Evidence map›Paper›PMID 35197076›Full record

ArticleVirology journal2022

Modulation of the tumor microenvironment by armed vesicular stomatitis virus in a syngeneic pancreatic cancer model.

Sijia Tang, Lei Shi, Breona T Luker, Channen Mickler, Bhavana Suresh, Gregory B Lesinski, Daping Fan, Yuan Liu, Ming Luo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. The role and mechanism of neutrophils in oncolytic virus therapy.Experimental biology and medicine (Maywood, N.J.) · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Oncolytic Viruses: Immunotherapy Drugs for Gastrointestinal Malignant Tumors.Frontiers in cellular and infection microbiology · 2022
    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

9 authors at 3 institutions in 1 country.

Sijia TangInstitute of Biomedical Sciences, Georgia State University, Atlanta, GA, 30302, USA.
Lei ShiDepartment of Biology, Georgia State University, Atlanta, GA, 30302, USA.
Breona T LukerDepartment of Chemistry, Georgia State University, Atlanta, GA, 30302, USA.
Channen MicklerDepartment of Chemistry, Georgia State University, Atlanta, GA, 30302, USA.
Bhavana SureshDepartment of Chemistry, Georgia State University, Atlanta, GA, 30302, USA.
Gregory B LesinskiDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA, 30322, USA.
Daping FanDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC, 29209, USA.
Yuan LiuDepartment of Biology, Georgia State University, Atlanta, GA, 30302, USA.
Ming LuoDepartment of Chemistry, Georgia State University, Atlanta, GA, 30302, USA. mluo@gsu.edu.ORCID 0000-0003-1766-3487
Georgia State University · USEmory University · USUniversity of South Carolina · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe immunosuppressive microenvironment in pancreatic ductal adenocarcinoma is a major factor that limits the benefits of immunotherapy, especially immune checkpoint blockade. One viable strategy for reverting the immunosuppressive conditions is the use of an oncolytic virus (OV) in combination with other immunotherapy approaches. Infection of PDAC cells with a robust OV can change the tumor microenvironment and increase tumor antigen release by its lytic activities. These changes in the tumor may improve responses to immunotherapy, including immune checkpoint blockade. However, a more potent OV may be required for efficiently infecting pancreatic tumors that may be resistant to OV.

methodsVesicular stomatitis virus, a rapid replicating OV, was armed to express the Smac protein during virus infection (VSV-S). Adaptation by limited dilution largely increased the selective infection of pancreatic cancer cells by VSV-S. The engineered OV was propagated to a large quantity and evaluated for their antitumor activities in an animal model.

resultsIn a syngeneic KPC model, intratumoral injection of VSV-S inhibited tumor growth, and induced increasing tumor infiltration of neutrophils and elimination of myeloid derived suppressor cells and macrophages in the tumor. More importantly, M2-like macrophages were eliminated preferentially over those with an M1 phenotype. Reduced levels of arginase 1, TGF-β and IL-10 in the tumor also provided evidence for reversion of the immunosuppressive conditions by VSV-S infection. In several cases, tumors were completely cleared by VSV-S treatment, especially when combined with anti-PD-1 therapy. A long-term survival of 44% was achieved.

conclusionsThe improved OV, VSV-S, was shown to drastically alter the immune suppressive tumor microenvironment when intratumorally injected. Our results suggest that the combination of potent OV treatment with immune checkpoint blockade may be a promising strategy to treat pancreatic cancer more effectively.

Indexed as

Oncolytic VirotherapyOncolytic VirusesPancreatic NeoplasmsVesicular StomatitisAnimalsCell Line, TumorTumor MicroenvironmentVesicular stomatitis Indiana virusM2 macrophagesMDSCNeutrophilSmacTumor microenvironment

Identifiers

PMID35197076
PMCPMC8867845
OpenAlexW4212969898

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.