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3. Shiau AL, Lin CY, Tzai TS, Wu CL: Postoperative immuno-gene therapy of murine bladder tumor by in vivo administration of retroviruses expressing mouse interferon-gamma. Cancer Gene Ther; 2001 Jan;8(1):73-81
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  • [Title] Postoperative immuno-gene therapy of murine bladder tumor by in vivo administration of retroviruses expressing mouse interferon-gamma.
  • The murine MBT-2 bladder tumor model in syngeneic C3H/HeN mice was used to investigate the feasibility of gene therapy based on the delivery of interferon-gamma (IFN-gamma) in vivo by retroviral vectors.
  • Because bladder is suitable for the intravesical instillation of therapeutic agents, in vivo administration of retroviral vectors encoding IFN-gamma may be explored for the treatment of bladder cancer.
  • [MeSH-major] Genetic Therapy. Interferon-gamma / therapeutic use. Lymphoma, T-Cell / therapy. Mastocytosis / therapy. Retroviridae / genetics. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Chromium / analysis. Chromium / metabolism. Cytotoxicity, Immunologic / immunology. DNA Primers / chemistry. Female. Gene Transfer Techniques. Genetic Vectors. Humans. In Vitro Techniques. Interleukin-2 / metabolism. Kanamycin Kinase / genetics. Kanamycin Kinase / metabolism. Mice. Mice, Inbred C3H. Neoplasm Transplantation. Postoperative Care. RNA, Viral / analysis. Recombinant Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transfection

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  • (PMID = 11219496.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Interleukin-2; 0 / RNA, Viral; 0 / Recombinant Proteins; 0R0008Q3JB / Chromium; 82115-62-6 / Interferon-gamma; EC 2.7.1.95 / Kanamycin Kinase
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4. 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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5. Hadaschik BA, ter Borg MG, Jackson J, Sowery RD, So AI, Burt HM, Gleave ME: Paclitaxel and cisplatin as intravesical agents against non-muscle-invasive bladder cancer. BJU Int; 2008 Jun;101(11):1347-55
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  • [Title] Paclitaxel and cisplatin as intravesical agents against non-muscle-invasive bladder cancer.
  • OBJECTIVES: To investigate the effects of cisplatin and paclitaxel against human bladder cancer cells in vitro, and to obtain both pharmacokinetic and pharmacodynamic data after intravesical administration in mice.
  • MATERIALS AND METHODS: Six bladder cancer cell lines (J82, KU7, RT4, SW780, T24, UMUC3) were treated with various combined doses of both drugs and cell proliferation was evaluated 3 days later.
  • After intravesical instillation, mouse serum concentrations of cisplatin and paclitaxel were in the low microgram/millilitre range and bladder tissue concentrations achieved were 82 and 241 microg/g, respectively.
  • Similar drug levels were reached using combined therapy.
  • In vivo, all chemotherapeutic agents significantly inhibited bladder tumour growth, with the best results for combined therapy and micellar paclitaxel alone.
  • However, there was toxicity in the combined treatment arm.
  • CONCLUSIONS: Both cisplatin and paclitaxel were absorbed at effective amounts into bladder tissues.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / therapeutic use. Paclitaxel / therapeutic use. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Intravesical. Animals. Cell Line, Tumor. Chromatography, High Pressure Liquid. Female. Mice. Mice, Nude. Neoplasm Invasiveness

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  • (PMID = 18384637.001).
  • [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] P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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6. Chen CL, Sung J, Cohen M, Chowdhury WH, Sachs MD, Li Y, Lakshmanan Y, Yung BY, Lupold SE, Rodriguez R: Valproic acid inhibits invasiveness in bladder cancer but not in prostate cancer cells. J Pharmacol Exp Ther; 2006 Nov;319(2):533-42
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  • [Title] Valproic acid inhibits invasiveness in bladder cancer but not in prostate cancer cells.
  • In addition, HDACIs can alter the expression of at least one cellular adhesion molecule, the coxsackie and adenovirus receptor, in bladder cancer.
  • We evaluated this hypothesis using valproic acid (VPA), a commonly prescribed anticonvulsant recently shown to have potent HDACI activity, in the bladder cancer cell lines T24 TCC-SUP, HT1376, and RT4.
  • Our results show that acute VPA treatment (72 h) causes a dose-dependent decrease in invasion for all bladder cancer cell lines, except RT4, a noninvasive papilloma.
  • Migration, in contrast, was not affected by VPA treatment.
  • The inhibitory effect of VPA may be cancer type-specific, because there was no difference in invasion between treated and untreated prostate cancer cell lines LNCaP, PC3, and DU145.
  • Our data suggest that VPA exerts some of its antineoplastic effects by inhibiting invasion as well as tumor growth, and thus it may represent a novel adjuvant strategy for patients at high risk of recurrence and/or progression of muscle invasive bladder cancer.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Prostatic Neoplasms / drug therapy. Urinary Bladder Neoplasms / drug therapy. Valproic Acid / pharmacology
  • [MeSH-minor] Acetylation. Animals. Cell Line, Tumor. Cell Movement / drug effects. Cell Survival / drug effects. Coxsackie and Adenovirus Receptor-Like Membrane Protein. Cyclin-Dependent Kinase Inhibitor p21 / analysis. Histones / metabolism. Humans. Male. Mice. Neoplasm Invasiveness. Receptors, Virus / drug effects

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  • (PMID = 16868035.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / CLMP protein, human; 0 / CLMP protein, mouse; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Receptors, Virus; 614OI1Z5WI / Valproic Acid
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7. Inamoto T, Papineni S, Chintharlapalli S, Cho SD, Safe S, Kamat AM: 1,1-Bis(3'-indolyl)-1-(p-chlorophenyl)methane activates the orphan nuclear receptor Nurr1 and inhibits bladder cancer growth. Mol Cancer Ther; 2008 Dec;7(12):3825-33
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  • [Title] 1,1-Bis(3'-indolyl)-1-(p-chlorophenyl)methane activates the orphan nuclear receptor Nurr1 and inhibits bladder cancer growth.
  • We show, for the first time, evidence that Nurr1 is expressed in a panel of 11 human bladder cancer cell lines.
  • Treatment of bladder cancer cells with Nurr1-active C-DIM resulted in decreased cell survival (MTT assay) and induction of cell death pathways, resulting in poly(ADP-ribose) polymerase cleavage and DNA fragmentation.
  • In an orthotopic model of human bladder tumors established in nude mice, administration of a Nurr1-active C-DIM suppressed bladder cancer growth.
  • These results identify Nurr1 as a potential target for bladder cancer therapy and also identify a novel agent for activating Nurr1.

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  • (PMID = 19074857.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA091846; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA124998; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA 91846; United States / NCI NIH HHS / CA / CA 124998
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,1-bis(3'-indolyl)-1-(4-chlorophenyl)methane; 0 / Benzhydryl Compounds; 0 / DNA-Binding Proteins; 0 / Indoles; 0 / Ligands; 0 / NR4A2 protein, human; 0 / Nr4a2 protein, mouse; 0 / Nuclear Receptor Subfamily 4, Group A, Member 2; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Transcription Factors; 298-93-1 / thiazolyl blue
  • [Other-IDs] NLM/ NIHMS486032; NLM/ PMC4948978
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8. Yang SM, Wen DG, Hou JQ, He J, Cen JN, Chen JH: [Establishment and application of an orthotopic murine bladder cancer model]. Ai Zheng; 2007 Apr;26(4):341-5
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  • [Title] [Establishment and application of an orthotopic murine bladder cancer model].
  • BACKGROUND & OBJECTIVE: The recurrence rate of superficial bladder cancer is still high even the patients received postoperative intravesical infusion of chemotherapeutic drugs, such as mitomycin C (MMC).
  • Some studies showed that intravesical infusion of small interfering RNA (siRNA) could suppress the growth of bladder cancer in nude mice.
  • This study was to establish an orthotopic animal model bearing human bladder cancer, monitor tumor progression by magnetic resonance imaging (MRI), and observe the synergistic effect of survivin short hairpin RNA (shRNA) in combination with MMC for intravesical treatment using this animal model.
  • METHODS: Human bladder cancer cell line T24 was inoculated into the bladders of 25 BALB/c nude mice to establish orthotopic bladder cancer model.
  • Eighteen mice bearing bladder cancer were randomized into 3 groups: untreated group, MMC group, and combination group.
  • RESULTS: All the 25 mice developed bladder cancer after T24 cell inoculation.
  • CONCLUSION: We successfully established an orthotopic bladder cancer model, which could simulate the progression of human bladder cancer approximately.
  • MRI is a reliable way for dynamic detection of murine orthotopic bladder tumor.
  • [MeSH-major] Disease Models, Animal. Microtubule-Associated Proteins / metabolism. Mitomycin / therapeutic use. RNA, Small Interfering / therapeutic use. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Contrast Media. Down-Regulation. Female. Gadolinium DTPA. Humans. Inhibitor of Apoptosis Proteins. Magnetic Resonance Imaging. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. RNA Interference. Random Allocation. Repressor Proteins. Urinary Bladder / pathology

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  • (PMID = 17430648.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Birc5 protein, mouse; 0 / Contrast Media; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 50SG953SK6 / Mitomycin; K2I13DR72L / Gadolinium DTPA
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9. 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
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  • [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
  • [MeSH-minor] Animals. Cyclohexanes. Female. Humans. Mice. Mice, SCID. Neoplasm Transplantation

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  • [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
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10. Kosugi M, Miyajima A, Kikuchi E, Kosaka T, Horiguchi Y, Murai M, Oya M: Angiotensin II type 1 receptor antagonist enhances cis-dichlorodiammineplatinum-induced cytotoxicity in mouse xenograft model of bladder cancer. Urology; 2009 Mar;73(3):655-60
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  • [Title] Angiotensin II type 1 receptor antagonist enhances cis-dichlorodiammineplatinum-induced cytotoxicity in mouse xenograft model of bladder cancer.
  • OBJECTIVES: To examine whether candesartan enhances the cytotoxicity of cis-dichlorodiammineplatinum (CDDP) in mice with bladder cancer as a method to enhance the therapeutic effects of CDDP.
  • CDDP is an antitumor agent conventionally used against bladder cancer; however, its therapeutic efficacy appears to not be fully satisfactory.
  • Recent studies have shown the antitumor activity of the angiotensin II type 1 receptor antagonist candesartan.
  • METHODS: A xenograft model was prepared in nude mice using human bladder cancer cells (KU-19-19).
  • RESULTS: Candesartan, CDDP, and candesartan-CDDP suppressed tumor growth to 41.9%, 33.8%, and 13.2%, respectively, of the tumor volume in the control group, showing that combined treatment significantly inhibited tumor growth compared with each single agent alone.
  • Furthermore, combined treatment with candesartan enhanced CDDP-induced cytotoxicity by further suppressing angiogenesis.
  • These results suggest that candesartan could be a candidate for innovational therapy of bladder cancer.
  • [MeSH-major] Angiotensin II Type 1 Receptor Blockers / pharmacology. Antineoplastic Agents / therapeutic use. Benzimidazoles / pharmacology. Cisplatin / therapeutic use. Tetrazoles / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Synergism. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 19167032.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Tetrazoles; Q20Q21Q62J / Cisplatin; S8Q36MD2XX / candesartan
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11. 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
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  • [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

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  • (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
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12. Kamat AM, Karashima T, Davis DW, Lashinger L, Bar-Eli M, Millikan R, Shen Y, Dinney CP, McConkey DJ: The proteasome inhibitor bortezomib synergizes with gemcitabine to block the growth of human 253JB-V bladder tumors in vivo. Mol Cancer Ther; 2004 Mar;3(3):279-90
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  • [Title] The proteasome inhibitor bortezomib synergizes with gemcitabine to block the growth of human 253JB-V bladder tumors in vivo.
  • Bortezomib (PS-341, Velcade) is a dipeptidyl boronic acid inhibitor of the 20S proteasome that was developed as a therapeutic agent for cancer.
  • Here, we investigated the effects of bortezomib on the growth of human 253JB-V bladder cancer cells.
  • Although the drug did not stimulate significant increases in levels of apoptosis, it inhibited cell growth in a concentration-dependent fashion and augmented the growth inhibitory effects of gemcitabine in vitro.
  • However, combination therapy with bortezomib plus gemcitabine produced synergistic tumor growth inhibition associated with strong suppression of tumor cell proliferation.
  • Together, our results demonstrate that bortezomib has significant antiproliferative activity in aggressive bladder cancer cells, which is best exploited within the context of combination chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Boronic Acids / pharmacology. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Drug Synergism. Multienzyme Complexes / antagonists & inhibitors. Pyrazines / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Bortezomib. CDC2-CDC28 Kinases / metabolism. Cell Death. Cell Division. Cell Line, Tumor. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. Cysteine Endopeptidases. DNA Fragmentation. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Humans. Immunoblotting. Immunohistochemistry. In Situ Nick-End Labeling. Interleukin-8 / metabolism. Male. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic. Proteasome Endopeptidase Complex. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15026548.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50CA91846-01
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Interleukin-8; 0 / Multienzyme Complexes; 0 / Pyrazines; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A; 0W860991D6 / Deoxycytidine; 69G8BD63PP / Bortezomib; B76N6SBZ8R / gemcitabine; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cdk2 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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13. Miyake H, Hara I, Kamidono S, Gleave ME: Synergistic chemsensitization and inhibition of tumor growth and metastasis by the antisense oligodeoxynucleotide targeting clusterin gene in a human bladder cancer model. Clin Cancer Res; 2001 Dec;7(12):4245-52
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  • [Title] Synergistic chemsensitization and inhibition of tumor growth and metastasis by the antisense oligodeoxynucleotide targeting clusterin gene in a human bladder cancer model.
  • Clusterin expression is highly up-regulated in several normal and malignant tissues undergoing apoptosis.
  • Although recent studies have demonstrated a protective role of clusterin expression against various kinds of apoptotic stimuli, the functional role of clusterin in the acquisition of a therapy-resistant phenotype in bladder cancer remains unknown.
  • The objectives of this study were to determine whether antisense (AS) oligodeoxynucleotide (ODN) targeting the clusterin gene enhances apoptosis induced by cisplatin and to evaluate the usefulness of combined treatment with AS clusterin ODN and cisplatin in the inhibition of KoTCC-1 tumor growth and metastasis in a human bladder cancer KoTCC-1 model.
  • We initially revealed the dose-dependent and sequence-specific inhibition of clusterin expression by AS clusterin ODN treatment in KoTCC-1 cells at both mRNA and protein levels.
  • Clusterin mRNA was increased in a dose-dependent manner by cisplatin treatment at concentrations < or =10 mg/ml, and clusterin mRNA up-regulation induced by 10 mg/ml cisplatin peaked by 48-h post-treatment and began decreasing by 72-h post-treatment.
  • Although there was no significant effect on growth of KoTCC-1 cells, AS clusterin ODN treatment significantly enhanced cisplatin chemosensitivity of KoTCC-1 cells in a dose-dependent manner, reducing the IC(50) by >50%.
  • Characteristic apoptotic DNA ladder formation and cleavage of poly(ADP-ribose) polymerase protein were detected after combined treatment with AS clusterin ODN and cisplatin but not either agent alone.
  • Furthermore, after the orthotopic implantation of KoTCC-1 cells, combined treatment with AS clusterin and cisplatin significantly inhibited the growth of primary KoTCC-1 tumors, as well as the incidence of lymph node metastasis.
  • Collectively, these findings demonstrated that clusterin helps confer a chemoresistant phenotype through inhibition of apoptosis and that combined AS clusterin ODN may be useful in enhancing the effects of cytotoxic chemotherapy in patients with bladder cancer.
  • [MeSH-major] Glycoproteins / genetics. Molecular Chaperones / genetics. Neoplasm Proteins / genetics. Oligodeoxyribonucleotides, Antisense / toxicity. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Animals. Clusterin. Drug Synergism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Kinetics. Lymphatic Metastasis / prevention & control. Mice. Mice, Nude. Models, Biological. Transcription, Genetic. Transplantation, Heterologous. Tubulin / genetics. Tumor Cells, Cultured

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  • (PMID = 11751526.001).
  • [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 / CLU protein, human; 0 / Clu protein, mouse; 0 / Clusterin; 0 / Glycoproteins; 0 / Molecular Chaperones; 0 / Neoplasm Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Tubulin
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14. Benedict WF, Tao Z, Kim CS, Zhang X, Zhou JH, Adam L, McConkey DJ, Papageorgiou A, Munsell M, Philopena J, Engler H, Demers W, Maneval DC, Dinney CP, Connor RJ: Intravesical Ad-IFNalpha causes marked regression of human bladder cancer growing orthotopically in nude mice and overcomes resistance to IFN-alpha protein. Mol Ther; 2004 Sep;10(3):525-32
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  • [Title] Intravesical Ad-IFNalpha causes marked regression of human bladder cancer growing orthotopically in nude mice and overcomes resistance to IFN-alpha protein.
  • We found sustained interferon protein levels for days, both in normal mouse urothelium and in human bladder cancer cells growing as superficial bladder tumors in nude mice using an orthotopic bladder model developed by us.
  • Tumor burden in the bladder was determined utilizing cancer cells containing the green fluorescent protein.
  • Surprisingly, in vitro, Ad-IFNalpha also caused caspase-dependent death of bladder cancer cell lines that were resistant to high concentrations of IFN-alpha protein, including the cell line used in vivo.
  • These findings demonstrate that Ad-IFNalpha can overcome resistance to IFN-alpha protein both in vitro and in vivo and support evaluation of intravesical Ad-IFNalpha/Syn3 for the treatment of superficial bladder cancer.
  • [MeSH-major] Adenoviridae / genetics. Genetic Therapy. Interferon-alpha / genetics. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Animals. Caspases / metabolism. Cell Death. Drug Resistance. Green Fluorescent Proteins / genetics. Humans. Immunochemistry. Mice. Mice, Nude. Neoplasm Transplantation. Nylons / pharmacology. Recombinant Proteins. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 15336652.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P50 CA091846
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Nylons; 0 / Recombinant Proteins; 147336-22-9 / Green Fluorescent Proteins; 43K1W2T1M6 / interferon alfa-2b; EC 3.4.22.- / Caspases
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15. Yamanaka K, Gleave M, Muramaki M, Hara I, Miyake H: Enhanced radiosensitivity by inhibition of the anti-apoptotic gene clusterin using antisense oligodeoxynucleotide in a human bladder cancer model. Oncol Rep; 2005 May;13(5):885-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced radiosensitivity by inhibition of the anti-apoptotic gene clusterin using antisense oligodeoxynucleotide in a human bladder cancer model.
  • In bladder cancer, our previous study demonstrated that overexpression of clusterin is closely associated with disease progression and recurrence.
  • The objective of this study was to investigate whether radiation sensitivity was enhanced by suppressing clusterin gene expression with antisense (AS) oligodeoxynucleotide (ODN) in the human bladder cancer KoTCC-1 model.
  • Clusterin mRNA in KoTCC-1 cells after radiation was up-regulated in a dose-dependent manner; however, AS clusterin ODN treatment resulted in a marked inhibition of clusterin mRNA even after irradiation.
  • Combined treatment of KoTCC-1 cells with radiation and AS clusterin ODN synergistically decreased plating efficacy and induced apoptotic cell death compared with either radiation or AS clusterin ODN treatment alone.
  • Collectively, these findings suggest that clusterin acts as a cell survival protein mediating radioresistance through the inhibition of apoptosis, and that inactivation of clusterin using AS technology might offer a novel strategy to improve the outcome of radiation therapy for patients with bladder cancer.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. Glycoproteins / genetics. Molecular Chaperones / genetics. Neoplasm Proteins / genetics. Oligonucleotides, Antisense / pharmacology. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Line, Tumor. Cisplatin / therapeutic use. Clusterin. Humans. Mice. Mice, Nude. RNA, Messenger / genetics. Transcription, Genetic / drug effects. Transplantation, Heterologous

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  • (PMID = 15809754.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CLU protein, human; 0 / Clu protein, mouse; 0 / Clusterin; 0 / Glycoproteins; 0 / Molecular Chaperones; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; Q20Q21Q62J / Cisplatin
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16. Mansure JJ, Nassim R, Chevalier S, Rocha J, Scarlata E, Kassouf W: Inhibition of mammalian target of rapamycin as a therapeutic strategy in the management of bladder cancer. Cancer Biol Ther; 2009 Dec;8(24):2339-47
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  • [Title] Inhibition of mammalian target of rapamycin as a therapeutic strategy in the management of bladder cancer.
  • We examined whether mTOR inhibition by RAD001 (Everolimus) could be therapeutically efficacious in the treatment of bladder cancer.
  • FACS analysis showed that treatment with RAD001 for 48 h induced a cell cycle arrest in the G(0)/G(1) phase in all cell lines, without eliciting apoptosis.
  • In conclusion inhibition of mTOR signaling in bladder cancer models demonstrated remarkable antitumor activity both in vitro and in vivo.
  • This is the first study showing that RAD001 could be exploited as a potential therapeutic strategy in bladder cancer.
  • [MeSH-major] Carcinoma / drug therapy. Intracellular Signaling Peptides and Proteins / metabolism. Protein-Serine-Threonine Kinases / metabolism. Sirolimus / analogs & derivatives. Urinary Bladder Neoplasms / drug therapy. Urothelium / pathology
  • [MeSH-minor] Animals. Apoptosis. Cell Cycle / drug effects. Cell Separation. Dose-Response Relationship, Drug. Everolimus. Female. Flow Cytometry. Humans. Mice. Neoplasm Transplantation. Neovascularization, Pathologic. Signal Transduction. TOR Serine-Threonine Kinases

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  • [CommentIn] Cancer Biol Ther. 2009 Dec;8(24):2348-50 [19949304.001]
  • (PMID = 20061787.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP 89796
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
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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.
  • 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.
  • However, in the orthotopic nude mouse model, after 4 weeks of treatment (100 micro g/week, i.p.
  • 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. Sänger C, Busche A, Bentien G, Spallek R, Jonas F, Böhle A, Singh M, Brandau S: Immunodominant PstS1 antigen of mycobacterium tuberculosis is a potent biological response modifier for the treatment of bladder cancer. BMC Cancer; 2004 Nov 26;4:86
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  • [Title] Immunodominant PstS1 antigen of mycobacterium tuberculosis is a potent biological response modifier for the treatment of bladder cancer.
  • BACKGROUND: Bacillus Calmette Guerin (BCG)-immunotherapy has a well-documented and successful clinical history in the treatment of bladder cancer.
  • Therefore, alternative treatment strategies are intensively being explored.
  • We report a novel approach of using a well defined immunostimulatory component of Mycobacterium tuberculosis for the treatment of bladder cancer.
  • This preclinical study was designed to test the potential of recombinant PstS1 to serve as a non-viable and defined immunotherapeutic agent for intravesical bladder cancer therapy.
  • In vivo studies in an orthotopic murine bladder cancer model demonstrated the therapeutic potential of intravesically applied PstS1.
  • In addition, intravesical PstS1 immunotherapy induced strong local and systemic immune responses together with substantial anti-tumor activity in a preclinical mouse model.
  • Thus, we have identified recombinant PstS1 antigen as a potent immunotherapeutic drug for cancer therapy.
  • [MeSH-major] Antigens, Bacterial / therapeutic use. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Animals. Cell Line. Cell Line, Tumor. Dendritic Cells / physiology. Female. Humans. Immunologic Factors / administration & dosage. Immunologic Factors / immunology. Immunologic Factors / therapeutic use. Immunotherapy / methods. Leukocytes, Mononuclear / physiology. Mice. Mice, Inbred C57BL. Mycobacterium tuberculosis / immunology. Neoplasm Transplantation / methods. Phosphate-Binding Proteins / administration & dosage. Phosphate-Binding Proteins / immunology. Phosphate-Binding Proteins / therapeutic use

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  • (PMID = 15566565.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Immunologic Factors; 0 / Phosphate-Binding Proteins
  • [Other-IDs] NLM/ PMC544192
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19. 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
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  • [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

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  • (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
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20. Korbelik M, Sun J, Posakony JJ: Interaction between photodynamic therapy and BCG immunotherapy responsible for the reduced recurrence of treated mouse tumors. Photochem Photobiol; 2001 Apr;73(4):403-9
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  • [Title] Interaction between photodynamic therapy and BCG immunotherapy responsible for the reduced recurrence of treated mouse tumors.
  • Subcutaneous mouse EMT6 tumors were treated by individual or combined regimens of a single Bacillus Calmette-Guérin (BCG) vaccine administration and photodynamic therapy (PDT).
  • Irrespective of the type of photosensitizer used, the optimized BCG protocols improved the cure rate of PDT-treated tumors.
  • The accumulation of activated myeloid cells that markedly increases in tumors treated by Photofrin-based PDT was not additionally affected by BCG treatment.
  • Since both these modalities are established for the treatment of superficial bladder carcinomas, use of their combination for this condition should be clinically tested.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. BCG Vaccine / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use
  • [MeSH-minor] Animals. Combined Modality Therapy. Dihematoporphyrin Ether / therapeutic use. Drug Combinations. Female. Mice. Mice, Inbred BALB C. Neoplasm Recurrence, Local / etiology

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  • (PMID = 11332036.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine; 0 / Drug Combinations; 0 / Photosensitizing Agents; 97067-70-4 / Dihematoporphyrin Ether
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21. Miyake M, Ishii M, Koyama N, Kawashima K, Kodama T, Anai S, Fujimoto K, Hirao Y, Sugano K: 1-tert-butyl-3-[6-(3,5-dimethoxy-phenyl)-2-(4-diethylamino-butylamino)-pyrido[2,3-d]pyrimidin-7-yl]-urea (PD173074), a selective tyrosine kinase inhibitor of fibroblast growth factor receptor-3 (FGFR3), inhibits cell proliferation of bladder cancer carrying the FGFR3 gene mutation along with up-regulation of p27/Kip1 and G1/G0 arrest. J Pharmacol Exp Ther; 2010 Mar;332(3):795-802
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  • [Title] 1-tert-butyl-3-[6-(3,5-dimethoxy-phenyl)-2-(4-diethylamino-butylamino)-pyrido[2,3-d]pyrimidin-7-yl]-urea (PD173074), a selective tyrosine kinase inhibitor of fibroblast growth factor receptor-3 (FGFR3), inhibits cell proliferation of bladder cancer carrying the FGFR3 gene mutation along with up-regulation of p27/Kip1 and G1/G0 arrest.
  • Activating mutation of the fibroblast growth factor receptor-3 (FGFR3) gene is known as a key molecular event in both oncogenesis and cell proliferation of low-grade noninvasive human bladder urothelial carcinoma (UC), which is characterized by frequent intravesical recurrence.
  • In this study, we investigated the antitumor potentiality of 1-tert-butyl-3-[6-(3,5-dimethoxy-phenyl)-2-(4-diethylamino-butylamino)-pyrido[2,3-d]pyrimidin-7-yl]-urea (PD173074), a small-molecule FGFR3-selective tyrosine kinase inhibitor (TKI), as a therapeutic modality using eight UC cell lines.
  • In contrast, the other six cell lines expressing wild-type FGFR3 or without FGFR3 expression were resistant to PD173074 treatment.
  • Furthermore, we observed an inverse relationship between Ki-67 and p27/Kip1 expression after PD173074 treatment, suggesting that up-regulation of p27 recruited UC cells harboring activating FGFR3 mutations in G(1) that was analogous with the other receptor TKIs acting on the epidermal growth factor receptors.
  • In the mouse xenograft models using subcutaneously transplanted UM-UC-14 and MGHU3, orally administered PD173074 suppressed tumor growth and induced apoptotic changes comparable with the results of our in vitro assay.
  • These findings elucidated the effectiveness of molecular targeted approach for bladder UC harboring FGFR3 mutations and the potential utility to decrease the intravesical recurrence of nonmuscle invasive bladder UC after transurethral surgical resection.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / biosynthesis. G0 Phase / drug effects. G1 Phase / drug effects. Pyrimidines / pharmacology. Receptor, Fibroblast Growth Factor, Type 3 / antagonists & inhibitors. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Female. Humans. Ki-67 Antigen / biosynthesis. Mice. Mice, SCID. Mutation. Neoplasm Transplantation. Phosphorylation. Transplantation, Heterologous. Up-Regulation

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  • (PMID = 19955487.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / PD 173074; 0 / Pyrimidines; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3
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22. Tannock IF, Lee CM, Tunggal JK, Cowan DS, Egorin MJ: Limited penetration of anticancer drugs through tumor tissue: a potential cause of resistance of solid tumors to chemotherapy. Clin Cancer Res; 2002 Mar;8(3):878-84
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  • [Title] Limited penetration of anticancer drugs through tumor tissue: a potential cause of resistance of solid tumors to chemotherapy.
  • PURPOSE: Potential causes of drug resistance in solid tumors include genetically determined factors expressed in individual cells and those related to the solid tumor environment.
  • Important among the latter is the requirement for drugs to penetrate into tumor tissue and to achieve a lethal concentration in all of the tumor cells.
  • The present study was designed to characterize further the multicellular layer (MCL) method for studying drug penetration through tumor tissue and to provide information about tissue penetration for drugs used commonly in the treatment of human cancer.
  • EXPERIMENTAL DESIGN: EMT-6 mouse mammary and MGH-U1 human bladder cancer cells were grown on collagen-coated semiporous Teflon membranes to form MCLs approximately 200 microm thick.
  • The penetration of drugs through the MCL was evaluated by using radiolabeled drugs or analytical methods.
  • RESULTS: The MCL developed an extracellular matrix containing both laminin and collagen, although there were some differences in expression of extracellular matrix proteins.
  • The penetration of cisplatin, etoposide, gemcitabine, paclitaxel, and vinblastine through tissue in the MCL was slow compared with penetration through the Teflon support membrane alone.
  • CONCLUSIONS: Our results suggest limited ability of anticancer drugs to reach tumor cells that are distant from blood vessels.
  • The limited penetration of anticancer drugs through tumor tissue may be an important cause of clinical resistance of solid tumors to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Mammary Neoplasms, Experimental / metabolism. Membranes, Artificial. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Animals. Biological Availability. Cisplatin / pharmacokinetics. Diffusion. Etoposide / pharmacokinetics. Humans. Mice. Neoplasm Staging. Paclitaxel / pharmacokinetics. Polytetrafluoroethylene. Tumor Cells, Cultured / metabolism. Vinblastine / pharmacokinetics

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  • (PMID = 11895922.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Membranes, Artificial; 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; 9002-84-0 / Polytetrafluoroethylene; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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23. Li ML, Jia YJ, Jiang MN, Shu XH, Li CG: [Changes and significance of peripheral blood platelet count in tumor shrinkage induced by a low dose of CTX in T739 mice]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2008 Jun;24(6):567-9
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  • AIM: To establish a mouse model for BTT739 tumor-bearing mice cured by a low dose of cyclophosphamide (CTX).
  • METHODS: Mouse bladder carcinoma tissues were inoculated subcutaneously into T739 mice.
  • Then another 12 tumor-bearing mice were randomly divided into 15 mg/kg CTX treatment group and control group.
  • Blood samples were obtained from orbital venous sinus on different times after CTX treatment.
  • RESULTS: Within 2 weeks after CTX treatment, the speed of tumor shrinkage had a positive relationship with the dose of CTX used; but the survival rate of the tumor-bearing mice had a negative relationship with the dose of CTX used in 2 months after CTX treatment.
  • The perpherial platelet count increased to (1483.4+/-184.4)x10(9)/L in mice 6 h after CTX treatment.
  • During the 2nd to 14th day after CTX treatment, there was no obvious difference in the platelet count between treatment group and control group (P>0.05).
  • CONCLUSION: CTX 15 mg/kg could cure most of bladder tumor-bearing T739 mice.
  • The transient increase of the peripheral platelet count in 6 h after CTX treatment may relate to the antitumor effects of CTX.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Carcinoma / drug therapy. Cyclophosphamide / administration & dosage. Platelet Count. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Animals. Blood Cell Count. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Male. Mice. Neoplasm Transplantation. Random Allocation

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  • (PMID = 18538085.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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24. 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
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  • 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

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  • (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
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25. Challita-Eid PM, Morrison K, Etessami S, An Z, Morrison KJ, Perez-Villar JJ, Raitano AB, Jia XC, Gudas JM, Kanner SB, Jakobovits A: Monoclonal antibodies to six-transmembrane epithelial antigen of the prostate-1 inhibit intercellular communication in vitro and growth of human tumor xenografts in vivo. Cancer Res; 2007 Jun 15;67(12):5798-805
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  • Six-transmembrane epithelial antigen of the prostate-1 (STEAP-1) is a novel cell surface protein highly expressed in primary prostate cancer, with restricted expression in normal tissues.
  • In this report, we show STEAP-1 expression in prostate metastases to lymph node and bone and in the majority of human lung and bladder carcinomas.
  • The successful generation of two monoclonal antibodies (mAb) that bind to cell surface STEAP-1 epitopes provided the tools to study STEAP-1 susceptibility to naked antibody therapy.
  • Furthermore, both mAbs significantly inhibited tumor growth in mouse models using patient-derived LAPC-9 prostate cancer xenografts and established UM-UC-3 bladder tumors.
  • These studies validate STEAP-1 as an attractive target for antibody therapy in multiple solid tumors and provide a putative mechanism for mAb-induced tumor growth inhibition.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, Neoplasm / drug effects. Cell Communication / drug effects. Oxidoreductases / drug effects. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Flow Cytometry. Humans. Immunohistochemistry. In Vitro Techniques. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Lymphatic Metastasis / pathology. Male. Mice. Neoplasm Transplantation. RNA, Small Interfering. Urinary Bladder Neoplasms / metabolism. Urinary Bladder Neoplasms / secondary. Xenograft Model Antitumor Assays

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  • (PMID = 17575147.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / RNA, Small Interfering; EC 1.- / Oxidoreductases; EC 1.16.1.- / STEAP1 protein, human
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26. Cheng JC, Matsen CB, Gonzales FA, Ye W, Greer S, Marquez VE, Jones PA, Selker EU: Inhibition of DNA methylation and reactivation of silenced genes by zebularine. J Natl Cancer Inst; 2003 Mar 5;95(5):399-409
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  • We then analyzed the ability of zebularine to inhibit DNA methylation in C3H 10T1/2 Cl8 (10T1/2) mouse embryo cells as assayed by induction of a myogenic phenotype and in T24 human bladder carcinoma cells, using the methylation-sensitive single nucleotide primer extension (Ms-SNuPE) assay.
  • We also evaluated the effects of zebularine (administered orally or intraperitoneally) on growth of EJ6 human bladder carcinoma cells grown in BALB/c nu/nu mice (five mice per group) and the in vivo reactivation of a methylated p16 gene in these cells.
  • Zebularine reactivated a silenced p16 gene and demethylated its promoter region in T24 bladder carcinoma cells in vitro and in tumors grown in mice.
  • CONCLUSIONS: Zebularine is a stable DNA demethylating agent and the first drug in its class able to reactivate an epigenetically silenced gene by oral administration.
  • [MeSH-major] Cinnamates. DNA Methylation / drug effects. DNA, Neoplasm / metabolism. Gene Silencing. Hygromycin B / analogs & derivatives. Neurospora crassa / genetics. Phosphotransferases (Alcohol Group Acceptor) / metabolism. Pyrimidine Nucleosides / pharmacology. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Administration, Oral. Animals. Blotting, Southern. Cytidine / analogs & derivatives. Dose-Response Relationship, Drug. Drug Administration Schedule. Embryo, Mammalian. Gene Expression Regulation, Fungal / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Infusions, Parenteral. Mice. Mice, Inbred BALB C. Mice, Nude. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Cells, Cultured

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  • (PMID = 12618505.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA82422; United States / NIGMS NIH HHS / GM / GM35690
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cinnamates; 0 / DNA, Neoplasm; 0 / Pyrimidine Nucleosides; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 3XQ2233B0B / Hygromycin B; 5CSZ8459RP / Cytidine; 6379-56-2 / hygromycin A; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.119 / hygromycin-B kinase
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27. Huang CH, Chang CC, Lin CM, Wang ST, Wu MT, Li EI, Chang HC, Lin CC: Promoting effect of Antrodia camphorata as an immunomodulating adjuvant on the antitumor efficacy of HER-2/neu DNA vaccine. Cancer Immunol Immunother; 2010 Aug;59(8):1259-72
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  • Importantly, AC has been shown to be highly beneficial in the treatment and prevention of cancer.
  • The goal of this study was to investigate whether AC is able to augment the antitumor immune properties of a HER-2/neu DNA vaccine in a mouse model in which p185neu is overexpressed in MBT-2 tumor cells.
  • Compared with the mice that received the HER-2/neu DNA vaccine alone, co-treatment with AC suppressed tumor growth and extended the survival rate.
  • Evidence for this came from the marked increase in the IFN-gamma mRNA expression in CD4+ T cells in the draining inguinal lymph nodes, an increase in the number of functional HER-2/neu-specific CTLs, and the increased tumor infiltration of both CD4+ and CD8+ T cells, depletion of which abolishes the antitumor effect of the HER-2/neu DNA vaccine-AC therapy.
  • Our results further indicate that the treatment of mice with AC enhanced DC activation and production of Th1-activating cytokines (e.g.
  • Overall, these results clearly demonstrate that AC represents a promising immunomodulatory adjuvant that could enhance the therapeutic potency of HER-2/neu DNA vaccines in cancer therapy.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Antrodia. Carcinoma / immunology. Lymphocytes, Tumor-Infiltrating / metabolism. Receptor, ErbB-2 / immunology. Urinary Bladder Neoplasms / immunology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Extracts / administration & dosage. Cell Extracts / immunology. Cell Line, Tumor. Cytotoxicity, Immunologic / drug effects. Female. Interferon-gamma / secretion. Mice. Mice, Inbred C3H. Neoplasm Transplantation. Th1 Cells / immunology. Vaccines, DNA

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  • (PMID = 20390417.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cell Extracts; 0 / Vaccines, DNA; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
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28. Kucerova L, Matuskova M, Pastorakova A, Tyciakova S, Jakubikova J, Bohovic R, Altanerova V, Altaner C: Cytosine deaminase expressing human mesenchymal stem cells mediated tumour regression in melanoma bearing mice. J Gene Med; 2008 Oct;10(10):1071-82
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  • BACKGROUND: Previously, we validated capability of human adipose tissue-derived mesenchymal stem cells (AT-MSC) to serve as cellular vehicles for gene-directed enzyme prodrug molecular chemotherapy.
  • Antitumour effect was tested on immunodeficient mouse model in vivo.
  • RESULTS: Although culture expansion of CD y-AT-MSC sensitized these cells to 5FC mediated suicide effect, expanded CD y-AT-MSC/5FC still exhibited strong bystander cytotoxic effect towards human melanoma, glioblastoma, colon, breast and bladder carcinoma in vitro.
  • Most efficient inhibition (91%) was observed in melanoma A375 cell line when directly cocultured with 2% of therapeutic cells CD y-AT-MSC/5FC.
  • The therapeutic paradigm of the CD y -AT-MSC/5FC system was further evaluated on melanoma A375 xenografts on nude mice in vivo.
  • More importantly, systemic CD y-AT-MSC administration resulted in therapeutic cell homing into subcutaneous melanoma and mediated tumour growth inhibition.
  • Our data further demonstrate beneficial biological properties of AT-MSC as a cellular vehicle for enzyme/prodrug therapy approach to molecular chemotherapy.
  • [MeSH-major] Cytosine Deaminase / genetics. Melanoma, Experimental / drug therapy. Mesenchymal Stromal Cells / enzymology
  • [MeSH-minor] Adipose Tissue / metabolism. Adult. Animals. Apoptosis. Cancer Vaccines / genetics. Cell Line, Tumor. Flucytosine / metabolism. Flucytosine / pharmacology. Genetic Therapy. Genetic Vectors / administration & dosage. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Pentosyltransferases / genetics. Pentosyltransferases / metabolism. Prodrugs / pharmacology. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transduction, Genetic

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  • [Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18671316.001).
  • [ISSN] 1521-2254
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Prodrugs; 0 / Recombinant Fusion Proteins; D83282DT06 / Flucytosine; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.9 / uracil phosphoribosyltransferase; EC 3.5.4.1 / Cytosine Deaminase
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29. Lee PC, Kakadiya R, Su TL, Lee TC: Combination of bifunctional alkylating agent and arsenic trioxide synergistically suppresses the growth of drug-resistant tumor cells. Neoplasia; 2010 May;12(5):376-87
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  • [Title] Combination of bifunctional alkylating agent and arsenic trioxide synergistically suppresses the growth of drug-resistant tumor cells.
  • Drug resistance is a crucial factor in the failure of cancer chemotherapy.
  • In this study, we explored the effect of combining alkylating agents and arsenic trioxide (ATO) on the suppression of tumor cells with inherited or acquired resistance to therapeutic agents.
  • We further demonstrated that the combination treatment of H460 cells with BO-1012 and ATO resulted in severe G(2)/M arrest and apoptosis.
  • In a xenograft mouse model, the combination treatment with BO-1012 and ATO synergistically reduced tumor volumes in nude mice inoculated with H460 cells.
  • Similarly, the combination of BO-1012 and ATO effectively reduced the growth of cisplatin-resistant NTUB1/P human bladder carcinoma cells.
  • Furthermore, the repair of BO-1012-induced DNA interstrand cross-links was significantly inhibited by ATO, and consequently, gammaH2AX was remarkably increased and formed nuclear foci in H460 cells treated with this drug combination.
  • In addition, Rad51 was activated by translocating and forming foci in nuclei on treatment with BO-1012, whereas its activation was significantly suppressed by ATO.
  • Taken together, the present study reveals that a combination of bifunctional alkylating agents and ATO may be a rational strategy for treating cancers with inherited or acquired drug resistance.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Arsenicals / administration & dosage. Carbamates / administration & dosage. Cell Proliferation / drug effects. Heterocyclic Compounds, 3-Ring / administration & dosage. Neoplasms, Experimental / drug therapy. Oxides / administration & dosage. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Line, Tumor. Cell Separation. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Flow Cytometry. Fluorescent Antibody Technique. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Xenograft Model Antitumor Assays

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  • (PMID = 20454509.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Arsenicals; 0 / BO-1012; 0 / Carbamates; 0 / Heterocyclic Compounds, 3-Ring; 0 / Oxides; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC2864475
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30. Heath-Engel HM, Lingwood CA: Verotoxin sensitivity of ECV304 cells in vitro and in vivo in a xenograft tumour model: VT1 as a tumour neovascular marker. Angiogenesis; 2003;6(2):129-41

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  • We investigated this potential using the ECV304 cell line, which, although identified as a bladder carcinoma cell line, displays some endothelial characteristics, including tubule formation (differentiation) following appropriate stimulation.
  • Intratumoural VT1 injection significantly reduced ECV304 xenograft growth and enhanced mouse survival.
  • Human bladder carcinoma samples were, in contrast, highly vascular and blood vessels were 100% co-labelled by anti-vWF antibody and VT1, with no extravascular staining.
  • These results suggest that ECV304 xenografts are not characteristic of bladder carcinoma in terms of Gb3 expression, and that VT1 staining may provide a new reliable index of tumour neovasculature.
  • We conclude that ECV304 cells are not an appropriate in vivo model of either tumour angiogenesis or bladder carcinoma.
  • These studies, nevertheless, further demonstrate the in vivo antineoplastic and antiangiogenic potential of VT1, and show that Gb3 is expressed in cells undergoing in vitro 'vascular' differentiation, and in the neovasculature of human bladder carcinomas.
  • [MeSH-major] Biomarkers, Tumor. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / metabolism. Neovascularization, Pathologic / drug therapy. Shiga Toxin 1 / pharmacology. Trihexosylceramides / biosynthesis
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Antineoplastic Agents / pharmacology. Cell Survival / drug effects. Humans. In Vitro Techniques. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Time Factors

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  • (PMID = 14739619.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Shiga Toxin 1; 0 / Trihexosylceramides; 71965-57-6 / globotriaosylceramide
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31. Kausch I, Jiang H, Brocks C, Albers A, Krüger S, Sczakiel G, Jocham D: [Ki-67 antisense therapy in murine renal cell carcinoma models]. Aktuelle Urol; 2005 Apr;36(2):142-8
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  • [Title] [Ki-67 antisense therapy in murine renal cell carcinoma models].
  • [Transliterated title] Ki-67 Antisense-Therapie in murinen Nierenzellkarzinom-Modellen.
  • Previously, it was shown that Ki-67 derived antisense oligonucleotides (asONs) specifically inhibit the proliferation of tumor cells and tumour growth in vitro and in subcutaneous bladder and prostate tumor models.
  • We intended to evaluate the effects of this therapeutic concept in two renal cell carcinoma (RCC) models.
  • Systemic administration of asONs significantly decreased the tumour growth in the RENCA model (p < 0.05) and in the SCID mouse model (p = 0.009).
  • Immunohistochemical staining of tumor specimens revealed a marked down-regulation of target protein and a slight increase in apoptotic cells after antisense treatment while the microvessel count was not significantly altered.
  • CONCLUSION: These results demonstrate that the Ki-67 antigen represents a suitable antiproliferative target and that asONs directed against this target are potent drugs that induce a significant inhibition of renal tumor growth in different mouse models.
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Cell Division / drug effects. Ki-67 Antigen / genetics. Kidney Neoplasms / pathology. Oligonucleotides, Antisense / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Neoplasm Transplantation. Neovascularization, Pathologic / pathology. Transfection

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  • (PMID = 15902575.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Oligonucleotides, Antisense
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32. Tu Y, Roberts L, Shetty K, Schneider SS: Rhodiola crenulata induces death and inhibits growth of breast cancer cell lines. J Med Food; 2008 Sep;11(3):413-23
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  • The phenolic secondary metabolites isolated from R. crenulata were recently analyzed in a preclinical setting for their ability to treat lymphosarcomas and superficial bladder cancers.
  • Experiments using aggressive human-derived MDA-MB-231 and mouse-derived V14 breast cancer cell lines demonstrated that phenolic-enriched R. crenulata extract was capable of inhibiting the proliferation, motility, and invasion of these cells.
  • Finally, an in vivo experiment showed that phenolic-enriched dietary R. crenulata is effective in preventing the initiation of tumors and slowing down the tumor growth in mice bearing tumor grafts, thereby further demonstrating its possible potential for treatment of breast cancer progression and metastasis.
  • [MeSH-major] Breast Neoplasms / drug therapy. Cell Death / drug effects. Cell Proliferation / drug effects. Phenols / pharmacology. Phytotherapy. Plant Extracts / pharmacology. Rhodiola / chemistry
  • [MeSH-minor] Animals. Caspases / pharmacology. Cell Line, Tumor. Cell Movement / drug effects. Epithelial Cells / drug effects. Epithelial Cells / physiology. Female. Humans. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Xenograft Model Antitumor Assays / methods


33. Takeuchi A, Kamiryou Y, Yamada H, Eto M, Shibata K, Haruna K, Naito S, Yoshikai Y: Oral administration of xanthan gum enhances antitumor activity through Toll-like receptor 4. Int Immunopharmacol; 2009 Dec;9(13-14):1562-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EXPERIMENTAL DESIGN: Cytokine production by XG-stimulated murine macrophage cell lines, J772 and RAW264.7, and peritoneal adherent cells from wild type C57BL/6 mice, TLR2 or MyD88-deficient mice, C3H/HeN, and TLR4-mutant C3H/HeJ mice were examined.
  • Tumor growth, mouse survival, NK activity, and tumor-specific cytotoxicity were examined.
  • The in vivo antitumor effects of XG were also dependent on TLR-4, as C3H/HeJ mice, which lack TLR4 signaling, exhibited no effect of XG on the growth of syngeneic bladder tumor, MBT-2.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Interleukin-12 / biosynthesis. Macrophages / drug effects. Melanoma, Experimental / drug therapy. Polysaccharides, Bacterial / administration & dosage. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Administration, Oral. Animals. Cell Growth Processes / drug effects. Cytotoxicity, Immunologic / drug effects. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. Mice, Knockout. Myeloid Differentiation Factor 88 / genetics. Neoplasm Transplantation. Toll-Like Receptor 2 / genetics. Toll-Like Receptor 4 / genetics. Toll-Like Receptor 4 / metabolism

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  • (PMID = 19788935.001).
  • [ISSN] 1878-1705
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Myeloid Differentiation Factor 88; 0 / Polysaccharides, Bacterial; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; TTV12P4NEE / xanthan gum
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34. Wickstrom E: Oligonucleotide treatment of ras-induced tumors in nude mice. Mol Biotechnol; 2001 May;18(1):35-55
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  • [Title] Oligonucleotide treatment of ras-induced tumors in nude mice.
  • Oligonucleotides have shown an ability to target specific oncogene transcripts and inhibit their expression in cells, but the degree to which sustained treatment can suppress the levels of an oncogenic protein enough to benefit a patient remains to be determined.
  • First, the relationship of antisense DNA inhibition to the predicted secondary structure of human H-RAS oncogene mRNA was examined in transformed mouse cells that form solid tumors.
  • The three days of treatment with the first intron antisense DNA reduced H-Ras cellular levels by more than 90% whereas a nonspecific control DNA reduced H-Ras levels by approx 20%.
  • Tumor growth of cells treated with H-RAS antisense oligonucleotide was significantly reduced for up to 14 d following the end of treatment and implantation into the mice, whereas the nonspecific control DNA had no significant effect.
  • Third, H-RAS transformed bladder cancer cells were implanted into nude mice, after which the mice were treated for 31 d with oligonucleotide phosphorothioates.
  • Tumor growth in mice treated with H-RAS 12th codon antisense oligonucleotide was reduced by about 80% throughout the treatment period, reiterating the sustained effect seen in pretreated tumor cells.
  • K-RAS transformed pancreatic cancer cells were implanted into nude mice, after which the mice were treated for 14 d with oligonucleotide phosphorothioates.
  • Tumor growth in mice treated with K-RAS 5'-UTR antisense oligonucleotide was reduced by about 50% throughout the treatment period, reiterating the sustained effect seen with H-RAS transformed cells.
  • The next logical steps include testing oligonucleotide efficacy against other tumor types, toxicological testing in higher species, and clinical trials in human subjects.
  • [MeSH-major] Genes, ras / genetics. Neoplasms, Experimental / therapy. Oligonucleotides, Antisense / therapeutic use. ras Proteins / biosynthesis
  • [MeSH-minor] 3T3 Cells. 5' Untranslated Regions. Animals. Cell Division. Cell Line, Transformed. Codon. Dose-Response Relationship, Drug. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Mutation. Neoplasm Transplantation. Nucleic Acid Conformation. RNA, Messenger / metabolism. Thermodynamics. Time Factors. Tumor Cells, Cultured

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  • (PMID = 11439698.001).
  • [ISSN] 1073-6085
  • [Journal-full-title] Molecular biotechnology
  • [ISO-abbreviation] Mol. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / Codon; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; EC 3.6.5.2 / ras Proteins
  • [Number-of-references] 73
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35. Molteni A, Ward WF, Ts'ao CH, Taylor J, Small W Jr, Brizio-Molteni L, Veno PA: Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists. Curr Pharm Des; 2003;9(9):751-61
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  • [Title] Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists.
  • Angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) type 1 receptor antagonists have strong cytostatic properties on in vitro cultures of many normal and neoplastic cells.
  • ACE inhibitors are also effective in protecting lungs, kidneys and bladders from the development of nephropathy, pneumopathy, cystitis, and eventually fibrosis in different models of organ-induced damage such as exposure to radiation, chronic hypoxia, administration of the alkaloid monocrotaline or bladder ligation.
  • ACE inhibitors and AII type 1 receptor antagonists are also effective in reducing excessive vascular neoformation in a model of injury to the cornea of rats and rabbits, and in controlling the excessive angiogenesis observed in the Solt-Farber model of experimentally induced hepatoma, in methylcholantrene or radiation-induced fibrosarcomas, in radiation-induced squamous cell carcinomas and in the MA-16 viral-induced mammary carcinoma of the mouse.
  • The mitogenic effect of AII is well established and a reduction of AII synthesis may well explain cell and neoplasm delayed growth.
  • Moreover, AII regulates and enhances the activity of several growth factors including transforming growth factor B (TGFB) and smooth muscle actin (SMA); and many of these factors are reduced in tissues of animals treated with ACE inhibitors and AII type 1 receptor antagonists.
  • The ACE inhibitors containing a sulphydril (SH) or thiol radical in their moiety (Captopril and CL242817) seemed to be more effective in controlling fibrosis and the growth of some neoplastic cells than those ACE inhibitors without this thiol radical in their structure, even if the second group of these drugs show in vitro a stronger inhibitory effect on converting enzyme activity.
  • However, although these additional properties are pharmacologically relevant, the blockade of AII synthesis plays an essential role in the cytostatic activity of these two categories of drugs.
  • These observations underline that in addition to the beneficial effect of these drugs on the cardiovascular system, new potential applications are opening for their wider deployment.
  • [MeSH-minor] Animals. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Receptors, Angiotensin / physiology

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  • (PMID = 12570792.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 24652; United States / NCI NIH HHS / CA / CA 52750; United States / NCI NIH HHS / CA / CA 64239; United States / NIDDK NIH HHS / DK / DK 15612; United States / NHLBI NIH HHS / HL / HL 25106
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiotensin Receptor Antagonists; 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antineoplastic Agents; 0 / Receptors, Angiotensin
  • [Number-of-references] 70
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