Evidence map›Paper›PMID 24614600›Full record

ArticlePloS one2014

Possible role of arginase-1 in concomitant tumor immunity.

Michael J Korrer, Yuwen Zhang, John M Routes

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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. Article
  2. Review
  3. Phase I Study of Niraparib in Combination with Radium-223 for the Treatment of Metastatic Castrate-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Michael J KorrerDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; Children's Research Institute, Milwaukee, Wisconsin, United States of America; Cancer Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Yuwen ZhangDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; 2 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; 3 Children's Research Institute, Milwaukee, Wisconsin, United States of America; 4 Cancer Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; 5 Department of Microbiology and Immunology, University of Louisville, Louisville, United States of America.
John M RoutesDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America; Children's Research Institute, Milwaukee, Wisconsin, United States of America; Cancer Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Children’s Institute · US

Funding

Anti-tumorigenic Activity of Adenovirus E1AR01CA125666 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI ROUTES, JOHN MICHAEL · 2007 to 2011
$1.5M
NCI NIH HHS CA125666-05NCI NIH HHS R01 CA125666
6 · The paper itself

Abstract

The expression of Adenovirus serotype 2 or serotype 5 (Ad2/5) E1A in tumor cells reduces their tumorigenicity in vivo by enhancing the NK cell mediated and T cell mediated anti-tumor immune response, an activity that correlates with the ability of E1A to bind p300. We determined if E1A could be used as a molecular adjuvant to enhance antigen-specific T cell responses to a model tumor antigen, ovalbumin (OVA). To achieve this goal, we stably expressed a fusion protein of E1A and OVA (MCA-205-E1A-OVA), OVA (MCA-205-OVA) or a mutant version of E1A unable to bind p300 and OVA (E1A-Δp300-OVA) in the B6-derived, highly tumorigenic MCA-205 tumor cell line. MCA-205-E1A-OVA tumor cells were over 10,000 fold less tumorigenic than MCA-205-OVA, MCA-205-E1A-Δp300-OVA, or MCA-205 in B6 mice. However, immunization of B6 mice with live MCA-205-OVA, MCA-205-E1A-Δp300-OVA and MCA-E1A-OVA tumor cells induced nearly equivalent OVA-specific CD4 T cells and CD8 CTL responses. Further studies revealed that mice with primary, enlarging MCA-205-OVA or MCA-205-E1A-Δp300-OVA tumors on one flank exhibited OVA-specific anti-tumor T cell responses that rejected a tumorigenic dose of MCA-205-OVA cells on the contralateral flank (concomitant tumor immunity). Next we found that tumor associated macrophages (TAMs) in progressive MCA-205-OVA tumors, but not MCA-205-E1A-OVA tumors that expressed high levels of arginase-1, which is known to have local immunosuppressive activities. In summary, immunization of mice with MCA-205 cells expressing OVA, E1A-Δp300-OVA or E1A-OVA induced equivalent OVA-specific CD4 and CD8 anti-tumor responses. TAMs found in MCA-205-OVA, but not MCA-205-E1A-OVA, tumors expressed high levels of arginase-1. We hypothesize that the production of arginase-1 by TAMs in MCA-205-OVA or MCA-205-E1A-Δp300-OVA tumor cells leads to an ineffective anti-tumor immune response in the tumor microenvironment, but does not result in inhibition of a systemic anti-tumor immunity.

Indexed as

ImmunityAdenovirus E1A ProteinsAnimalsArginaseCarcinogenesisCD3 ComplexCD8-Positive T-LymphocytesCytotoxicity, ImmunologicImmunizationMacrophagesMice, Inbred C57BLNeoplasmsOvalbuminRecombinant Fusion ProteinsTransfectionAdenovirus E1A ProteinsArginaseCD3 ComplexOvalbuminRecombinant Fusion Proteins

Identifiers

PMID24614600
PMCPMC3948845
OpenAlexW2032458197

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.