7 results match your criteria dl520

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Boosting oncolytic adenovirus potency with magnetic nanoparticles and magnetic force.

Mol Pharm 2010 Aug;7(4):1069-89

Institute of Experimental Oncology and Therapy Research, Technische Universitat Munchen, Munich 81675, Germany.

Oncolytic adenoviruses rank among the most promising innovative agents in cancer therapy. We examined the potential of boosting the efficacy of the oncolytic adenovirus dl520 by associating it with magnetic nanoparticles and magnetic-field-guided infection in multidrug-resistant (MDR) cancer cells in vitro and upon intratumoral injection in vivo. The virus was complexed by self-assembly with core-shell nanoparticles having a magnetite core of about 10 nm and stabilized by a shell containing 68 mass % lithium 3-[2-(perfluoroalkyl)ethylthio]propionate) and 32 mass % 25 kDa branched polyethylenimine. Read More

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Adenovirus-based virotherapy enabled by cellular YB-1 expression in vitro and in vivo.

Cancer Gene Ther 2009 Oct 10;16(10):753-63. Epub 2009 Apr 10.

Institute of Experimental Oncology and Therapeutics, Klinikum Rechts der Isar, Technische Universitaet Muenchen, Muenchen 81675, Germany.

We have earlier described the oncolytic adenovirus vector dl520 that was rendered cancer-specific by deletion of the transactivation domain CR3 of the adenoviral E1A13S protein; this deletion causes antitumor activity in drug-resistant cells displaying nuclear YB-1 expression. We hypothesized that the anticancer activity of dl520 could be further improved by introducing the RGD motif in the fiber knob and by deletion of the adenoviral E1B19K protein (Ad-Delo3-RGD). In this study, the in vitro and in vivo antitumor activity of Ad-Delo3-RGD was investigated focussing on two pancreatic cancer cell lines MiaPaCa-2 and BxPC3 alone and in combination with cytotoxic drugs. Read More

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October 2009

Impact of radiation therapy on the oncolytic adenovirus dl520: implications on the treatment of glioblastoma.

Radiother Oncol 2008 Mar 29;86(3):419-27. Epub 2007 Oct 29.

Institute of Experimental Oncology, Technical University of Munich, Germany.

Background And Purpose: Viral oncolytic therapy is emerging as a new form of anticancer therapy and has shown promising preclinical results, especially in combination with radio- and chemotherapy. We recently reported that nuclear localization of the human transcription factor YB-1 in multidrug-resistant cells facilitates E1-independent adenoviral replication. The aim of this study was to evaluate the combined treatment of the conditionally-replicating adenovirus dl520 and radiotherapy in glioma cell lines in vitro and in human tumor xenografts. Read More

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Novel three-pronged strategy to enhance cancer cell killing in glioblastoma cell lines: histone deacetylase inhibitor, chemotherapy, and oncolytic adenovirus dl520.

Hum Gene Ther 2006 Jan;17(1):55-70

Institute of Experimental Oncology, Technical University of Munich, Klinikum Rechts-der-Isar, 81675 Munich, Germany.

Resistance to radiation and chemotherapy remains an obstacle to the treatment of brain tumors. We have demonstrated that the replication-deficient adenovirus d1520, which lacks the E1A 13S protein, replicates efficiently and exhibits oncolytic potential in multidrug-resistant cells with nuclear localization of the human transcription factor YB-1. However, besides others, key factors regarding oncolytic virotherapy are limited tumor transduction rate and low replication efficiency. Read More

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January 2006

Expression of E1A in terminally differentiated muscle cells reactivates the cell cycle and suppresses tissue-specific genes by separable mechanisms.

Mol Cell Biol 1996 Oct;16(10):5302-12

Molecular Oncogenesis Laboratory, Regina Elena Cancer Center, Rome, Italy.

Terminally differentiated cells are characterized by permanent withdrawal from the cell cycle; they do not enter S phase even when stimulated by growth factors or retroviral oncogenes. We have shown, however, that the adenovirus E1A oncogene can reactivate the cell cycle in terminally differentiated cells. In this report, we describe the molecular events triggered by E1A in terminally differentiated skeletal muscle cells. Read More

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October 1996

Multiple pathways for activation of E2A expression in human KB cells by the 243R E1A protein of adenovirus type 5.

Virus Res 1994 Jul;33(1):89-97

Department of Biochemistry, McMaster University, Hamilton, Ontario, Canada.

Adenovirus type 5 (Ad5) mutant dl520, which produces only the smaller 243 residue (243R) E1A protein, induced efficient production of the viral E2A 72-kDa DNA binding protein (DBP) in human KB cells, but not in human WI38, 143, or HeLa cells. In transient expression assays, the 243R E1A protein induced transcription from the E2 early promoter in KB but not in HeLa cells; there was no transcription from the E3 promoter in either cell line. In KB cells, truncation of the E2 promoter from -285 to -97 basepairs dramatically reduced transactivation by the 243R E1A product but not by wt E1A, suggesting that the 243R protein acts through factors binding in this region. Read More

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Induction of gene expression by exon 2 of the major E1A proteins of adenovirus type 5.

J Virol 1993 Dec;67(12):6922-8

Department of Biochemistry, McMaster University, Hamilton, Ontario, Canada.

We have constructed an adenovirus type 5 (Ad5) E1A mutant, dl1119/520, that produces essentially only exon 2 of the major E1A proteins. In infected primary baby rat kidney cells, this mutant induced expression of the E1B 55-kDa protein, and in infected human KB cells, it induced expression of this protein, the E2A 72-kDa protein, and hexon. In KB cells, this mutant grew substantially better than Ad5 dl312, which lacks E1A, and as well as Ad5 dl520, an E1A mutant producing only the 243-residue protein. Read More

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December 1993
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