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Colonization of xenograft tumors by oncolytic vaccinia virus (VACV) results in enhanced tumor killing due to the involvement of myeloid cells

Overview of attention for article published in Journal of Translational Medicine, December 2016
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (62nd percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

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1 tweeter
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2 patents

Citations

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4 Dimensions

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15 Mendeley
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Title
Colonization of xenograft tumors by oncolytic vaccinia virus (VACV) results in enhanced tumor killing due to the involvement of myeloid cells
Published in
Journal of Translational Medicine, December 2016
DOI 10.1186/s12967-016-1096-1
Pubmed ID
Authors

Mehmet Okyay Kilinc, Klaas Ehrig, Maysam Pessian, Boris R. Minev, Aladar A. Szalay

Abstract

The mechanisms by which vaccinia virus (VACV) interacts with the innate immune components are complex and involve different mechanisms. iNOS-mediated NO production by myeloid cells is one of the central antiviral mechanisms and this study aims to investigate specifically whether iNOS-mediated NO production by myeloid cells, is involved in tumor eradication following the virus treatment. Human colon adenocarcinoma (HCT-116) xenograft tumors were infected by VACV. Infiltration of iNOS(+) myeloid cell population into the tumor, and virus titer was monitored following the treatment. Single-cell suspensions were stained for qualitative and quantitative flow analysis. The effect of different myeloid cell subsets on tumor growth and colonization were investigated by depletion studies. Finally, in vitro culture experiments were carried out to study NO production and tumor cell killing. Student's t test was used for comparison between groups in all of the experiments. Infection of human colon adenocarcinoma (HCT-116) xenograft tumors by VACV has led to recruitment of many CD11b(+) ly6G(+) myeloid-derived suppressor cells (MDSCs), with enhanced iNOS expression in the tumors, and to an increased intratumoral virus titer between days 7 and 10 post-VACV therapy. In parallel, both single and multiple rounds of iNOS-producing cell depletions caused very rapid tumor growth within the same period after virus injection, indicating that VACV-induced iNOS(+) MDSCs could be an important antitumor effector component. A continuous blockade of iNOS by its specific inhibitor, L-NIL, showed similar tumor growth enhancement 7-10 days post-infection. Finally, spleen-derived iNOS(+) MDSCs isolated from virus-injected tumor bearing mice produced higher amounts of NO and effectively killed HCT-116 cells in in vitro transwell experiments. We initially hypothesized that NO could be one of the factors that limits active spreading of the virus in the cancerous tissue. In contrast to our initial hypothesis, we observed that PMN-MDSCs were the main producer of NO through iNOS and NO provided a beneficial antitumor effect, The results strongly support an important novel role for VACV infection in the tumor microenvironment. VACV convert tumor-promoting MDSCs into tumor-killing cells by inducing higher NO production.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 15 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 15 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 4 27%
Student > Ph. D. Student 4 27%
Researcher 2 13%
Professor 1 7%
Student > Master 1 7%
Other 1 7%
Unknown 2 13%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 20%
Agricultural and Biological Sciences 3 20%
Medicine and Dentistry 2 13%
Psychology 1 7%
Immunology and Microbiology 1 7%
Other 2 13%
Unknown 3 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 29 March 2022.
All research outputs
#6,582,406
of 20,993,108 outputs
Outputs from Journal of Translational Medicine
#1,039
of 3,630 outputs
Outputs of similar age
#124,286
of 339,941 outputs
Outputs of similar age from Journal of Translational Medicine
#67
of 261 outputs
Altmetric has tracked 20,993,108 research outputs across all sources so far. This one has received more attention than most of these and is in the 68th percentile.
So far Altmetric has tracked 3,630 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.0. This one has gotten more attention than average, scoring higher than 69% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 339,941 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 62% of its contemporaries.
We're also able to compare this research output to 261 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 72% of its contemporaries.