ArticleGene therapy2006
Hypoxia- and radiation-activated Cre/loxP 'molecular switch' vectors for gene therapy of cancer.
Article in Gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Hypoxia-inducible tumour-specific promoters as a dual-targeting transcriptional regulation system for cancer gene therapy.Ecancermedicalscience · 2017Review
- STAT3/NF-κB-Regulated Lentiviral TK/GCV Suicide Gene Therapy for Cisplatin-Resistant Triple-Negative Breast Cancer.Theranostics · 2017Article
- Study of the combined treatment of lung cancer using gene-loaded immunomagnetic albumin nanospheres in vitro and in vivo.International journal of nanomedicine · 2016Article
- p53 activated by AND gate genetic circuit under radiation and hypoxia for targeted cancer gene therapy.Cancer science · 2015Article
- Detailed assessment of gene activation levels by multiple hypoxia-responsive elements under various hypoxic conditions.Annals of nuclear medicine · 2014Article
- Evaluation of p21 promoter for interleukin 12 radiation induced transcriptional targeting in a mouse tumor model.Molecular cancer · 2013Article
- Long-term and stable correction of uremic anemia by intramuscular injection of plasmids containing hypoxia-regulated system of erythropoietin expression.Experimental & molecular medicine · 2012Article
- The radiation dose-regulated AND gate genetic circuit, a novel targeted and real-time monitoring strategy for cancer gene therapy.Cancer gene therapy · 2012Article
- Using HSV-TK/GCV suicide gene therapy to inhibit lens epithelial cell proliferation for treatment of posterior capsular opacification.Molecular vision · 2011Article
- Radiation-inducible silencing of uPA and uPAR in vitro and in vivo in meningioma.International journal of oncology · 2010Article
- Systemic administration of a PEGylated adenovirus vector with a cancer-specific promoter is effective in a mouse model of metastasis.Gene therapy · 2009Article
- Translation of the radio- and chemo-inducible TNFerade vector to the treatment of human cancers.Cancer gene therapy · 2009Article
- Targeted molecular imaging in oncology: focus on radiation therapy.Seminars in radiation oncology · 2008Review
- The radiation-inducible pE9 promoter driving inducible nitric oxide synthase radiosensitizes hypoxic tumour cells to radiation.Gene therapy · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although a significant negative prognostic factor, tumor hypoxia can be exploited for gene therapy. To maximize targeting within the tumor mass, we have developed synthetic gene promoters containing hypoxia-responsive elements (HREs) from the erythropoietin (Epo) gene as well as radiation-responsive CArG elements from the early growth response (Egr) 1 gene. Furthermore, to achieve high and sustained expression of the suicide gene herpes simplex virus thymidine kinase (HSVtk), our gene therapy vectors contain an expression amplification system, or 'molecular switch', based on Cre/loxP recombination. In human glioma and breast adenocarcinoma cells exposed to hypoxia and/or radiation, the HRE/CArG promoter rapidly activated Cre recombinase expression leading to selective and sustained HSVtk synthesis. Killing of transfected tumor cells was measured after incubation with the prodrug ganciclovir (GCV; converted by HSVtk into a cytotoxin). In vitro, higher and more selective GCV-mediated toxicity was achieved with the switch vectors, when compared with the same inducible promoters driving HSVtk expression directly. In tumor xenografts implanted in nude mice, the HRE/CArG-switch induced significant growth delay and tumor eradication. In conclusion, hypoxia- and radiation-activated 'molecular switch' vectors represent a promising strategy for both targeted and effective gene therapy of solid tumors.
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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.