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1. 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
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  • [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

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  • (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
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2. 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
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  • [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

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  • (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
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3. 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
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  • [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

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  • [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
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4. 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
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  • [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.

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  • [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
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5. 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
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  • 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

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  • (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
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6. 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
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  • [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

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  • (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
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7. 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
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  • [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

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  • (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
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8. Kassouf W, Dinney CP, Brown G, McConkey DJ, Diehl AJ, Bar-Eli M, Adam L: Uncoupling between epidermal growth factor receptor and downstream signals defines resistance to the antiproliferative effect of Gefitinib in bladder cancer cells. Cancer Res; 2005 Nov 15;65(22):10524-35
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  • [Title] Uncoupling between epidermal growth factor receptor and downstream signals defines resistance to the antiproliferative effect of Gefitinib in bladder cancer cells.
  • Activation of the epidermal growth factor receptor (EGFR) and downstream signaling pathways, such as phosphatidylinositol-3 kinase/Akt and Ras/mitogen-activated protein kinase (MAPK), have been implicated in causing resistance to EGFR-targeted therapy in solid tumors, including the urogenital tumors.
  • To investigate the mechanism of resistance to EGFR inhibition in bladder cancer, we compared EGFR tyrosine kinase inhibitor (Gefitinib, Iressa, ZD1839) with respect to its inhibitory effects on three kinases situated downstream of EGFR: MAPK, Akt, and glycogen synthase kinase-3beta (GSK-3beta).
  • We found that the resistance to the antiproliferative effects of gefitinib, in vitro as well as in vivo in nude mice models, was associated with uncoupling between EGFR and MAPK inhibition, and that GSK-3beta activation and degradation of its target cyclin D1 were indicators of a high cell sensitivity to gefitinib.
  • Further analysis of one phenotypic sensitive (253J B-V) and resistant (UM-UC13) cell lines revealed that platelet-derived growth factor receptor-beta (PDGFRbeta) activation was responsible for short circuiting the EGFR/MAPK pathway for mitogenic stimuli.
  • In conclusion, our data show that the uncoupling of EGFR with mitogenic pathways can cause resistance to EGFR inhibition in bladder cancer.
  • Although this uncoupling may arise through different mechanisms, we suggest that the resistance of bladder cancer cells to EGFR blockade can be predicted early in the course of treatment by measuring the activation of GSK-3beta and of nuclear cyclin D1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / metabolism. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / pathology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Cyclin D1 / metabolism. Drug Resistance, Neoplasm. Enzyme Activation. Enzyme Induction. Glycogen Synthase Kinase 3 / metabolism. Humans. MAP Kinase Signaling System / drug effects. Mitogen-Activated Protein Kinases / biosynthesis. Mitogen-Activated Protein Kinases / metabolism. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism


9. 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
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  • 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

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  • (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
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10. 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
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  • [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

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  • (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
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11. 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
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  • [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

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  • (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
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12. 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.
  • 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

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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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13. 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
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  • [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

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  • (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
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14. 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
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  • [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

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  • (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
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15. 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
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  • [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

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  • (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
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16. 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
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  • [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

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  • (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
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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
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  • [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

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  • (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
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18. 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
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  • [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

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  • (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
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