ArticleNeoplasia (New York, N.Y.)2005
Properties of a telomerase-specific Cre/Lox switch for transcriptionally targeted cancer gene therapy.
Article in Neoplasia (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 19 citations in OpenAlex.
- Use of the XRCC2 promoter for in vivo cancer diagnosis and therapy.Cell death & disease · 2018Article
- Mathematical model of a telomerase transcriptional regulatory network developed by cell-based screening: analysis of inhibitor effects and telomerase expression mechanisms.PLoS computational biology · 2014Article
- Novel therapeutic approaches for various cancer types using a modified sleeping beauty-based gene delivery system.PloS one · 2014Article
- TCEAL7 inhibition of c-Myc activity in alternative lengthening of telomeres regulates hTERT expression.Neoplasia (New York, N.Y.) · 2010Article
- Use of the Rad51 promoter for targeted anti-cancer therapy.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- A review of the past, present, and future directions of neoplasia.Neoplasia (New York, N.Y.) · 2005Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomerase expression represents a good target for cancer gene therapy. The promoters of the core telomerase catalytic [human telomerase reverse transcriptase (hTERT)] and RNA [human telomerase RNA (hTR)] subunits show selective activity in cancer cells but not in normal cells. This property can be harnessed to express therapeutic transgenes in a wide range of cancer cells. Unfortunately, weak hTR and hTERT promoter activities in some cancer cells could limit the target cell range. Therefore, strategies to enhance telomerase-specific gene therapy are of interest. We constructed a Cre/Lox reporter switch coupling telomerase promoter specificity with Cytomegalovirus (CMV) promoter activity, which is generally considered to be constitutively high. In this approach, a telomerase-specific vector expressing Cre recombinase directs excisive recombination on a second vector, removing a transcriptional blockade to CMV-dependent luciferase expression. We tested switch activation in cell lines over a wide range of telomerase promoter activities. However, Cre/Lox-dependent luciferase expression was not enhanced relative to expression using hTR or hTERT promoters directly. Cell-specific differences between telomerase and CMV promoter activities and incomplete sigmoid switch activation were limiting factors. Notably, CMV activity was not always significantly stronger than telomerase promoter activity. Our conclusions provide a general basis for a more rational design of novel recombinase switches in gene therapy.
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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.