Evidence map›Paper›PMID 33803211›Full record

ReviewCancers2021

Expanding the Spectrum of Pancreatic Cancers Responsive to Vesicular Stomatitis Virus-Based Oncolytic Virotherapy: Challenges and Solutions.

Molly C Holbrook, Dakota W Goad, Valery Z Grdzelishvili

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. 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
2.8field-weighted citation impact, top 9% 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, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Activation and Evasion of the FEAR Pathway by RNA Viruses.bioRxiv : the preprint server for biology · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Neutrophils in oncolytic virus immunotherapy.Frontiers in immunology · 2024
    Review
  17. Article
  18. Review
  19. Oncolytic Virotherapy.Cancer treatment and research · 2023
    Article
  20. 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

3 authors at 1 institution in 1 country.

Molly C HolbrookDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
Dakota W GoadDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
Valery Z GrdzelishviliDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
University of North Carolina at Charlotte · US

Funding

Rational Oncolytic Virotherapy For Pancreatic Cancer Using Vesicular Stomatitis VirusR15CA238864 · NCI · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI GRDZELISHVILI, VALERY ZURABOVICH · 2019 to 2019
$440k
NCI NIH HHS 1R15CA238864NCI NIH HHS R15 CA238864
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a devastating malignancy with poor prognosis and a dismal survival rate, expected to become the second leading cause of cancer-related deaths in the United States. Oncolytic virus (OV) is an anticancer approach that utilizes replication-competent viruses to preferentially infect and kill tumor cells. Vesicular stomatitis virus (VSV), one such OV, is already in several phase I clinical trials against different malignancies. VSV-based recombinant viruses are effective OVs against a majority of tested PDAC cell lines. However, some PDAC cell lines are resistant to VSV. Upregulated type I IFN signaling and constitutive expression of a subset of interferon-simulated genes (ISGs) play a major role in such resistance, while other mechanisms, such as inefficient viral attachment and resistance to VSV-mediated apoptosis, also play a role in some PDACs. Several alternative approaches have been shown to break the resistance of PDACs to VSV without compromising VSV oncoselectivity, including (i) combinations of VSV with JAK1/2 inhibitors (such as ruxolitinib); (ii) triple combinations of VSV with ruxolitinib and polycations improving both VSV replication and attachment; (iii) combinations of VSV with chemotherapeutic drugs (such as paclitaxel) arresting cells in the G2/M phase; (iv) arming VSV with p53 transgenes; (v) directed evolution approach producing more effective OVs. The latter study demonstrated impressive long-term genomic stability of complex VSV recombinants encoding large transgenes, supporting further clinical development of VSV as safe therapeutics for PDAC.

Indexed as

oncolytic viruspancreatic cancerpancreatic ductal adenocarcinomavesicular stomatitis virusvirotherapy

Identifiers

PMID33803211
PMCPMC7963195
OpenAlexW3134348101

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.