bax.
  • [MeSH-major] Apoptosis / drug effects. Carotenoids / pharmacology. Carotenoids / therapeutic use. Cell Proliferation / drug effects. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Animals. Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / pathology. Carcinoma, Transitional Cell / ultrastructure. Cell Cycle / drug effects. Cell Line, Tumor. Cyclin D1 / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Electron, Transmission. Microtubule-Associated Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Repressor Proteins. Transplantation, Heterologous

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. Crocin .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19007019.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Birc5 protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Repressor Proteins; 136601-57-5 / Cyclin D1; 36-88-4 / Carotenoids; 42553-65-1 / crocin
  •  go-up   go-down


10. Lee SJ, Cho YH, Park K, Kim EJ, Kang BS, Jung KH, Kim CH, Kim WJ, Moon SK: Inhibitory effects of the aqueous extract of Magnolia officinalis on the responses of human urinary bladder cancer 5637 cells in vitro and mouse urinary bladder tumors induced by N-Butyl-N-(4-hydroxybutyl) nitrosamine in vivo. Phytother Res; 2009 Jan;23(1):20-7
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of the aqueous extract of Magnolia officinalis on the responses of human urinary bladder cancer 5637 cells in vitro and mouse urinary bladder tumors induced by N-Butyl-N-(4-hydroxybutyl) nitrosamine in vivo.
  • This study investigated the anticancer activity of Magnolia officinalis on urinary bladder cancer in vitro and in vivo, and elucidated the mechanism of its activity.
  • An aqueous extract of M. officinalis inhibited cell viability and DNA synthesis in cultured human urinary bladder cancer 5637 cells.
  • Inhibition of proliferation was the result of apoptotic induction, because FACS analyses of 5637 cells treated with M. officinalis showed a sub-G1 phase accumulation. M. officinalis extract also increased cytoplasmic DNA-histone complex dose-dependently.
  • Treatment of 5637 cells with M. officinalis extract suppressed the expression of matrix metalloproteinase 2 (MMP-2) and MMP-9, as revealed by zymographic and immunoblot analyses.
  • When M. officinalis extract was given to mice simultaneously with the carcinogen N-butyl-N-(4-hydroxybutyl) nitrosamine, which induces urinary bladder tumors, the size of the induced tumors was smaller.
  • Finally, histological data indicated that the histological grade of carcinoma and the depth of invasion were dramatically decreased by treatment with M. officinalis extract in mice with N-butyl-N-(4-hydroxybutyl) nitrosamine-induced urinary bladder tumors.
  • In conclusion, the findings showed that M. officinalis extract exhibited potential chemopreventive activity against urinary bladder tumor in vitro and in vivo.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Butylhydroxybutylnitrosamine / toxicity. Carcinoma, Transitional Cell / drug therapy. Magnolia / chemistry. Plant Extracts / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cytochromes c / metabolism. DNA / biosynthesis. Dose-Response Relationship, Drug. Humans. Male. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Nucleic Acid Synthesis Inhibitors / pharmacology. bcl-2-Associated X Protein / metabolism

  • Genetic Alliance. consumer health - Bladder cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 John Wiley & Sons, Ltd.
  • (PMID = 19048611.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Plant Extracts; 0 / bcl-2-Associated X Protein; 3817-11-6 / Butylhydroxybutylnitrosamine; 9007-43-6 / Cytochromes c; 9007-49-2 / DNA; EC 3.4.22.- / Caspase 3; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


11. Ikeda N, Honda I, Yano I, Koyama A, Toida I: Bacillus calmette-guerin Tokyo172 substrain for superficial bladder cancer: characterization and antitumor effect. J Urol; 2005 May;173(5):1507-12
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bacillus calmette-guerin Tokyo172 substrain for superficial bladder cancer: characterization and antitumor effect.
  • PURPOSE: We investigated the preparation of bacillus Calmette-Guerin (BCG) Tokyo172 substrain (Japan BCG Laboratory, Ltd., Tokyo, Japan) on the characteristics of bacilli and antitumor activity in a mouse model in comparison with a preparation of the Connaught substrain (Aventis Pasteur, Ltd., Toronto, Ontario, Canada).
  • MATERIALS AND METHODS: Lyophilized BCG preparations of Tokyo172 and Connaught for superficial bladder cancer were tested.
  • The number of bacilli and cfu per dose, dispersion, size and attachment to murine bladder tumor cells were determined after reconstitution.
  • [MeSH-major] BCG Vaccine / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Urinary Bladder Neoplasms / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15821469.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCG Vaccine
  •  go-up   go-down


12. Rooks V, Beecken WD, Iordanescu I, Taylor GA: Sonographic evaluation of orthotopic bladder tumors in mice treated with TNP-470, an angiogenic inhibitor. Acad Radiol; 2001 Feb;8(2):121-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sonographic evaluation of orthotopic bladder tumors in mice treated with TNP-470, an angiogenic inhibitor.
  • RATIONALE AND OBJECTIVES: The purpose of this study was to determine the feasibility of using transabdominal ultrasonography (US) to monitor tumor growth and response to therapy in a mouse model of orthotopic bladder carcinoma.
  • MATERIALS AND METHODS: Human bladder carcinoma cell suspensions were injected into the bladders of 18 SCID mice, allowed to grow for 3 weeks, and monitored weekly with gray-scale US.
  • Eight of the treated animals were imaged and sacrificed after 14 days of treatment.
  • RESULTS: While saline-treated tumors continued to grow, the growth of TNP-470-treated tumors was arrested within 7 days of therapy (P < .02).
  • Although tumor neovascularity was identified in every animal, the pattern of neovascularity did not correlate with tumor volume or therapy.
  • CONCLUSION: US can provide accurate intermediate end points for monitoring experimental intraabdominal tumor growth and response to therapy in the mouse model.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / ultrasonography. Sesquiterpenes / therapeutic use. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / ultrasonography

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Acad Radiol. 2001 Feb;8(2):119-20 [11227639.001]
  • (PMID = 11227640.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol
  •  go-up   go-down


13. Ogihara M, Yamaguchi O: Potentiation of effects of anticancer agents by local electric pulses in murine bladder cancer. Urol Res; 2000 Dec;28(6):391-7
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potentiation of effects of anticancer agents by local electric pulses in murine bladder cancer.
  • Electrochemotherapy is a novel cancer treatment in which electric pulses (EP) are used as a means of delivering anticancer agents to the cytoplasm of cancer cells (electroporation).
  • The present study evaluates whether electrochemotherapy has in vitro and in vivo anticancer effects in murine bladder cancer.
  • Using mouse bladder tumor cells (MBT-2 cells), in vitro electrochemotherapy was performed by applying EP to the cell suspension immediately after the addition of anticancer agents.
  • Then, tumor growth rate (TGR) was determined and compared to that in the sham-treated control group, the EP-only group and the drug-only group.
  • It is clear from in vitro and in vivo studies that, in a murine bladder tumor, the anticancer effect of BLM can be considerably potentiated by applying EP.
  • Thus, BLM seems to be the most suitable anticancer agent for electrochemotherapy of bladder cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Transitional Cell / drug therapy. Doxorubicin / pharmacology. Electric Stimulation Therapy / methods. Electroporation / methods. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Bleomycin / pharmacology. Cisplatin / pharmacology. Combined Modality Therapy. Fadrozole. Female. In Vitro Techniques. Mice. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. BLEOMYCIN .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11221918.001).
  • [ISSN] 0300-5623
  • [Journal-full-title] Urological research
  • [ISO-abbreviation] Urol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 11056-06-7 / Bleomycin; 80168379AG / Doxorubicin; H3988M64PU / Fadrozole; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


14. Wu Q, Mahendran R, Esuvaranathan K: Nonviral cytokine gene therapy on an orthotopic bladder cancer model. Clin Cancer Res; 2003 Oct 1;9(12):4522-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonviral cytokine gene therapy on an orthotopic bladder cancer model.
  • PURPOSE: The purpose is to assess cytokine gene transfection in tumor cells and its therapeutic efficacy in an orthotopic mouse bladder cancer model after liposome-mediated gene transfer.
  • EXPERIMENTAL DESIGN: A total of 1 x 10(5) MB49 cells was instilled into the bladder of C57BL/6 mice after electrocautery to establish the tumor model.
  • RESULTS: Superficial bladder tumors were established by intravesical instillation of MB49 into cauterized bladders.
  • The expression level of cytokines in transfected cell lines was increased significantly.
  • In situ gene transfer to bladder tumors was accomplished via intravesical instillation of plasmid DNA/N-[1-(2,3-dioleoyloxyl)propyl]-N,N,N-trimethylammoniummethyl sulfate/methyl-beta-cyclodextrin-solubilized cholesterol after a single 2 h in situ transfection.
  • The tumor incidence in the treatment groups was dramatically decreased from 76.9% in the control group to 15.4-30.8% in the treatment groups.
  • CONCLUSIONS: We demonstrated in the orthotopic mouse bladder cancer model that successful inhibition of tumor cell growth could be obtained with cytokine gene therapy.
  • The results suggest that our liposome transfection system appears to be a promising method for gene therapy of bladder cancer in vivo.
  • [MeSH-major] Genetic Therapy. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Interferon-alpha / therapeutic use. Neoplasms, Experimental / therapy. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Animals. Carcinoma, Transitional Cell / immunology. Carcinoma, Transitional Cell / prevention & control. Carcinoma, Transitional Cell / therapy. Cell Division. Cholesterol / metabolism. Disease Models, Animal. Drug Therapy, Combination. Enzyme-Linked Immunosorbent Assay. Female. Flow Cytometry. Immunoenzyme Techniques. Lipid Metabolism. Liposomes. Mice. Mice, Inbred C57BL. Mice, Transgenic. Plasmids. Transfection. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14555526.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Liposomes; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 97C5T2UQ7J / Cholesterol
  •  go-up   go-down


15. Nativ O, Dalal E, Laufer M, Sabo E, Aronson M: Antineoplastic effect of gemcitabine in an animal model of superficial bladder cancer. Urology; 2004 Oct;64(4):845-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antineoplastic effect of gemcitabine in an animal model of superficial bladder cancer.
  • OBJECTIVES: To evaluate the safety and efficacy of gemcitabine in an animal model of superficial bladder cancer because of the promising results for treatment of patients with advanced urothelial carcinoma using gemcitabine.
  • The substantial failure rate and toxicity of currently available intravesical agents for treating superficial bladder cancer emphasize the need for alternative drugs.
  • METHODS: The mouse bladder tumor (MBT-2) model was used in female C3H/eb mice to evaluate gemcitabine toxicity (n = 45) and efficacy (n = 402).
  • RESULTS: Treatment with varying doses (0.5, 2.5, and 10 mg) of intravesical gemcitabine was well tolerated with no demonstrable side effects.
  • No statistically significant differences in the histologic changes in the bladder wall were observed among the various treatment groups.
  • The efficacy of the drug was tested in two sets of experiments and showed a statistically significant decrease in the bladder weight of the animals treated with gemcitabine compared with those treated with phosphate-buffered saline or untreated controls (61.4 +/- 24.1 mg versus 106.2 +/- 50 mg and 105.5 +/- 46 mg, respectively [P = 0.0001], for an aggressive tumor variant).
  • In the second set of experiments, gemcitabine was given both intraperitoneally and intravesically and resulted in a lower bladder weight (44.5 +/- 15.75 mg and 59.71 +/- 22.5 mg, respectively) compared with the control groups (116.43 +/- 53.91 mg and 122.29 +/- 50 mg, respectively, P = 0.0004).
  • This drug displayed significant antineoplastic activity against superficial bladder cancer.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Intravesical. Animals. Cystitis / chemically induced. Drug Screening Assays, Antitumor. Female. Fibrosis. Hyperplasia. Injections, Intraperitoneal. Mice. Mice, Inbred C3H. Neoplasm Transplantation. Organ Size / drug effects. Single-Blind Method. Urothelium / drug effects. Urothelium / pathology

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15491745.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  •  go-up   go-down


16. Zhang J, Ramesh N, Chen Y, Li Y, Dilley J, Working P, Yu DC: Identification of human uroplakin II promoter and its use in the construction of CG8840, a urothelium-specific adenovirus variant that eliminates established bladder tumors in combination with docetaxel. Cancer Res; 2002 Jul 1;62(13):3743-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of human uroplakin II promoter and its use in the construction of CG8840, a urothelium-specific adenovirus variant that eliminates established bladder tumors in combination with docetaxel.
  • UPII gene expression is bladder specific and differentiation dependent, but very little is known about its transcription response elements.
  • Transient transfection experiments showed that the DNA segment located between -1809 and +1 bp resulted in preferential expression in bladder carcinoma cells with negligible expression in nonurothelial cells.
  • This promoter was engineered into adenovirus (Ad) type 5 to drive the expression of the E1A and E1B genes and to create an attenuated replication-competent Ad variant, termed CG8840.
  • Viral replication and the cytopathic effect of CG8840 were evaluated by virus yield and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays in bladder transitional cell carcinoma (TCC) cell lines RT4 and SW780; nonbladder cancer cell lines G361 (melanoma), LNCaP (prostate cancer), PA-1 (ovarian cancer), and U118 (brain cancer); and human primary cells including lung fibroblasts, bladder smooth muscle cells, and mammary epithelial cells.
  • CG8840 replicated in and eliminated bladder TCC efficiently with high specificity (10,000:1) in comparison with nonbladder cells.
  • Intratumoral and i.v. administration of CG8840 in RT4 human bladder cancer xenografts caused significant (P < 0.01) inhibition of tumor growth.
  • Synergistic antitumor efficacy was observed when CG8840 was combined with docetaxel, resulting in significant regression of RT4 bladder cancer xenograft tumors within 6 weeks after i.v. administration of CG8840 (3.33 x 10(9) plaque-forming units/animal on day 1) and docetaxel (20 mg/kg on days 2, 6, and 9).
  • These results demonstrate the utility of the UPII promoter in the generation of urothelium-specific adenoviral vectors and provide a potential foundation for the development of bladder tumor-specific oncolytic viral therapies.
  • [MeSH-major] Adenoviruses, Human / physiology. Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Transitional Cell / therapy. Membrane Proteins / genetics. Paclitaxel / analogs & derivatives. Paclitaxel / pharmacology. Taxoids. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Adenovirus E1B Proteins / genetics. Animals. Combined Modality Therapy. Cytopathogenic Effect, Viral. Drug Synergism. Gene Deletion. Genes, Regulator. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Promoter Regions, Genetic / genetics. Uroplakin II. Virus Replication / genetics. Virus Replication / physiology. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12097284.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1B Proteins; 0 / Antineoplastic Agents, Phytogenic; 0 / Membrane Proteins; 0 / Taxoids; 0 / UPK2 protein, human; 0 / Upk2 protein, mouse; 0 / Uroplakin II; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


17. Mian BM, Dinney CP, Bermejo CE, Sweeney P, Tellez C, Yang XD, Gudas JM, McConkey DJ, Bar-Eli M: Fully human anti-interleukin 8 antibody inhibits tumor growth in orthotopic bladder cancer xenografts via down-regulation of matrix metalloproteases and nuclear factor-kappaB. Clin Cancer Res; 2003 Aug 1;9(8):3167-75
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fully human anti-interleukin 8 antibody inhibits tumor growth in orthotopic bladder cancer xenografts via down-regulation of matrix metalloproteases and nuclear factor-kappaB.
  • PURPOSE: We previously demonstrated that overexpression of interleukin 8 (IL-8) in human transitional cell carcinoma (TCC) resulted in increased tumorigenicity and metastasis.
  • EXPERIMENTAL DESIGN: To investigate whether targeting IL-8 with a fully human anti-IL-8 antibody (ABX-IL8) could be a potential therapeutic strategy for controlling TCC growth, we studied its effects on TCC growth in vitro and in an in vivo mouse model.
  • Human TCC cell lines 253J B-V and UM UC3 (high IL-8 producers), 253J (low IL-8), and 253J transfected with the IL-8 gene (high producer) were used.
  • RESULTS: ABX-IL8 had no effect on TCC cell proliferation in vitro.
  • However, in the orthotopic nude mouse model, after 4 weeks of treatment (100 micro g/week, i.p.
  • ), a significant decrease in tumor growth of both cell lines was observed.
  • CONCLUSIONS: Our data point to the potential use of ABX-IL8 as a modality to treat bladder cancer and other solid tumors, either alone or in combination with conventional chemotherapy or other antitumor agents.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Down-Regulation. Interleukin-8 / chemistry. Interleukin-8 / immunology. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 9 / biosynthesis. NF-kappa B / biosynthesis. Urinary Bladder Neoplasms / metabolism. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Animals. Blotting, Western. Carcinoma, Transitional Cell / metabolism. Cell Division. Cell Line, Tumor. Cell Nucleus / metabolism. Collagen / pharmacology. Drug Combinations. Humans. Laminin / pharmacology. Luciferases / metabolism. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis. Neoplasm Transplantation. Nucleic Acid Hybridization. Promoter Regions, Genetic. Proteoglycans / pharmacology. RNA, Messenger / metabolism. Time Factors. Transcription, Genetic. Up-Regulation

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12912969.001).
  • [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 / CA16672; United States / NCI NIH HHS / CA / P50 CA 91846
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Drug Combinations; 0 / Interleukin-8; 0 / Laminin; 0 / NF-kappa B; 0 / Proteoglycans; 0 / RNA, Messenger; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 1.13.12.- / Luciferases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


18. Chen F, Zhang G, Cao Y, Hessner MJ, See WA: MB49 murine urothelial carcinoma: molecular and phenotypic comparison to human cell lines as a model of the direct tumor response to bacillus Calmette-Guerin. J Urol; 2009 Dec;182(6):2932-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MB49 murine urothelial carcinoma: molecular and phenotypic comparison to human cell lines as a model of the direct tumor response to bacillus Calmette-Guerin.
  • PURPOSE: The mouse urothelial carcinoma cell line MB49 is widely used as an in vitro and in vivo model of urothelial carcinoma.
  • Little comparative data exist on the molecular and phenotypic responses of this cell line relative to human cell lines.
  • We compared the effect of bacillus Calmette-Guerin on the MB49 cell line relative to responses previously observed in the human urothelial carcinoma lines T24 (ATCC) and 253J.
  • Phenotypic response end points were direct cytotoxicity using dye exclusion, viability on MTT assay, apoptotic sensitivity and cell cycle compartmentalization.
  • Bacillus Calmette-Guerin decreased cell viability and induced G1 cell cycle arrest.
  • Treatment of MB49 cells with bacillus Calmette-Guerin induced caspase independent cell death while simultaneously decreasing sensitivity to pro-apoptotic agents.
  • Cell death was associated with release of the necrotic cell death marker HMGB1.
  • CONCLUSIONS: MB49 cells show molecular and phenotypic responses to bacillus Calmette-Guerin that replicate those observed in human urothelial carcinoma lines.
  • MB49 cells appear to be an excellent model in which to study bacillus Calmette-Guerin as an antitumor agent for urothelial carcinoma.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. BCG Vaccine / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / genetics. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor / drug effects. Cell Line, Tumor / physiology. Humans. Mice. Phenotype. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19853870.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine
  •  go-up   go-down


19. Yao X, Chang JW, Li WL, Niu RF, Sun BC, Ma TX: [Inhibitory effects of antisense TGF beta1 on in vitro and in vivo proliferation of human bladder cancer cells]. Zhonghua Zhong Liu Za Zhi; 2004 Jan;26(1):18-21
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Inhibitory effects of antisense TGF beta1 on in vitro and in vivo proliferation of human bladder cancer cells].
  • OBJECTIVE: To investigate the inhibitory effects of antisense TGF beta1 on proliferation of human bladder transitional cell carcinoma in vitro and in vivo.
  • METHODS: Human bladder carcinoma cell line EJ was transfected with pRevT beta-AS, a replication defective retroviral vector carried antisense TGF beta1 fragment.
  • Cell cycle was determined by flow cytometry.
  • RESULTS: The expression of TGF beta1 mRNA and protein in EJ cells was inhibited by pRevT beta-AS, G(1) to S transition was restrained in cell cycle and cell proliferation decreased in vitro.
  • CONCLUSION: TGF beta1 plays a role in vitro proliferation and in vivo growth of bladder transitional cell carcinoma.
  • [MeSH-major] RNA, Antisense / therapeutic use. Transforming Growth Factor beta / antagonists & inhibitors. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Female. Humans. Mice. Mice, SCID. Transforming Growth Factor beta1

  • Genetic Alliance. consumer health - Bladder cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15059346.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Antisense; 0 / TGFB1 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1
  •  go-up   go-down


20. Kemberling JK, Hampton JA, Keck RW, Gomez MA, Selman SH: Inhibition of bladder tumor growth by the green tea derivative epigallocatechin-3-gallate. J Urol; 2003 Sep;170(3):773-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of bladder tumor growth by the green tea derivative epigallocatechin-3-gallate.
  • PURPOSE: We evaluated the green tea derivative epigallocatechin-3-gallate (EGCG) as an intravesical agent for the prevention of transitional cell tumor implantation.
  • MATERIALS AND METHODS: In vitro studies were performed in the AY-27 rat transitional cell cancer and the L1210 mouse leukemia cell lines.
  • Surviving cell colonies were then determined.
  • A DNA ladder assay was performed in the 2 cell lines.
  • Rats were sacrificed 3 weeks following treatment.
  • RESULTS: At 6.0 x 104 cells per 100 mm dish a time dose dependent response was observed.
  • After 2 hours of treatment with EGCG 100% cell lethality of the AY-27 cell line occurred at concentrations greater than 100 microM.
  • Strong banding on the DNA ladder assay was seen with the L1210 mouse leukemia cell line.
  • Only weak banding patterns were found in the AY-27 cell line treated with EGCG (100 and 200 microM) for 24 hours.
  • CONCLUSIONS: The clonal assays showed a time dose related response to EGCG.
  • Intravesical instillation of EGCG inhibits the growth of AY-27 rat transitional cells implanted in this model.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Catechin / analogs & derivatives. Catechin / therapeutic use. Free Radical Scavengers / therapeutic use. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Rats. Rats, Inbred F344. Tea. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Green tea .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12913695.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Free Radical Scavengers; 0 / Tea; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate
  •  go-up   go-down


21. Zi X, Simoneau AR: Flavokawain A, a novel chalcone from kava extract, induces apoptosis in bladder cancer cells by involvement of Bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice. Cancer Res; 2005 Apr 15;65(8):3479-86
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flavokawain A, a novel chalcone from kava extract, induces apoptosis in bladder cancer cells by involvement of Bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice.
  • We have identified flavokawain A, B, and C but not the major kavalactone, kawain, in kava extracts as causing strong antiproliferative and apoptotic effect in human bladder cancer cells.
  • Flavokawain A results in a significant loss of mitochondrial membrane potential and release of cytochrome c into the cytosol in an invasive bladder cancer cell line T24.
  • These effects of flavokawain A are accompanied by a time-dependent decrease in Bcl-x(L), a decrease in the association of Bcl-x(L) to Bax, and an increase in the active form of Bax protein.
  • Using the primary mouse embryo fibroblasts Bax knockout and wild-type cells as well as a Bax inhibitor peptide derived from the Bax-binding domain of Ku70, we showed that Bax protein was, at least in part, required for the apoptotic effect of flavokawain A.
  • Because both X-linked inhibitor of apoptosis and survivin are main factors for apoptosis resistance and are overexpressed in bladder tumors, our data suggest that flavokawain A may have a dual efficacy in induction of apoptosis preferentially in bladder tumors.
  • Finally, the anticarcinogenic effect of flavokawain A was evident in its inhibitory growth of bladder tumor cells in a nude mice model (57% of inhibition) and in soft agar.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Transitional Cell / drug therapy. Chalcone / analogs & derivatives. Chalcone / pharmacology. Flavonoids / pharmacology. Kava / chemistry. Mitochondria / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Caspase 3. Caspase 9. Caspases / metabolism. Cell Growth Processes / drug effects. Cytochromes c / secretion. Humans. Inhibitor of Apoptosis Proteins. Membrane Potentials / drug effects. Mice. Mice, Nude. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins. Plant Extracts / pharmacology. Poly(ADP-ribose) Polymerases / metabolism. Proteins / metabolism. X-Linked Inhibitor of Apoptosis Protein. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15833884.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-109428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BIRC5 protein, human; 0 / Bax protein, mouse; 0 / Flavonoids; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Plant Extracts; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 0 / bcl-2-Associated X Protein; 0 / flavokawain A; 0 / flavokawain B; 5S5A2Q39HX / Chalcone; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp9 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
  •  go-up   go-down


22. Schwartz L, Abolhassani M, Guais A, Sanders E, Steyaert JM, Campion F, Israël M: A combination of alpha lipoic acid and calcium hydroxycitrate is efficient against mouse cancer models: preliminary results. Oncol Rep; 2010 May;23(5):1407-16
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A combination of alpha lipoic acid and calcium hydroxycitrate is efficient against mouse cancer models: preliminary results.
  • Our hypothesis is that a combination of these drugs may have antitumoral potential.
  • The efficacy of these molecules was screened in vitro by treatment of different human cancer and murine cell lines.
  • Lipoic acid reduced the cell number by 10-50% depending on concentrations (0.1-10 microM) and cell types.
  • Calcium hydroxycitrate reduced the cell number by 5-60% at different concentrations (10-500 microM).
  • When hydroxycitrate and lipoic acid were used together, there was a major cytotoxic effect: complete cell death was seen following 8 microM lipoic acid and 300 microM hydroxycitrate treatment for 72 h.
  • The combination was used to treat mouse syngenic cancer models: MBT-2 bladder transitional cell carcinoma, B16-F10 melanoma and LL/2 Lewis lung carcinoma.
  • The efficacy of this combination appears similar to conventional chemotherapy (cisplatin or 5-fluorouracil) as it resulted in significant tumor growth retardation and enhanced survival.
  • This preliminary study suggests that this combination of drugs is efficient against cancer cell proliferation both in vitro and in vivo.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Lewis Lung / drug therapy. Melanoma, Experimental / drug therapy. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] ATP Citrate (pro-S)-Lyase / antagonists & inhibitors. ATP Citrate (pro-S)-Lyase / metabolism. Animals. Antineoplastic Agents / administration & dosage. Cell Death / drug effects. Cell Proliferation / drug effects. Cisplatin / pharmacology. Citrates / administration & dosage. Dose-Response Relationship, Drug. Energy Metabolism / drug effects. Enzyme Inhibitors / administration & dosage. Fluorouracil / pharmacology. HT29 Cells. Humans. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. Pyruvate Dehydrogenase (Lipoamide) / metabolism. Thioctic Acid / administration & dosage. Time Factors. Tumor Burden / drug effects

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20372858.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Citrates; 0 / Enzyme Inhibitors; 73Y7P0K73Y / Thioctic Acid; 8W94T9026R / hydroxycitric acid; EC 1.2.4.1 / Pyruvate Dehydrogenase (Lipoamide); EC 2.3.3.8 / ATP Citrate (pro-S)-Lyase; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


23. De Boer EC, Rooijakkers SJ, Schamhart DH, Kurth KH: Cytokine gene expression in a mouse model: the first instillations with viable bacillus Calmette-Guerin determine the succeeding Th1 response. J Urol; 2003 Nov;170(5):2004-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine gene expression in a mouse model: the first instillations with viable bacillus Calmette-Guerin determine the succeeding Th1 response.
  • PURPOSE: Bacillus Calmette-Guerin (BCG) therapy for superficial bladder cancer is immune dependent and activation of a Th1 immune response is probably required for clinical efficacy.
  • Given the empirical approach to improving BCG therapy we investigated in a mouse model the consequences of modifications in BCG therapy with regard to Th1 and Th2 cytokine responses in the bladder.
  • These studies may provide a rationale for possible modifications of the established clinical treatment protocol.
  • RESULTS: During 6 weekly BCG instillations a dose and time dependent induction of the various Th1 as well as Th2 cytokines was observed.
  • However, when mice were first treated 3 times with viable BCG and subsequently received 3 instillations with killed BCG, the Th1 and Th2 cytokine pattern was comparable to the standard 6-week regimen with viable BCG.
  • CONCLUSIONS: The model seems an appropriate one in which to investigate changes in Th1 and Th2 cytokine gene expression levels in bladders resulting from modifications in intravesical BCG treatment.
  • Whether such an approach could decrease BCG therapy toxicity, while maintaining antitumor efficacy, remains to be further investigated in patients.
  • [MeSH-major] BCG Vaccine / pharmacology. Cytokines / genetics. Th1 Cells / drug effects. Th2 Cells / drug effects. Urinary Bladder / drug effects
  • [MeSH-minor] Administration, Intravesical. Animals. Carcinoma, Transitional Cell / immunology. Female. Gene Expression Regulation / drug effects. Mice. Mice, Inbred C57BL. Urinary Bladder Neoplasms / immunology. Vaccines, Inactivated / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14532842.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCG Vaccine; 0 / Cytokines; 0 / Vaccines, Inactivated
  •  go-up   go-down


24. Otto T, Luemmen G, Bex A, Suhr J, Goebell PJ, Raz A, Ruebben H: Tumor cell motility as a novel target in cancer--experimental and clinical results. Onkologie; 2002 Apr;25(2):172-7
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor cell motility as a novel target in cancer--experimental and clinical results.
  • BACKGROUND: Surgery, chemotherapy and radiotherapy are the mainstay of tumor management.
  • Based on cell biological research we have characterized the process of tumor progression and metastasis and disclosed that the loss of cell-cell adhesion in association with an increased tumor cell motility is an essential feature of the malignant potential of a tumor.
  • METHODS: According to this principle we derived therapeutical methods differing from hitherto existing treatments by being exclusively focused on tumor cell motility.
  • Characterization of so-called anti-motility factors was performed biochemically as well as with motility assays by in vitro studies in established bladder carcinoma cell lines.
  • RESULTS: We evaluated the potential therapeutic benefit in a model of chemically induced bladder carcinoma followed by a phase I/II trial applying antimotility factors in patients with advanced bladder cancer.
  • CONCLUSION: Both basic research as well as the results of first clinical trials confirm, that advanced carcinomas can be influenced by inhibition of tumor cell motility.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Transitional Cell / pathology. Cell Adhesion / drug effects. Cell Movement / drug effects. Tumor Cells, Cultured / drug effects. Urinary Bladder Neoplasms / pathology. Virulence Factors, Bordetella / pharmacology
  • [MeSH-minor] Adult. Aged. Animals. Cadherins / metabolism. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dose-Response Relationship, Drug. Female. Humans. Male. Mice. Middle Aged. Prognosis. Receptors, Autocrine Motility Factor. Receptors, Cytokine / metabolism. Ubiquitin-Protein Ligases

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002 S. Karger GmbH, Freiburg
  • (PMID = 12006769.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Receptors, Cytokine; 0 / Virulence Factors, Bordetella; EC 2.3.2.27 / AMFR protein, human; EC 2.3.2.27 / Amfr protein, mouse; EC 2.3.2.27 / Receptors, Autocrine Motility Factor; EC 2.3.2.27 / Ubiquitin-Protein Ligases
  •  go-up   go-down


25. Saga Y, Hashimoto H, Yachiku S, Iwata T, Tokumitsu M: Reversal of acquired cisplatin resistance by modulation of metallothionein in transplanted murine tumors. Int J Urol; 2004 Jun;11(6):407-15
Hazardous Substances Data Bank. GLYCINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study, the mechanism of acquired resistance to cisplatin was studied in C3H mice inoculated with MBT-2 murine bladder tumor cells.
  • METHODS: C3H mice were subcutaneously inoculated with 1.0 x 10(6) MBT-2 cells/mouse on day 0.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Transitional Cell / drug therapy. Cisplatin / pharmacology. Drug Resistance, Neoplasm / drug effects. Glycine / analogs & derivatives. Metallothionein / drug effects. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Alkynes / pharmacology. Animals. Cystathionine gamma-Lyase / antagonists & inhibitors. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Female. Glutathione / metabolism. Injections, Intraperitoneal. Mice. Mice, Inbred C3H. Neoplasm Transplantation

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15157211.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Alkynes; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 64165-64-6 / propargylglycine; 9038-94-2 / Metallothionein; EC 4.4.1.1 / Cystathionine gamma-Lyase; GAN16C9B8O / Glutathione; Q20Q21Q62J / Cisplatin; TE7660XO1C / Glycine
  •  go-up   go-down


26. Izbicka E, Sommer E, Skopinska-Rozewska E, Davidson K, Wu RS, Orlowski T, Pastewka K: Tetracationic porphyrins inhibit angiogenesis induced by human tumor cells in vivo. Anticancer Res; 2000 Sep-Oct;20(5A):3205-10
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Either subcutaneous injections (> or = 50 micrograms/mouse) or preincubation with > or = 5 microM porphyrins significantly inhibited angiogenesis.
  • [MeSH-minor] Adenocarcinoma, Clear Cell / blood supply. Adenocarcinoma, Clear Cell / pathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. Carcinoma, Small Cell / blood supply. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / blood supply. Carcinoma, Squamous Cell / pathology. Carcinoma, Transitional Cell / blood supply. Carcinoma, Transitional Cell / pathology. Endothelial Growth Factors / metabolism. Fibroblast Growth Factor 2 / metabolism. Humans. Kidney Neoplasms / blood supply. Kidney Neoplasms / pathology. Lung Neoplasms / blood supply. Lung Neoplasms / pathology. Lymphokines / metabolism. Mice. Mice, Inbred BALB C. Neovascularization, Pathologic. Piroxicam / pharmacology. Tumor Cells, Cultured. Urinary Bladder Neoplasms / blood supply. Urinary Bladder Neoplasms / pathology. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11062744.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Porphyrins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 13T4O6VMAM / Piroxicam; 38673-65-3 / tetra(4-N-methylpyridyl)porphine; 59728-89-1 / tetra(2-N-methylpyridyl)porphine; R16CO5Y76E / Aspirin
  •  go-up   go-down






Advertisement