ArticleGene therapy2001
Tumour-specific therapeutic adenovirus vectors: repression of transgene expression in healthy cells by endogenous p53.
Article in Gene therapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Selective killing of Smad4-negative tumor cells via a designed repressor strategy.Molecular pharmacology · 2008Article
- Antitumor immune responses mediated by adenoviral GDEPT using nitroreductase/CB1954 is enhanced by high-level coexpression of heat shock protein 70.Cancer gene therapy · 2005Article
- Tumor-specific adenoviral gene therapy: transcriptional repression of gene expression by utilizing p53-signal transduction pathways.Cancer gene therapy · 2004Article
- Transcriptional Targeting in Cancer Gene Therapy.Journal of biomedicine & biotechnology · 2003Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 50% of human tumours lack functional p53 suppressor protein. A promoter that is repressed by p53 in healthy cells could thus provide tumour-specific gene expression for a huge subset of tumours. In this report we describe a double recombinant adenovirus vector, 'Ad.p53R', encoding a therapeutic gene that is indirectly repressed by endogenous wild-type p53. Ad.p53R contains two independent expression cassettes; (1) the E. coli nitroreductase gene (NTR) driven by the human hsp70 promoter containing LacI binding sites (hsp70lacO-NTR) and (2) a p53-inducible lac repressor gene (tkGC3-lacI). In p53 null cells (Hep3B), Ad.p53R directed the same level of NTR expression as Ad.p53NR which lacks the tkGC3-lacI cassette. Moreover, injection of SW480 xenografts (mutated p53) with Ad.p53R resulted in a clear inhibition of growth in response to the prodrug CB1954. In cells retaining wt p53 (HepG2 and primary human endothelial cells), Ad.p53R expressed significantly less NTR (approximately 70%) than Ad.p53NR. Ad.p53R administered by i.v. injection also produced significantly less NTR than Ad.p53NR in normal tissues in vivo. Finally, adenovirus infection per se of cultured HepG2 cells at low MOI induced p53 stabilisation suggesting that adenovirus-mediated gene delivery may contribute to p53-based selectivity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.