Evidence map›Paper›PMID 26053394›Full record

ArticleInternational journal of molecular sciences2015

Specific Colon Cancer Cell Cytotoxicity Induced by Bacteriophage E Gene Expression under Transcriptional Control of Carcinoembryonic Antigen Promoter.

Ana R Rama, Rosa Hernandez, Gloria Perazzoli, Miguel Burgos, Consolación Melguizo, Celia Vélez, Jose Prados

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Bacteriophages as Therapeutic and Diagnostic Vehicles in Cancer.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Toward Precision Medicine: How Far Is the Goal?International journal of molecular sciences · 2016
    Article
  11. 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

7 authors at 3 institutions in 1 country.

Ana R RamaDepartment of Health Science, University of Jaén, Jaén 23071, Spain. arama@ujaen.es.
Rosa HernandezInstitute of Biopathology and Regenerative Medicine (IBIMER), Granada 18100, Spain. r_faraya@hotmail.com.
Gloria PerazzoliInstitute of Biopathology and Regenerative Medicine (IBIMER), Granada 18100, Spain. gperazzoli@ugr.es.
Miguel BurgosInstitute of Biotechnology and Department of Genetics, University of Granada, Granada 18071, Spain. mburgos@ugr.es.
Consolación MelguizoInstitute of Biopathology and Regenerative Medicine (IBIMER), Granada 18100, Spain. melguizo@ugr.es.
Celia VélezInstitute of Biopathology and Regenerative Medicine (IBIMER), Granada 18100, Spain. mariaceliavelez@ugr.es.
Jose PradosInstitute of Biopathology and Regenerative Medicine (IBIMER), Granada 18100, Spain. jcprados@ugr.es.
Universidad de Granada · ESInstituto de Investigación Biosanitaria de Granada · ESUniversidad de Jaén · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer is one of the most prevalent cancers in the world. Patients in advanced stages often develop metastases that require chemotherapy and usually show a poor response, have a low survival rate and develop considerable toxicity with adverse symptoms. Gene therapy may act as an adjuvant therapy in attempts to destroy the tumor without affecting normal host tissue. The bacteriophage E gene has demonstrated significant antitumor activity in several cancers, but without any tumor-specific activity. The use of tumor-specific promoters may help to direct the expression of therapeutic genes so they act against specific cancer cells. We used the carcinoembryonic antigen promoter (CEA) to direct E gene expression (pCEA-E) towards colon cancer cells. pCEA-E induced a high cell growth inhibition of human HTC-116 colon adenocarcinoma and mouse MC-38 colon cancer cells in comparison to normal human CCD18co colon cells, which have practically undetectable levels of CEA. In addition, in vivo analyses of mice bearing tumors induced using MC-38 cells showed a significant decrease in tumor volume after pCEA-E treatment and a low level of Ki-67 in relation to untreated tumors. These results suggest that the CEA promoter is an excellent candidate for directing E gene expression specifically toward colon cancer cells.

Indexed as

AnimalsBacteriophagesCaco-2 CellsCarcinoembryonic AntigenCell Line, TumorCell ProliferationColonic NeoplasmsGenetic TherapyHCT116 CellsHT29 CellsHumansMiceNeoplasm TransplantationPromoter Regions, GeneticRecombinant ProteinsViral ProteinsCarcinoembryonic AntigenRecombinant ProteinsViral Proteinscarcinoma embryonic antigencolorectal cancerE genepromoter tissue specificsuicide gene therapy

Identifiers

PMID26053394
PMCPMC4490463
OpenAlexW1570129449

What OpenQuestion holds

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LicenceCC BY
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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.