Evidence map›Paper›PMID 17989705›Full record

ArticleGene therapy2008

Alpha-fetoprotein promoter-targeted sodium iodide symporter gene therapy of hepatocellular carcinoma.

M J Willhauck, B R Sharif Samani, K Klutz, N Cengic, I Wolf, L Mohr, M Geissler, R Senekowitsch-Schmidtke, B Göke, J C Morris and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  9. Lung microenvironment promotes the metastasis of human hepatocellular carcinoma cells to the lungs.International journal of clinical and experimental medicine · 2015
    Article
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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

11 authors at 4 institutions in 2 countries.

M J WillhauckDepartment of Internal Medicine II, Ludwig-Maximilians-University, Munich, Germany.
B R Sharif Samani
K Klutz
N Cengic
I Wolf
L Mohr
M Geissler
R Senekowitsch-Schmidtke
B Göke
J C Morris
C Spitzweg
Ludwig-Maximilians-Universität München · DETechnical University of Munich · DEUniversity of Freiburg · DEMayo Clinic · US

Funding

Utility of serum and Tissue Biomarkers for Predicting Response to Androgen DeprivP50CA091956 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2001 to 2010
$23.4M
NCI NIH HHS CA91956
6 · The paper itself

Abstract

Due to limited treatment options the prognosis of patients with advanced hepatocellular cancer (HCC) has remained poor. To investigate an alternative therapeutic approach, we examined the feasibility of radioiodine therapy of HCC following human sodium iodide symporter (NIS) gene transfer using a mouse alpha-fetoprotein (AFP) promoter construct to target NIS expression to HCC cells. For this purpose, the murine Hepa 1-6 and the human HepG2 hepatoma cell lines were stably transfected with NIS cDNA under the control of the tumor-specific AFP promoter. The stably transfected Hepa 1-6 cell line showed a 10-fold increase in iodide accumulation, while HepG2 cells accumulated (125)I approximately 60-fold. Tumor-specific NIS expression was confirmed on mRNA level by northern blot analysis, and on protein level by immunostaining, that revealed primarily membrane-associated NIS-specific immunoreactivity. In an in vitro clonogenic assay up to 78% of NIS-transfected Hepa 1-6 and 93% of HepG2 cells were killed by (131)I exposure, while up to 96% of control cells survived. In vivo NIS-transfected HepG2 xenografts accumulated 15% of the total (123)I administered per gram tumor with a biological half-life of 8.38 h, resulting in a tumor absorbed dose of 171 mGy MBq(-1) (131)I. After administration of a therapeutic (131)I dose (55.5 MBq) tumor growth of NIS expressing HepG2 xenografts was significantly inhibited. In conclusion, tumor-specific iodide accumulation was induced in HCC cells by AFP promoter-directed NIS expression in vitro and in vivo, which was sufficiently high to allow a therapeutic effect of (131)I. This study demonstrates the potential of tumor-specific NIS gene therapy as an innovative treatment strategy for HCC.

Indexed as

Promoter Regions, Geneticalpha-FetoproteinsAnimalsCarcinoma, HepatocellularCombined Modality TherapyGene ExpressionGenetic TherapyHumansIodine RadioisotopesLiver NeoplasmsMiceRadiopharmaceuticalsSodium-Iodide SymportersSymportersTransfectionalpha-FetoproteinsIodine RadioisotopesRadiopharmaceuticalsSodium-Iodide SymportersSymporters

Identifiers

PMID17989705
OpenAlexW2057572740

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.