Evidence map›Paper›PMID 29563582›Full record

ArticleGene therapy2018

Evaluation of the Glypican 3 promoter for transcriptional targeting of hepatocellular carcinoma.

Bijay Dhungel, Slawomir Andrzejewski, Aparna Jayachandran, Ritu Shrestha, Charmaine A Ramlogan-Steel, Christopher J Layton, Jason C Steel

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Gene Therapy Strategies for Uveal Melanoma: Adeno-associated Virus Delivery Challenges and Translational Opportunities.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
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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

7 authors at 3 institutions in 1 country.

Bijay DhungelGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.ORCID http://orcid.org/0000-0001-5130-5224
Slawomir AndrzejewskiGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.
Aparna JayachandranGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.
Ritu ShresthaGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.
Charmaine A Ramlogan-SteelGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.
Christopher J LaytonGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia.ORCID http://orcid.org/0000-0001-6933-9991
Jason C SteelGallipoli Medical Research Institute, Greenslopes Private Hospital, 102 Newdegate Street, Brisbane, QLD 4120, Australia. j.steel2@uq.edu.au.
The University of Queensland · AUGreenslopes Private Hospital · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a major health problem as evidenced by its increasing incidence and high morbidity and mortality rates. Most patients with HCC have underlying liver disease and dysfunction which limits the current therapeutic options. Treatments that spare the liver and destroy the HCC are needed. Targeting transcriptional differences between HCC and liver cells may provide this therapeutic window. In this study, we examine the potential of the Glypican 3 (GPC3) promoter as a targeting strategy. GPC3 is an oncofetal protein belonging to the proteoglycan family which is normally only expressed during fetal development. However, in HCC, the expression of this protein is reactivated. Here, we show that GPC3 is expressed primarily in HCC and not in normal liver lines. We show that the GPC3 promoter can be used to drive expression of significantly more luciferase and eYFP in HCC cell lines compared to normal liver cells. Further, we show that vectors containing cytosine deaminase (CD) under GPC3 promotor control induced significantly more killing of HCC cell lines after treatment with 5-FC compared to normal liver cell lines. These data suggest that transcriptionally targeted delivery of transgene in HCC cells can be achieved using the GPC3 promoter and this targeting strategy produces limited toxicity to normal liver cells.

Indexed as

Genetic TherapyPromoter Regions, GeneticTranscription, Geneticalpha-FetoproteinsCarcinoma, HepatocellularCase-Control StudiesDependovirusGlypicansHumansLiver Neoplasmsalpha-FetoproteinsGlypicansGPC3 protein, human

Identifiers

PMID29563582
OpenAlexW2785040715

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.