Evidence map›Paper›PMID 12438603›Full record

ArticleJournal of virology2002

Tissue-specific transcriptional targeting of a replication-competent retroviral vector.

Christopher R Logg, Aki Logg, Robert J Matusik, Bernard H Bochner, Noriyuki Kasahara

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  12. Retroviral replicating vectors in cancer.Methods in enzymology · 2012
    Article
  13. Adenovirus-retrovirus hybrid vectors achieve highly enhanced tumor transduction and antitumor efficacy in vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2011
    Article
  14. Article
  15. Article
  16. Article
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  18. Splicing mediates the activity of four putative cellular internal ribosome entry sites.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  19. Viruses as anticancer drugs.Trends in pharmacological sciences · 2007
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Christopher R LoggInstitute for Genetic Medicine, Keck School of Medicine, University of Southern California, 2250 Alcazar Street, Los Angeles, CA 90033, USA.
Aki Logg
Robert J Matusik
Bernard H Bochner
Noriyuki Kasahara
Memorial Sloan Kettering Cancer Center · USUniversity of Southern California · USVanderbilt University · US

Funding

TARGETING OF RETROVIRAL REPLICATION TO TUMORSP01CA059318 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KEDES, LAURENCE H · 1992 to 2005
$8.4M
TRANSCRIPTIONAL TARGETING OF RETROVIRAL REPLICATIONR01CA085908 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KASAHARA, NORIYUKI · 2000 to 2001
$402k
NCI NIH HHS P01 CA059318NCI NIH HHS P01 CA 59318NCI NIH HHS R01 CA085908NCI NIH HHS R01 CA 85908
6 · The paper itself

Abstract

The inability of replication-defective viral vectors to efficiently transduce tumor cells in vivo has prevented the successful application of such vectors in gene therapy of cancer. To address the need for more efficient gene delivery systems, we have developed replication-competent retroviral (RCR) vectors based on murine leukemia virus (MLV). We have previously shown that such vectors are capable of transducing solid tumors in vivo with very high efficiency. While the natural requirement of MLV infection for cell division imparts a certain degree of specificity for tumor cells, additional means for confining RCR vector replication to tumor cells are desirable. Here, we investigated the parameters critical for successful tissue-specific transcriptional control of RCR vector replication by replacing various lengths of the MLV enhancer/promoter with sequences derived either from the highly prostate-specific probasin (PB) promoter or from a more potent synthetic variant of the PB promoter. We assessed the transcriptional specificity of the resulting hybrid long terminal repeats (LTRs) and the cell type specificity and efficiency of replication of vectors containing these LTRs. Incorporation of PB promoter sequences effectively restricted transcription from the LTR to prostate-derived cells and imparted prostate-specific RCR vector replication but required the stronger synthetic promoter and retention of native MLV sequences in the vicinity of the TATA box for optimal replicative efficiency and specificity. Our results have thus identified promoter strength and positioning within the LTR as important determinants for achieving both high transduction efficiency and strict cell type specificity in transcriptionally targeted RCR vectors.

Indexed as

Transcription, GeneticVirus ReplicationAndrogen-Binding ProteinAnimalsDNA, ViralFemaleGenetic VectorsHumansLeukemia Virus, MurineMaleOrgan SpecificityProstateProvirusesRatsTerminal Repeat SequencesTumor Cells, CulturedAndrogen-Binding ProteinDNA, Viralprobasin

Identifiers

PMID12438603
PMCPMC136666
OpenAlexW2135478494

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.