ArticleGene therapy2007
p21((WAF1))-mediated transcriptional targeting of inducible nitric oxide synthase gene therapy sensitizes tumours to fractionated radiotherapy.
Article in Gene therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 42 citations in OpenAlex.
- Non-Clinical In Vitro Evaluation of Antibiotic Resistance Gene-Free Plasmids Encoding Human or Murine IL-12 Intended for First-in-Human Clinical Study.Pharmaceutics · 2021Article
- Multiple functions of p21 in cancer radiotherapy.Journal of cancer research and clinical oncology · 2021Review
- Article
- Systemic RALA/iNOS Nanoparticles: A Potent Gene Therapy for Metastatic Breast Cancer Coupled as a Biomarker of Treatment.Molecular therapy. Nucleic acids · 2017Article
- Retargeted adenoviruses for radiation-guided gene delivery.Cancer gene therapy · 2016Article
- Demonstration of Tightly Radiation-Controlled Molecular Switch Based on CArG Repeats by In Vivo Molecular Imaging.Molecular imaging and biology · 2015Article
- Evaluation of p21 promoter for interleukin 12 radiation induced transcriptional targeting in a mouse tumor model.Molecular cancer · 2013Article
- Chapter seven--Cancer treatment with gene therapy and radiation therapy.Advances in cancer research · 2012Review
- Radiation-inducible silencing of uPA and uPAR in vitro and in vivo in meningioma.International journal of oncology · 2010Article
- NO to breast: when, why and why not?Current pharmaceutical design · 2010Review
- Astatine Radiopharmaceuticals: Prospects and Problems.Current radiopharmaceuticals · 2008Article
- The radiation-inducible pE9 promoter driving inducible nitric oxide synthase radiosensitizes hypoxic tumour cells to radiation.Gene therapy · 2008Article
- A kit method for the high level synthesis of [211At]MABG.Bioorganic & medicinal chemistry · 2007Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer gene therapy that utilizes toxic transgene products requires strict transcriptional targeting to prevent adverse normal tissue effects. We report on the use of a promoter derived from the cyclin dependent kinase inhibitor, p21((WAF1)), to control transgene expression. We demonstrate that this promoter is relatively silent in normal cells (L132, FSK, HMEC-1) compared to the almost constitutive expression obtained in tumour cells (DU145, LNCaP, HT29 and MCF-7) of varying p53 status, a characteristic that will be important in gene therapy protocols. In addition, we found that the p21((WAF1)) promoter could be further induced by both external beam radiation (up to eight-fold in DU145 cells), intracellular-concentrated radionuclides ([(211)At]MABG) (up to 3.5-fold in SK-N-BE(2c) cells) and hypoxia (up to four-fold in DU145 cells). We have previously achieved significant radiosensitization of tumour cells both in vitro and in vivo by using inducible nitric oxide synthase (iNOS) gene therapy to generate the potent radiosensitizer, nitric oxide (NO(.-)). Here, we report that a clinically relevant schedule of p21((WAF1))-driven iNOS gene therapy significantly sensitized both p53 wild-type RIF-1 tumours and p53 mutant HT29 tumours to fractionated radiotherapy. Our data highlight the utility of this p21((WAF1))/iNOS-targeted approach.
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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.