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1. Vojtechová M, Turecková J, Kucerová D, Sloncová E, Vachtenheim J, Tuhácková Z: Regulation of mTORC1 signaling by Src kinase activity is Akt1-independent in RSV-transformed cells. Neoplasia; 2008 Feb;10(2):99-107
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  • Increased activity of the Src tyrosine protein kinase that has been observed in a large number of human malignancies appears to be a promising target for drug therapy.
  • In the present study, a critical role of the Src activity in the deregulation of mTOR signaling pathway in Rous sarcoma virus (RSV)-transformed hamster fibroblasts, H19 cells, was shown using these cells treated with the Src-specific inhibitor, SU6656, and clones of fibroblasts expressing either the active Src or the dominant-negative Src kinase-dead mutant.
  • These observations might have an implication in drug resistance to mTOR inhibitor-based cancer therapy in certain cell types.
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line. Cell Line, Transformed. Cricetinae. Indoles / pharmacology. Phosphorylation. Protein Kinase Inhibitors / pharmacology. Rous sarcoma virus / genetics. Signal Transduction. Sulfonamides / pharmacology

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  • (PMID = 18283331.001).
  • [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 / Indoles; 0 / Protein Kinase Inhibitors; 0 / SU 6656; 0 / Sulfonamides; EC 2.7.- / Protein Kinases
  • [Other-IDs] NLM/ PMC2244684
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2. Wierdl M, Morton CL, Harris LC, Danks MK, Schuetz JD, Potter PM: p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11). J Pharmacol Exp Ther; 2003 Feb;304(2):699-705
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  • We have exploited the ability of wild-type (wt) p53 to repress gene expression and produce tumor-selective cytotoxicity using viral-directed enzyme prodrug therapy.
  • Vectors containing either the cytomegalovirus or Rous sarcoma virus promoter regulating transcription of a rabbit liver carboxylesterase (CE) have been constructed.
  • Transduction of isogenic cell lines with adenovirus containing CE under control of the Rous sarcoma virus promoter confirmed the decreased sensitization of cells expressing wtp53 to CPT-11.
  • These studies indicate that the inactivation of wtp53 by mutant p53 in human tumor cells may be sufficient enough to generate a therapeutic window for enhanced cytotoxicity with CPT-11.
  • [MeSH-major] Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Carboxylic Ester Hydrolases / antagonists & inhibitors. Carboxylic Ester Hydrolases / biosynthesis. Gene Expression Regulation, Enzymologic / drug effects. Liver / drug effects. Liver / enzymology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Animals. Carboxylesterase. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Humans. Rabbits. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology

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  • (PMID = 12538824.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA66124; United States / NCI NIH HHS / CA / CA76202; United States / NCI NIH HHS / CA / CA79763; United States / NIEHS NIH HHS / ES / ES05851
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Tumor Suppressor Protein p53; 7673326042 / irinotecan; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.1 / Carboxylesterase; XT3Z54Z28A / Camptothecin
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3. Voeks D, Martiniello-Wilks R, Madden V, Smith K, Bennetts E, Both GW, Russell PJ: Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models. Gene Ther; 2002 Jun;9(12):759-68
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  • [Title] Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models.
  • A gene-directed enzyme pro-drug therapy (GDEPT) based on purine nucleoside phosphorylase (PNP), that converts the prodrug, fludarabine to 2-fluoroadenine, has been described, but studies are limited compared with other GDEPTs.
  • The PNP gene controlled by Rous sarcoma virus (RSV) constitutive promoter was delivered using a recombinant ovine adenovirus vector (OAdV220) that uses a different receptor from human adenovirus type 5.
  • Transduction of RM1 cells with OAdV220 before implantation in immunocompetent mice dramatically inhibited subcutaneous (s.c.) tumor growth when fludarabine phosphate was administered systemically and increased mouse survival in a dose-dependent manner.
  • In tumor-bearing C57BL/6 mice, a single intratumoral injection of OAdV220 produced detectable PNP activity for at least 6 days and with prodrug, retarded the growth of aggressive RM1 s.c. tumors by 35% at day 14.
  • A similar regimen induced significant therapeutic efficacy in human PC3 xenografts.
  • [MeSH-major] Adenine / analogs & derivatives. Avian Sarcoma Viruses / genetics. Genetic Therapy / methods. Prodrugs / administration & dosage. Prostatic Neoplasms / therapy. Purine-Nucleoside Phosphorylase / genetics. Vidarabine Phosphate / administration & dosage
  • [MeSH-minor] Animals. Gene Expression. Genetic Vectors / administration & dosage. Humans. Male. Mastadenovirus / genetics. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasms, Experimental / therapy. Transduction, Genetic / methods. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 12040457.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Prodrugs; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate; 700-49-2 / 2-fluoroadenine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; JAC85A2161 / Adenine
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4. Majhen D, Brozovic A, Buger T, Gabrilovac J, Osmak M, Ambriović-Ristov A: Vincristine-resistant human laryngeal carcinoma cells demonstrate increased Rous sarcoma virus promoter activity. Life Sci; 2010 Oct 9;87(15-16):468-74
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  • [Title] Vincristine-resistant human laryngeal carcinoma cells demonstrate increased Rous sarcoma virus promoter activity.
  • AIMS: Gene therapy is a candidate approach for treating cancer patients whose tumors have developed resistance to some drugs.
  • Our results point out that (i) drug-resistance may be accompanied with an alteration in promoter activity;.
  • (ii) the proper choice of promoter could contribute to a decrease in the vector dose required to achieve a therapeutic effect during gene therapy.
  • [MeSH-major] Adenoviridae / genetics. Gene Expression Regulation, Neoplastic. Gene Transfer Techniques. Laryngeal Neoplasms / therapy. Rous sarcoma virus / genetics
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Cell Line, Tumor. Coxsackie and Adenovirus Receptor-Like Membrane Protein. Drug Resistance, Neoplasm. Genetic Therapy / methods. Genetic Vectors. Humans. Promoter Regions, Genetic. Receptors, Virus / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transgenes. Vincristine / pharmacology

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20837033.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / CLMP protein, human; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / Receptors, Virus; 5J49Q6B70F / Vincristine
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5. Trask TW, Trask RP, Aguilar-Cordova E, Shine HD, Wyde PR, Goodman JC, Hamilton WJ, Rojas-Martinez A, Chen SH, Woo SL, Grossman RG: Phase I study of adenoviral delivery of the HSV-tk gene and ganciclovir administration in patients with current malignant brain tumors. Mol Ther; 2000 Feb;1(2):195-203
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  • Between December 1996 and September 1998, 13 patients with advanced recurrent malignant brain tumors (9 with glioblastoma multiforme, 1 with gliosarcoma, and 3 with anaplastic astrocytoma) were treated with a single intratumoral injection of 2 x 10(9), 2 x 10(10), 2 x 10(11), or 2 x 10(12) vector particles (VP) of a replication-defective adenoviral vector bearing the herpes simplex virus thymidine kinase gene driven by the Rous sarcoma virus promoter (Adv.RSVtk), followed by ganciclovir (GCV) treatment.
  • Our primary objective was to determine the safety of this treatment.
  • One patient is living and stable 29.2 months after treatment.
  • Two patients survived >25 months before succumbing to tumor progression.
  • Ten patients died within 10 months of treatment, 9 from tumor progression and 1 with sepsis and endocarditis.
  • Neuropathologic examination of postmortem tissue demonstrated cavitation at the injection site, intratumoral foci of coagulative necrosis, and variable infiltration of the residual tumor with macrophages and lymphocytes.
  • [MeSH-major] Adenoviridae / genetics. Antiviral Agents / pharmacology. Brain Neoplasms / genetics. Brain Neoplasms / therapy. Ganciclovir / pharmacology. Genetic Therapy. Simplexvirus / enzymology. Thymidine Kinase / genetics
  • [MeSH-minor] Adult. Aged. Astrocytoma / genetics. Astrocytoma / mortality. Astrocytoma / therapy. Avian Sarcoma Viruses / genetics. Combined Modality Therapy. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Genetic Vectors / administration & dosage. Glioblastoma / diagnostic imaging. Glioblastoma / genetics. Glioblastoma / mortality. Glioblastoma / therapy. Gliosarcoma / genetics. Gliosarcoma / mortality. Gliosarcoma / therapy. Humans. Male. Middle Aged. Promoter Regions, Genetic. Radiography. Time Factors. Treatment Outcome

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  • (PMID = 10933931.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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6. Hu J, Renaud G, Golmes T, Ferris A, Hendrie PC, Donahue RE, Hughes SH, Wolfsberg TG, Russell DW, Dunbar CE: Reduced Genotoxicity of Avian Sarcoma Leukosis Virus Vectors in Rhesus Long-term Repopulating Cells Compared to Standard Murine Retrovirus Vectors. Mol Ther; 2008 Sep;16(9):1617-1623

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  • [Title] Reduced Genotoxicity of Avian Sarcoma Leukosis Virus Vectors in Rhesus Long-term Repopulating Cells Compared to Standard Murine Retrovirus Vectors.
  • : Insertional mutagenesis continues to be a major concern in hematopoietic stem-cell gene therapy.
  • Nonconventional gene transfer vectors with more favorable integration features in comparison with conventional retrovirus and lentivirus vectors are being developed and optimized.
  • In this study, we report for the first time a systematic analysis of 198 avian sarcoma leukosis virus (ASLV) insertion sites identified in rhesus long-term repopulating cells, and a comparison of ASLV insertion patterns to Moloney murine leukemia virus (MLV) (n = 396) and simian immunodeficiency virus (SIV) (n = 289) using the newly released rhesus genome databank.

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  • [Copyright] Copyright © 2008 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28189014.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Liu Y, Okada T, Nomoto T, Ke X, Kume A, Ozawa K, Xiao S: Promoter effects of adeno-associated viral vector for transgene expression in the cochlea in vivo. Exp Mol Med; 2007 Apr 30;39(2):170-5
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  • The aims of this study were to evaluate the expression of enhanced green fluorescent protein (EGFP) driven by 6 different promoters, including cytomegalovirus IE enhancer and chicken beta-actin promoter (CAG), cytomegalovirus promoter (CMV), neuron-specific enolase promoter (NSE), myosin 7A promoter (Myo), elongation factor 1alpha promoter (EF-1alpha), and Rous sarcoma virus promoter (RSV), and assess the dose response of CAG promoter to transgene expression in the cochlea.
  • Our results might provide important information with regard to the role of promoters in regulating transgene expression and for the proper design of vectors for gene expression and gene therapy.
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Female. Green Fluorescent Proteins / metabolism. Humans. Mice. Mice, Inbred C57BL

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  • (PMID = 17464178.001).
  • [ISSN] 1226-3613
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
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8. Sirninger J, Muller C, Braag S, Tang Q, Yue H, Detrisac C, Ferkol T, Guggino WB, Flotte TR: Functional characterization of a recombinant adeno-associated virus 5-pseudotyped cystic fibrosis transmembrane conductance regulator vector. Hum Gene Ther; 2004 Sep;15(9):832-41
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  • Despite extensive experience with recombinant adeno-associated virus (rAAV) 2 vectors in the lung, gene expression has been low in the context of cystic fibrosis (CF) gene therapy, where the large size of the cystic fibrosis transmembrane conductance regulator (CFTR) coding sequence has prompted the use of compact endogenous promoter elements.
  • The relative activities of the cytomegalovirus (CMV) Rous sarcoma virus (RSV) promoter, the CMV enhancer/beta-actin (CB) promoter combination, and the CMV enhancer/RSV promoter hybrid were assessed in vitro in a CF bronchial cell line.
  • [MeSH-major] Cystic Fibrosis / therapy. Cystic Fibrosis Transmembrane Conductance Regulator / genetics. Dependovirus / genetics. Genetic Vectors
  • [MeSH-minor] Actins / genetics. Animals. Chloride Channels / drug effects. Cloning, Molecular. DNA, Recombinant / therapeutic use. Gene Expression. Genetic Therapy. Luciferases / analysis. Luciferases / genetics. Mice. Pneumonia / microbiology. Pneumonia / pathology. Promoter Regions, Genetic. Pseudomonas aeruginosa / pathogenicity. Weight Loss

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  • (PMID = 15353038.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL51811; United States / NHLBI NIH HHS / HL / HL67260
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Chloride Channels; 0 / DNA, Recombinant; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator; EC 1.13.12.- / Luciferases
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9. Wessler S, Otto C, Wilck N, Stangl V, Fritzemeier KH: Identification of estrogen receptor ligands leading to activation of non-genomic signaling pathways while exhibiting only weak transcriptional activity. J Steroid Biochem Mol Biol; 2006 Jan;98(1):25-35
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  • Treatment of breast cancer cells and osteosarcoma cells with estradiol, estren, substance A and substance B led to non-genomic activation of Akt (protein kinase B) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling cascades mediated by Src (Rous Sarcoma Virus, non-receptor tyrosine kinase) and phosphatidylinositol-3-kinase (PI3K) stimulation.
  • We assume that these pathway-selective estrogen receptor ligands may serve as potent lead structures for novel hormone replacement strategies exhibiting lesser side effects than the existing treatment paradigms.
  • [MeSH-major] Receptors, Estrogen / metabolism. Signal Transduction. Transcription, Genetic / drug effects
  • [MeSH-minor] Animals. Aorta / drug effects. Blotting, Western. Bone Neoplasms / drug therapy. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Estradiol / pharmacology. Humans. Immunoprecipitation. Ligands. Male. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Osteosarcoma / drug therapy. Osteosarcoma / metabolism. Osteosarcoma / pathology. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Rats. Rats, Wistar. Tumor Cells, Cultured. Vasodilation / drug effects. src-Family Kinases / metabolism

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  • (PMID = 16203130.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Estrogen; 4TI98Z838E / Estradiol; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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10. Homsi J, Cubitt C, Daud A: The Src signaling pathway: a potential target in melanoma and other malignancies. Expert Opin Ther Targets; 2007 Jan;11(1):91-100
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  • Although Src was the first oncogene to be discovered as the transforming protein of the Rous sarcoma virus almost three decades ago, the role of Src and the Src family kinases in human oncogenesis is still not completely understood.
  • Recent studies have shown that Src regulates cell adhesion, invasiveness and motility in cancer cells and in tumor vasculature, rather than directly influencing cell replication.
  • Cumulatively, these data mark Src signaling as attractive therapeutic targets in melanoma.
  • Studies are currently underway with novel Src inhibitors in melanoma and in other tumor types.
  • [MeSH-minor] Animals. Clinical Trials as Topic. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Protein Kinase Inhibitors / therapeutic use. Signal Transduction

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  • (PMID = 17150037.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 99
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11. Kieback DG: Adenovirus-mediated thymidine kinase gene therapy induces apoptosis in human epithelial ovarian cancer cells and damages PARP-1. In Vivo; 2009 Jan-Feb;23(1):77-80
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  • [Title] Adenovirus-mediated thymidine kinase gene therapy induces apoptosis in human epithelial ovarian cancer cells and damages PARP-1.
  • Adenoviral (ADV) gene therapy with the thymidine kinase gene (TK) under control of the Rous sarcoma virus (RSV) promotor followed by the administration of acyclovir leads to replication errors in transcription and to cell death.
  • This concept of ADV-RSV-TK has been established for the treatment of ovarian cancer cells.
  • The purpose of this investigation was to clarify whether cell death after ADV-RSV-TK gene therapy and acyclovir administration is indeed due to apoptosis induction, whether the synergistic effect of ADV-RSV-TK gene therapy with chemotherapy was limited to the primary mechanism of action or whether the vector transduction itself exerted any pro-apoptotic effect was examined using the epithelial cell lines OVCAR-3 and MDAH-2774, established from human poorly differentiated serous ovarian cancer.
  • Apoptosis induction was established in this investigation as the mechanism of the ADV-RSV-TK gene therapy effect of acyclovir administration by caspase activity and subsequent CK 18 cleavage.
  • The synergistic effect of TK gene therapy and chemotherapeutic agents was shown to be TK induced.
  • Significant anti-PARP 1 activity was found to be an ADV-RSV-TK treatment effect after acyclovir addition.
  • [MeSH-major] Apoptosis / genetics. Cystadenocarcinoma, Serous / therapy. Genetic Therapy / methods. Ovarian Neoplasms / therapy. Poly(ADP-ribose) Polymerases / metabolism. Thymidine Kinase / genetics
  • [MeSH-minor] Acyclovir / pharmacology. Adenoviridae / genetics. Antiviral Agents / pharmacology. Cell Line, Tumor. Combined Modality Therapy. Drug Synergism. Female. Genetic Vectors. Humans. Rous sarcoma virus / genetics


12. Wiedmann MW, Caca K: Molecularly targeted therapy for gastrointestinal cancer. Curr Cancer Drug Targets; 2005 May;5(3):171-93
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  • [Title] Molecularly targeted therapy for gastrointestinal cancer.
  • Receptor and non-receptor tyrosine kinases (TKs) have emerged as clinically useful drug target molecules for treating gastrointestinal cancer.
  • Imatinib mesilate (STI-571, Gleevec(TM)), an inhibitior of bcr-abl TK, which was primarily designed to treat chronic myeloid leukemia is also an inhibitor of c-kit receptor TK, and is currently the drug of choice for the therapy of metastatic gastrointestinal stromal tumors (GISTs), which frequently express constitutively activated forms of the c-kit-receptor.
  • In addition, erlotinib has been evaluated in a Phase III study for the treatment of pancreatic cancer.
  • Cetuximab (IMC-C225, Erbitux(TM)), a monoclonal EGFR antibody, has been FDA approved for the therapy of irinotecan resistant colorectal cancer and has been tested for pancreatic cancer.
  • Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) are critical regulators of tumor angiogenesis.
  • Bevacizumab (Avastin(TM)), a monoclonal antibody against VEGF, was efficient in two randomized clinical trials investigating the treatment of metastatic colorectal cancer.
  • It is also currently investigated for the therapy of pancreatic cancer in combination with gemcitabine.
  • Other promising new drugs currently under preclinical and clinical evaluation, are VEGFR2 inhibitor PTK787/ZK 222584, thalidomide, farnesyl transferase inhibitor R115777 (tipifarnib, Zarnestra(TM)), matrix metalloproteinase inhibitors, proteasome inhibitor bortezomib (Velcade(TM)), mammalian target of rapamycin (mTOR) inhibitors, cyclooxygenase-2 (COX-2) inhibitors, platelet derived growth factor receptor (PDGF-R) inhibitors, protein kinase C (PKC) inhibitors, mitogen-activated protein kinase kinase (MEK) 1/2 inhibitors, Rous sarcoma virus transforming oncogene (SRC) kinase inhibitors, histondeacetylase (HDAC) inhibitors, small hypoxia-inducible factor (HIF) inhibitors, aurora kinase inhibitors, hedgehog inhibitors, and TGF-beta signalling inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gastrointestinal Neoplasms / drug therapy
  • [MeSH-minor] Animals. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / drug effects. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Epidermal Growth Factor / drug effects. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / metabolism. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15892618.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 102
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13. Louzier V, Eddahibi S, Raffestin B, Déprez I, Adam M, Levame M, Eloit M, Adnot S: Adenovirus-mediated atrial natriuretic protein expression in the lung protects rats from hypoxia-induced pulmonary hypertension. Hum Gene Ther; 2001 Mar 20;12(5):503-13
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  • We built a recombinant adenovirus type 5 containing ANP cDNA under the control of the Rous sarcoma virus long terminal repeat (Ad.ANP).
  • As compared with Ad.beta GAL-treated controls, rats given Ad.ANP (5 x 10(8) TCID(50)) on the day before a 2-week exposure to hypoxia (10% O(2)) had lower values for pulmonary artery pressure (32.1 +/- 1.93 vs. 35.5 +/- 2 mmHg, p < 0.01) and Fulton's index (0.52 +/- 0.089 vs. 0.67 +/- 0.12, p < 0.001) and less severe right ventricular hypertrophy and distal vessel muscularization.
  • These results suggest that induction of ANP expression in the lung may hold promise in the treatment of pulmonary hypertension.
  • [MeSH-minor] Animals. Anoxia. Avian Sarcoma Viruses / genetics. Body Weight. Bronchoalveolar Lavage Fluid. Cells, Cultured. Culture Media, Conditioned. Cyclic GMP / metabolism. DNA, Complementary / metabolism. Dose-Response Relationship, Drug. Epinephrine / pharmacology. Gene Transfer Techniques. Immunohistochemistry. Muscle, Smooth / metabolism. RNA, Messenger / metabolism. Rats. Rats, Wistar. Time Factors. Tissue Distribution. Trachea / metabolism. Transfection. Transgenes

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  • (PMID = 11268283.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / DNA, Complementary; 0 / RNA, Messenger; 85637-73-6 / Atrial Natriuretic Factor; H2D2X058MU / Cyclic GMP; YKH834O4BH / Epinephrine
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14. Tözsér J, Zahuczky G, Bagossi P, Louis JM, Copeland TD, Oroszlan S, Harrison RW, Weber IT: Comparison of the substrate specificity of the human T-cell leukemia virus and human immunodeficiency virus proteinases. Eur J Biochem; 2000 Oct;267(20):6287-95
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  • Human T-cell leukemia virus type-1 (HTLV-1) is associated with a number of human diseases.
  • Based on the therapeutic success of human immunodeficiency virus type 1 (HIV-1) PR inhibitors, the proteinase (PR) of HTLV-1 is a potential target for chemotherapy.
  • A molecular model of the HTLV-1 PR in complex with this substrate was built, based on the crystal structure of the S9 mutant of Rous sarcoma virus PR, in order to understand the molecular basis of the enzyme specificity.

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  • (PMID = 11012683.001).
  • [ISSN] 0014-2956
  • [Journal-full-title] European journal of biochemistry
  • [ISO-abbreviation] Eur. J. Biochem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM062920; United States / NIAID NIH HHS / AI / AI4380; United States / FIC NIH HHS / TW / TW01001
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HIV Protease; EC 3.4.23.- / HTLV-1 protease
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15. Deng W, Bivalacqua TJ, Chattergoon NN, Jeter JR Jr, Kadowitz PJ: Engineering ex vivo-expanded marrow stromal cells to secrete calcitonin gene-related peptide using adenoviral vector. Stem Cells; 2004;22(7):1279-91
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  • Calcitonin gene-related peptide (CGRP) is a target for cardiovascular gene therapy.
  • Marrow stromal cells (MSCs) hold promise for use in adult stem cell-based cell and gene therapy.
  • Adprepro-CGRP and AdntlacZ, adenoviral vectors containing prepro-CGRP or nuclear-targeted beta-galactosidase reporter gene ntlacZ under the control of Rous sarcoma virus promoter, were used.
  • These findings suggest that replication-deficient recombinant adenovirus can be used to gene engineer ex vivo-expanded MSCs and that high-level secretion of biologically active CGRP can be achieved, underscoring the clinical potential of using this novel adult stem cell-based cell and gene therapy strategy for the treatment of cardiovascular diseases.
  • [MeSH-minor] Adipocytes / cytology. Adipocytes / metabolism. Animals. Avian Sarcoma Viruses / genetics. Blotting, Western. Cell Differentiation. Cell Proliferation. Cell Survival. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Genes, Reporter. Genetic Vectors. Humans. Immunoenzyme Techniques. Male. Osteoblasts / cytology. Osteoblasts / metabolism. Rats. Time Factors. Transgenes. beta-Galactosidase / metabolism

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  • (PMID = 15579646.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-65600; United States / NHLBI NIH HHS / HL / HL-62000
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 83652-28-2 / Calcitonin Gene-Related Peptide; E0399OZS9N / Cyclic AMP; EC 3.2.1.23 / beta-Galactosidase
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16. Cheon J, Moon DG, Cho HY, Park HS, Kim JJ, Gardner TA, Kao C: Adenovirus-mediated suicide-gene therapy in an orthotopic murine bladder tumor model. Int J Urol; 2002 May;9(5):261-7
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  • [Title] Adenovirus-mediated suicide-gene therapy in an orthotopic murine bladder tumor model.
  • BACKGROUND: Patients with high-grade transitional-cell carcinoma (TCC) of the bladder frequently experience recurrence and progress and have a low response rate to chemotherapy in metastatic TCC.
  • In this study, we evaluated the feasibility and long-term efficacy of suicide-gene therapy using adenovirus (Ad)-mediated herpes simplex virus thymidine kinase gene (HSV-TK) and prodrug ganciclovir (GCV) as a potential therapeutic approach in murine-orthotopic models of TCC.
  • METHODS: A replication defective adenoviral vectors containing toxic HSV-TK gene under the transcriptional control of RSV (Rous sarcoma virus) promoter (Ad-RSV-TK) was used.
  • Intratumoral injection of Ad-RSV-TK in combination with GCV (20 mg/kg body weight/day i.p. b.i.d. x 7 days) was administered in vivo for the determination of treatment efficacy and long-term host survival in separate controlled experiments.
  • RESULTS: In vivo experiments demonstrated greater than three-fold reductions in MBT-2 tumor growth for the animals treated with Ad-RSV-TK (5 x 108 plaque forming units (pfu)/GCV therapy (P < 0.01)).
  • Central tumor necrosis and apoptosis were revealed by histomorphology and immunohistochemistry compared with other control animals (non-treated, GCV alone, Ad-RSV-TK alone).
  • CONCLUSIONS: Suicide-gene therapy using Ad-RSV-TK/GCV provides an effective therapy in an experimental murine orthotopic bladder cancer by significantly inhibiting tumor growth and improving long-term host survival.
  • [MeSH-major] Carcinoma, Transitional Cell / therapy. Genetic Therapy. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Antiviral Agents / therapeutic use. Disease Models, Animal. Female. Ganciclovir / therapeutic use. Mice. Mice, Inbred C3H. Simplexvirus. Thymidine Kinase / genetics

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  • (PMID = 12060439.001).
  • [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 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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17. Nyati MK, Sreekumar A, Li S, Zhang M, Rynkiewicz SD, Chinnaiyan AM, Rehemtulla A, Lawrence TS: High and selective expression of yeast cytosine deaminase under a carcinoembryonic antigen promoter-enhancer. Cancer Res; 2002 Apr 15;62(8):2337-42
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  • Yeast cytosine deaminase (yCD)-based gene therapy offers the potential for selective production of the cytotoxic and radiosensitizing drug 5-fluorouracil (5-FU) from the benign prodrug 5-fluorocytosine within colorectal cancers.
  • Although previous attempts to target therapy to colorectal cancer using the carcinoembryonic antigen (CEA) promoter have demonstrated specificity, this has been achieved at the cost of 10- to 300-fold loss in activity compared with strong but nonspecific rous sarcoma virus (RSV) or cytomegalovirus promoters.
  • We developed a highly specific and active gene transfer method for colorectal cancer using CEA under control of a promoter-enhancer.
  • This specificity was also achieved while maintaining a higher yCD enzyme activity than we obtained with RSV/yCD adenovirus in an HT-29 intrahepatic tumor model.
  • We then compared the response of HT-29 xenografts to treatment with 5-fluorocytosine and yCD adenovirus driven by either the RSV or the CEA promoter-enhancer and found similar tumor growth inhibition.

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  • (PMID = 11956093.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA080145; United States / NCI NIH HHS / CA / CA 46592; United States / NCI NIH HHS / CA / CA 80145
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen; EC 3.5.4.- / Nucleoside Deaminases; EC 3.5.4.1 / Cytosine Deaminase
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18. Morioka J, Kajiwara K, Yoshikawa K, Ideguchi M, Uchida T, Suzuki M: Vaccine therapy for murine glioma using tumor cells genetically modified to express B7.1. Neurosurgery; 2004 Jan;54(1):182-9; discussion 189-90
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  • [Title] Vaccine therapy for murine glioma using tumor cells genetically modified to express B7.1.
  • OBJECTIVE: In a syngeneic mouse brain tumor model, we tested the hypothesis that vaccination with tumor cells genetically modified to express B7.1 molecules induces tumor-specific T cells and immunological antitumor effects.
  • METHODS: Malignant glioma cells (RSV-MG) derived from a C3H/He mouse induced by Schmidt-Ruppin Rous sarcoma virus (RSV) were infected with an adenovirus encoding the B7.1 gene (AdB7).
  • The C3H/He mice were vaccinated with AdB7 transfectants injected subcutaneously and 2 weeks later were challenged intracerebrally with wild-type RSV-MG cells to determine whether or not the expression of B7.1 would enhance the immunogenicity of RSV-MG cells.
  • In the vaccine experiments, the mice immunized with AdB7 transfectants survived longer than did the mice of the other groups, and a significant difference in survival times was noted.
  • In addition, a cytotoxicity assay confirmed that vaccination with the AdB7 transfectants induced tumor-specific cytotoxicity.
  • CONCLUSION: These results demonstrate the therapeutic potential of vaccination with tumor cells expressing B7.1 for the treatment of malignant glioma.
  • [MeSH-major] Antigens, CD80 / administration & dosage. Antigens, CD80 / genetics. Brain Neoplasms / drug therapy. Gene Transfer Techniques. Glioma / drug therapy. Immunotherapy, Active / methods
  • [MeSH-minor] Adenoviridae. Animals. Avian Sarcoma Viruses. Cell Line, Tumor. Disease Models, Animal. Gene Expression. Genetic Vectors. Mice. Mice, Inbred C3H

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  • (PMID = 14683556.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80
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19. Urtti A, Polansky J, Lui GM, Szoka FC: Gene delivery and expression in human retinal pigment epithelial cells: effects of synthetic carriers, serum, extracellular matrix and viral promoters. J Drug Target; 2000;7(6):413-21
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  • Non-viral gene therapy is a potential treatment to many incurable retinal diseases.
  • In RPE cells, Rous sarcoma virus and cytomegalovirus (CMV) were more efficient promoters than SV40 in driving luciferase expression, and CMV was chosen for further experiments.
  • Despite low percentage of transfected cells the transgene expression per RPE cell is high, important feature in the retinal tissue with small dimensions, in particular in the case of secreted gene products.
  • [MeSH-major] Extracellular Matrix / physiology. Genetic Therapy. Pigment Epithelium of Eye / metabolism

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  • (PMID = 10758912.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-46052; United States / NEI NIH HHS / EY / EY 02162; United States / NEI NIH HHS / EY / EY 02477
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Liposomes; 0 / Polymers; EC 1.13.12.- / Luciferases
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20. Correale P, Del Vecchio MT, La Placa M, Montagnani F, Di Genova G, Savellini GG, Terrosi C, Mannucci S, Giorgi G, Francini G, Cusi MG: Chemotherapeutic drugs may be used to enhance the killing efficacy of human tumor antigen peptide-specific CTLs. J Immunother; 2008 Feb-Mar;31(2):132-47
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  • [Title] Chemotherapeutic drugs may be used to enhance the killing efficacy of human tumor antigen peptide-specific CTLs.
  • The effects of anticancer chemotherapy on antigen-specific cytotoxic T lymphocytes (CTLs) are mostly unknown.
  • We tested the effects of cytotoxic drugs such as 5-fluorouracil, gemcitabine, and oxaliplatin on the functional activity of antigen-specific CTL cultures derived from the peripheral blood mononuclear cells of human donors.
  • We found that a biweekly drug-exposure of human HLA-A(*)02.01+ CTLs derived from bulk cultures led to completely different effects if occurring early (day second) or late (day thirteenth) after the in vitro stimulations with the cognate peptides.
  • Results of immunocytofluorimetric studies and CTL/natural killer inhibition assays suggested that the latter effect could be related to a more selective drug-mediated inhibition of cohabitant T regulatory (reg) cells.
  • These results were translated in an in vivo therapeutic mouse model where humanized HLA-A(*)02.01 transgenic mice inoculated with EL-4/humanized HLA-A(*)02.01 transgenic mice showed a prolonged survival and the greatest rate of cure when receiving a combined treatment with a thymidylate synthase-specific peptide vaccine and a multidrug chemotherapy regimen administered late after immunization.
  • Tumor samples derived from this group of mice showed a reduced expression of the target thymidylate synthase antigen, a marked reduction of T(reg)s, and a noteworthy infiltration of C8+ T cells.
  • These results may have clinical implications for the design of new translational anticancer regimens aimed at combining chemotherapy and immunotherapy.
  • [MeSH-major] Antigens, Neoplasm / immunology. Antineoplastic Agents / pharmacology. Cytotoxicity, Immunologic / drug effects. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoembryonic Antigen / immunology. Cell Line. Cell Line, Tumor. Colonic Neoplasms / immunology. Colonic Neoplasms / pathology. Deoxycytidine / therapeutic use. Dose-Response Relationship, Drug. Fluorouracil / therapeutic use. HLA-A Antigens / genetics. HLA-A Antigens / immunology. HLA-A2 Antigen. Humans. Interleukin-2 Receptor alpha Subunit / analysis. Leucovorin / therapeutic use. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell / pathology. Lymphoma, T-Cell / therapy. Mice. Mice, Inbred Strains. Mice, Transgenic. Organoplatinum Compounds / therapeutic use. Peptides / immunology. Peptides / pharmacology. Peptides / therapeutic use. Rous sarcoma virus / immunology. Sandfly fever Naples virus / immunology. Survival Analysis. T-Lymphocytes, Regulatory / chemistry. T-Lymphocytes, Regulatory / drug effects. T-Lymphocytes, Regulatory / immunology. Thymidylate Synthase / metabolism

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  • (PMID = 18481383.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Carcinoembryonic Antigen; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Organoplatinum Compounds; 0 / Peptides; 0W860991D6 / Deoxycytidine; EC 2.1.1.45 / Thymidylate Synthase; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; GOLF protocol
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21. Uckun FM, Erbeck D, Qazi S, Venkatachalam T, Tibbles HE, Vassilev A: Effect of targeting janus kinase 3 on the development of intestinal tumors in the adenomatous polyposis coli(min) mouse model of familial adenomatous polyposis. Arzneimittelforschung; 2007;57(6):320-9
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  • Familial adenomatous polyposis (FAP) is associated with germ-line mutations in the tumor suppressor gene, adenomatous polyposis coli (APC) located on chromosome 5q21.
  • In contrast, Compound DDE24, a synthetically activated genistein, an inhibitor of Epidermal Growth Factor receptor (EGF-R), cellular homologue of oncogene product from Raus Avian sarcoma virus (SRC) and Syk tyrosine kinases, which Thus, selective targeting of JAK3 was highly effective in preventing development of intestinal tumors in Min mice resulting in markedly improved survival outcomes.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Enzyme Inhibitors / pharmacology. Intestinal Neoplasms / drug therapy. Janus Kinase 3 / antagonists & inhibitors. Quinazolines / pharmacology
  • [MeSH-minor] Animals. Chromatography, High Pressure Liquid. Male. Mice. Mice, Inbred C57BL. Point Mutation / physiology. Survival Analysis. Tissue Distribution. beta Catenin / biosynthesis

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  • (PMID = 17688077.001).
  • [ISSN] 0004-4172
  • [Journal-full-title] Arzneimittel-Forschung
  • [ISO-abbreviation] Arzneimittelforschung
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Quinazolines; 0 / WHI P131; 0 / beta Catenin; EC 2.7.10.2 / Janus Kinase 3
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22. Jaskolski M, Alexandratos JN, Bujacz G, Wlodawer A: Piecing together the structure of retroviral integrase, an important target in AIDS therapy. FEBS J; 2009 Jun;276(11):2926-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Piecing together the structure of retroviral integrase, an important target in AIDS therapy.
  • Although the Protein Data Bank contains a number of NMR structures of the N-terminal and C-terminal domains of HIV-1 and HIV-2, simian immunodeficiency virus and avian sarcoma virus IN, as well as X-ray structures of the core domain of HIV-1, avian sarcoma virus and foamy virus IN, plus several models of two-domain constructs, no structure of the complete molecule of retroviral IN has been solved to date.
  • We also attempt to reconcile the differences between the reported structures, and discuss the relationship between the structure and function of this enzyme, which is an important, although so far rather poorly exploited, target for designing drugs against HIV-1 infection.
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / drug therapy. Acquired Immunodeficiency Syndrome / virology. Amino Acid Sequence. Humans. Models, Molecular. Molecular Sequence Data. Sequence Homology, Amino Acid

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  • (PMID = 19490099.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010348-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viral Proteins; EC 2.7.7.- / Integrases
  • [Number-of-references] 108
  • [Other-IDs] NLM/ NIHMS140284; NLM/ PMC2747025
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