ArticleCancer gene therapy2010
Adenoviral targeting of gene expression to tumors.
Article in Cancer gene therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Therapeutic improvement of a stroma-targeted CRAd by incorporating motives responsive to the melanoma microenvironment.The Journal of investigative dermatology · 2013Article
- MicroRNA silencing improves the tumor specificity of adenoviral transgene expression.Cancer gene therapy · 2012Article
- Peptide targeting of adenoviral vectors to augment tumor gene transfer.Cancer gene therapy · 2012Article
- A novel hybrid promoter responsive to pathophysiological and pharmacological regulation.Journal of molecular medicine (Berlin, Germany) · 2012Article
- Targeting different types of human meningioma and glioma cells using a novel adenoviral vector expressing GFP-TRAIL fusion protein from hTERT promoter.Cancer cell international · 2011Article
- FGF15/19 regulates hepatic glucose metabolism by inhibiting the CREB-PGC-1α pathway.Cell metabolism · 2011Article
- Retargeting adenoviral vectors to improve gene transfer into tumors.Cancer gene therapy · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Using biochemical, imaging and histological methods, we employed transcriptional targeting to increase the specificity of tumor gene expression in vivo for intravenously administered recombinant adenovirus vectors. Surprisingly, the relative specificity of tumor expression in comparison with other tissues was increased for a constitutively expressing recombinant adenovirus, AdCMVLuc, by simply reducing the viral dose. Even at lower doses, however, the high frequency of viral infection and transgene expression in the liver using constitutive promoters still represents a substantial problem. To further augment tumor specificity, we constructed a series of adenoviruses expressing luciferase from several other promoters and tested their ability to selectively transcribe genes in tumor cells, both in vitro and in vivo. Constitutively active viral promoters (RSV, SRalpha) varied widely in their tumor selectivity, but hypoxia-responsive promoters (carbonic anhydrase 9, PAI-1, SOD2 and several chimeric constructs) showed the most tumor-selective expression. Our results show that tumor targeting to HT1080 fibrosarcomas was readily achieved using transcriptional targeting mechanisms. We attribute the relatively high level of gene transfer and expression in HT1080 tumors in vivo to increased viral access to the tumor, presumably due to discontinuities in tumor vasculature and augmented expression from stress-responsive promoters in the hypoxic and inflammatory tumor microenvironment.
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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.