Evidence map›Paper›PMID 12489029›Full record

ArticleCancer gene therapy2003

Recombinant adenoviruses expressing dominant negative insulin-like growth factor-I receptor demonstrate antitumor effects on lung cancer.

Choon-Taek Lee, Kyung-Ho Park, Yasushi Adachi, Ja Young Seol, Chul-Gyu Yoo, Young Whan Kim, Sung Koo Han, Young-Soo Shim, Keith Coffee, Mikhail M Dikov and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  6. The effect of IGF-I receptor blockade for human esophageal squamous cell carcinoma and adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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  12. The proliferating role of insulin and insulin-like growth factors in cancer.Trends in endocrinology and metabolism: TEM · 2010
    Review
  13. Article
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  15. Article
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  19. Article
  20. Cancer.Advances in experimental medicine and biology · 2005
    Review
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 3 institutions in 2 countries.

Choon-Taek LeeDepartment of Internal Medicine, Seoul National University College of Medicine, South Korea.
Kyung-Ho Park
Yasushi Adachi
Ja Young Seol
Chul-Gyu Yoo
Young Whan Kim
Sung Koo Han
Young-Soo Shim
Keith Coffee
Mikhail M Dikov
David P Carbone
Seoul National University Hospital · KRVanderbilt University · USSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The continuous growth of tumors depends on the altered regulation of the cell cycle, which is in turn modulated by signals from growth factors and their receptors. Blockade of insulin-like growth factor (IGF)-I and IGF-IR by antisense or dominant negative plasmid transfection can suppress tumorigenicity and induce regression of established tumors. We have constructed two recombinant adenoviruses: an adenovirus expressing truncated IGF-IR (ad-IGF-IR/950) with an engineered stop codon at amino acid residue 950, and an adenovirus expressing the soluble extracellular domain of IGF-IR (ad-IGF-IR/482) with an engineered stop codon at amino acid residue 482. Ad-IGF-IR/950 produces a defective receptor with an intact alpha subunit and a defective beta subunit lacking the tyrosine kinase domain. Dominant negative inhibition results from competition of the defective receptor with normal IGF-IR subunits, or the competition with normal IGF-IR for ligand by the soluble receptor. We were able to show here that ad-IGF-IR/950 induced the increased expression of IGF-IR on the cell surface and ad-IGF-IR/482 induced the secretion of the soluble fragment of IGF-IR. The transduction of both ad-IGF-IR/950 and ad-IGF-IR/482 could blunt the growth-stimulatory effect of IGF-I on human lung cancer cell lines. Both ad-IGF-IR/950 and ad-IGF-IR/482 effectively blocked IGF-I-induced Akt kinase activation. Intratumoral injection of ad-IGF-IR/482 virus showed significant growth suppression in established lung cancer xenografts. These findings suggest that these ad-IGF-IR/dn (950, 482) have the potential to be effective and practical cancer gene therapy strategies.

Indexed as

Protein Serine-Threonine KinasesAdenocarcinoma, Bronchiolo-AlveolarAdenoviridaeAnimalsCarcinoma, Large CellCell DivisionColony-Forming Units AssayFemaleGenes, DominantGenetic TherapyHumansInsulin-Like Growth Factor ILung NeoplasmsMiceMice, Inbred BALB CMice, NudeAKT1 protein, humanInsulin-Like Growth Factor IProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor, IGF Type 1Recombinant ProteinsThymidine

Identifiers

PMID12489029
OpenAlexW2011158774

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.