Evidence map›Paper›PMID 22737605›Full record

ArticleOncoimmunology2012

Development of immune memory to glial brain tumors after tumor regression induced by immunotherapeutic Toll-like receptor 7/8 activation.

Apostolis Stathopoulos, Chrystel Pretto, Laurent Devillers, Denis Pierre, Florence M Hofman, Carol Kruse, Martin Jadus, Thomas C Chen, Virgil E J C Schijns

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. High expression of Toll-like receptor 7 is a survival factor in pediatric medulloblastoma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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 6 institutions in 3 countries.

Apostolis StathopoulosDepartment of Neurosurgery; Arlon Hospital; Arlon, Belgium ; Epitopoietic Research Corporation (ERC); Namur, Belgium.
Chrystel Pretto
Laurent Devillers
Denis Pierre
Florence M Hofman
Carol Kruse
Martin Jadus
Thomas C Chen
Virgil E J C Schijns
Epicura · BEIndiana University School of MedicineSouthern California University for Professional Studies · USUniversity of California, Irvine · USUniversity of Southern California · USWageningen University & Research · NL

Funding

Adoptive Transfer of AlloCTL for Immunotherapy of Recurrent GliomasR01CA125244 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LIAU, LINDA M · 2010 to 2014
$2.4M
Optimizing Induction Conditions for Immunotherapeutic CTLR01CA154256 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PRINS, ROBERT M · 2010 to 2014
$1.9M
NCI NIH HHS R01 CA125244NCI NIH HHS R01 CA154256
6 · The paper itself

Abstract

The efficacy of immunotherapeutic TLR7/8 activation by resiquimod (R848) was evaluated in vivo, in the CNS-1 rat glioma model syngeneic to Lewis rats. The immune treatment was compared with cytotoxic cyclophosphamide chemotherapy, and as well, was compared with the combination cytotoxic and immunotherapeutic treatments. We found that parenteral treatment with the TLR7/8 agonist, resiquimod, eventually induced complete tumor regression of CNS-1 glioblastoma tumors in Lewis rats. Cyclophosphamide (CY) treatment also resulted in dramatic CNS-1 remission, while the combined treatment showed similar antitumor effects. The resiquimod efficacy appeared not to be associated with direct injury to CNS-1 growth, while CY proved to exert tumoricidal cytotoxicity to the tumor cells. Rats that were cured by treatment with the innate immune response modifier resiquimod proved to be fully immune to secondary CNS-1 tumor rechallenge. They all remained tumor-free and survived. In contrast, rats that controlled CNS-1 tumor growth as a result of CY treatment did not develop immune memory, as demonstrated by their failure to reject a secondary CNS-1 tumor challenge; they showed a concomittant outgrowth of the primary tumor upon secondary tumor exposure. Rechallenge of rats that initially contained tumor growth by combination chemo-immunotherapy also failed to reject secondary tumor challenge, indicating that the cytotoxic effect of the CY likely extended to the endogenous memory immune cells as well as to the tumor. These data demonstrate strong therapeutic antitumor efficacy for the immune response modifier resiquimod leading to immunological memory, and suggest that CY treatment, although effective as chemotherapeutic agent, may be deleterious to maintenance of long-term antitumor immune memory. These data also highlight the importance of the sequence in which a multi-modal therapy is administered.

Identifiers

PMID22737605
PMCPMC3382858
OpenAlexW2043629087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.