Evidence map›Paper›PMID 25423447›Full record

ArticleHuman gene therapy2015

Targeted oncolytic herpes simplex virus type 1 eradicates experimental pancreatic tumors.

Marion Gayral, Hubert Lulka, Naima Hanoun, Coline Biollay, Janick Sèlves, Alix Vignolle-Vidoni, Hervé Berthommé, Pascal Trempat, Alberto L Epstein, Louis Buscail and 2 more

Open access · greenAbstract read
In one paragraph

Article in Human gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. New avenues for the treatment of immunotherapy-resistant pancreatic cancer.World journal of gastrointestinal oncology · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Reshaping the Immune Microenvironment by Oncolytic Herpes Simplex Virus in Murine Pancreatic Ductal Adenocarcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Gene Therapy for Pancreatic Diseases: Current Status.International journal of molecular sciences · 2018
    Review
  16. Gene Therapy for Pancreatic Cancer: Specificity, Issues and Hopes.International journal of molecular sciences · 2017
    Review
  17. Review
  18. Oncolytic Viral Therapy for Mesothelioma.Frontiers in oncology · 2017
    Review
  19. 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

12 authors at 4 institutions in 3 countries.

Marion Gayral1 Université Toulouse III-Paul Sabatier , UMR1037 CRCT, F-31000 Toulouse, France .
Hubert Lulka
Naima Hanoun
Coline Biollay
Janick Sèlves
Alix Vignolle-Vidoni
Hervé Berthommé
Pascal Trempat
Alberto L Epstein
Louis Buscail
Jean-Luc Béjot
Pierre Cordelier
Université Toulouse III - Paul Sabatier · FRItron (France) · FRUniversitas Bung Karno · IDUniversité de Versailles Saint-Quentin-en-Yvelines · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As many other cancers, pancreatic ductal adenocarcinoma (PDAC) progression is associated with a series of hallmark changes for cancer cells to secure their own growth success. Yet, these very changes render cancer cells highly sensitive to viral infection. A promising strategy may rely on and exploit viral replication for tumor destruction, whereby infection of tumor cells by a replication-conditional virus may lead to cell destruction and simultaneous release of progeny particles that can spread and infect adjacent tumor cells, while sparing healthy tissues. In the present study, we used Myb34.5, a second-generation replication-conditional herpes simplex virus type 1 (HSV-1) mutant in which ICP6 gene expression is defective and expression of the HSV-1 γ134.5 gene is regulated by the cellular B-myb promoter. We found that B-myb is present in experimental PDAC and tumors, and is overexpressed in patients' tumors, as compared with normal adjacent pancreas. Myb34.5 replicates to high level in human PDAC cell lines and is associated with cell death by apoptosis. In experimental models of PDAC, mice receiving intratumoral Myb34.5 injections appeared healthy and tumor progression was inhibited, with evidence of tumor necrosis, hemorrhage, viral replication, and cancer cell death by apoptosis. Combining standard-of-care chemotherapy with Myb34.5 successfully led to a very impressive antitumoral effect that is rarely achieved in this experimental model, and resulted in a greater reduction in tumor growth than chemotherapy alone. These promising results warrant further evaluation in early phase clinical trial for patients diagnosed with PDAC for whom no effective treatment is available.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Pancreatic DuctalCell Cycle ProteinsCell Line, TumorDeoxycytidineDisease Models, AnimalGemcitabineGene Expression RegulationGenetic EngineeringHerpesvirus 1, HumanHumansInjections, IntralesionalMiceMice, NudeAntineoplastic AgentsCell Cycle ProteinsDeoxycytidineGemcitabineherpes simplex virus type 1-protein ICP6MYBL2 protein, humanTrans-ActivatorsViral Proteins

Identifiers

PMID25423447
PMCPMC4326267
OpenAlexW1778578100

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.