ArticleGut2006
Treatment of pancreatic carcinoma by adenoviral mediated gene transfer of vasostatin in mice.
Article in Gut, 2006. 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.
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.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Persistent Infection of a Canine Histiocytic Sarcoma Cell Line with Attenuated Canine Distemper Virus Expressing Vasostatin or Granulocyte-Macrophage Colony-Stimulating Factor.International journal of molecular sciences · 2022Article
- Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism.American journal of hematology · 2016Article
- Gene therapy in pancreatic cancer.World journal of gastroenterology · 2014Review
- Chromogranin A and its fragments as regulators of small intestinal neuroendocrine neoplasm proliferation.PloS one · 2013Article
- Antiangiogenic and antitumor effects of Trypanosoma cruzi Calreticulin.PLoS neglected tropical diseases · 2010Article
- The Chick Embryo Chorioallantoic Membrane as an In Vivo Assay to Study Antiangiogenesis.Pharmaceuticals (Basel, Switzerland) · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumour growth is angiogenesis dependent and antiangiogenesis therapy may represent a promising therapeutic option.
aimsTo evaluate the inhibitory effect of vasostatin gene mediated by a replication deficient recombinant adenovirus (Ad) on human pancreatic cancer in vivo and to investigate the mechanism of action of vasostatin.
methodsHuman umbilical vein endothelium derived ECV304 cells were infected with Ad-vasostatin and Ad-lacZ, and compared with phosphate buffered saline (PBS). MTT (3,-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay was used to estimate the proliferation of ECV304 cells; tube formation assay and choriallantoic membrane assay were used to evaluate angiogenesis in vivo and in vitro. Xenografted nude mice with pancreatic cancer were established to observe in vivo tumour growth suppression. Microvessel density revealed by CD31 immunohistochemical staining was measured.
resultsGrowth and tube formation of ECV304 cells infected with Ad-vasostatin were suppressed significantly compared with cells infected with Ad-lacZ or cells treated with PBS. Neovascularisation in the Ad-vasostatin group was less than that in the PBS and Ad-lacZ groups, based on chorioallantoic membrane results. Volumes of pancreatic tumours in the Ad-vasostatin group were significantly smaller than those in the PBS and Ad-lacZ groups at the end of the treatment period. Microvessel density in the Ad-vasostatin group was significantly lower than that in the Ad-lacZ and PBS groups.
conclusionThe vasostatin gene mediated by adenovirus is efficient for gene therapy for pancreatic carcinoma. Suppression of vasostatin on proliferation of vascular endothelium cells and angiogenesis may account for its effect.
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Registered trials
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