Evidence map›Paper›PMID 29465830›Full record

ArticleCancer science2018

Toll-like receptor 3 signal augments radiation-induced tumor growth retardation in a murine model.

Sumito Yoshida, Hiroaki Shime, Yohei Takeda, Jin-Min Nam, Ken Takashima, Misako Matsumoto, Hiroki Shirato, Masanori Kasahara, Tsukasa Seya

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

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  17. Significance and Role of Pattern Recognition Receptors in Malignancy.Archivum immunologiae et therapiae experimentalis · 2019
    Review
  18. Review
  19. Article
  20. Article
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 2 institutions in 1 country.

Sumito YoshidaDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Hiroaki ShimeDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Yohei TakedaDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Jin-Min NamDepartment of Radiation Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Ken TakashimaDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Misako MatsumotoDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Hiroki ShiratoDepartment of Radiation Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Masanori KasaharaDepartment of Pathology I, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Tsukasa SeyaDepartment of Vaccine Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.ORCID http://orcid.org/0000-0002-0808-5710
Hokkaido University of Science · JPSapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy induces anti-tumor immunity by induction of tumor antigens and damage-associated molecular patterns (DAMP). DNA, a representative DAMP in radiotherapy, activates the stimulator of interferon genes (STING) pathway which enhances the immune response. However, the immune response does not always parallel the inflammation associated with radiotherapy. This lack of correspondence may, in part, explain the radiation-resistance of tumors. Additive immunotherapy is expected to revive tumor-specific CTL facilitating radiation-resistant tumor shrinkage. Herein pre-administration of the double-stranded RNA, polyinosinic-polycytidylic acid (polyI:C), in conjunction with radiotherapy, was shown to foster tumor suppression in mice bearing radioresistant, ovalbumin-expressing Lewis lung carcinoma (LLC). Extrinsic injection of tumor antigen was not required for tumor suppression. No STING- and CTL-response was induced by radiation in the implant tumor. PolyI:C was more effective for induction of tumor growth retardation at 1 day before radiation than at post-treatment. PolyI:C targeted Toll-like receptor 3 with minimal effect on the mitochondrial antiviral-signaling protein pathway. Likewise, the STING pathway barely contributed to LLC tumor suppression. PolyI:C primed antigen-presenting dendritic cells in draining lymph nodes to induce proliferation of antigen-specific CTL. By combination therapy, CTL efficiently infiltrated into tumors with upregulation of relevant chemokine transcripts. Batf3-positive DC and CD8

Indexed as

AnimalsAntigens, NeoplasmCarcinoma, Lewis LungCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationCombined Modality TherapyDendritic CellsDisease Models, AnimalImmunotherapy, AdoptiveMacrophagesMiceMice, Inbred C57BLPoly I-CT-Lymphocytes, CytotoxicToll-Like Receptor 3Antigens, NeoplasmPoly I-CTLR3 protein, mouseToll-Like Receptor 3cytotoxic T lymphocytedendritic cellradiationToll-like receptor 3tumor necrosis factor-α

Identifiers

PMID29465830
PMCPMC5891207
OpenAlexW2789593042

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.