Evidence map›Paper›PMID 32047957›Full record

ArticleCancer immunology, immunotherapy : CII2020

Activation of TLR4 signaling inhibits progression of osteosarcoma by stimulating CD8-positive cytotoxic lymphocytes.

Kenichiro Yahiro, Yoshihiro Matsumoto, Hisakata Yamada, Makoto Endo, Nokitaka Setsu, Toshifumi Fujiwara, Makoto Nakagawa, Atsushi Kimura, Eijiro Shimada, Seiji Okada and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 44 citations in OpenAlex.

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  16. Strategies to Overcome Resistance to Immune-Based Therapies in Osteosarcoma.International journal of molecular sciences · 2023
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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

12 authors at 1 institution in 3 countries.

Kenichiro YahiroDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Yoshihiro MatsumotoDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan. ymatsu@ortho.med.kyushu-u.ac.jp.
Hisakata YamadaDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Makoto EndoDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Nokitaka SetsuDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Toshifumi FujiwaraDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Makoto NakagawaDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Atsushi KimuraDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Eijiro ShimadaDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Seiji OkadaDepartment of Immunobiology and Neuroscience Medical. Medical Institute of Bioregulation, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Yoshinao OdaDepartment of Anatomic Pathology, Pathological Sciences, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Yasuharu NakashimaDepartment of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Fukuoka, Japan.
Kyushu University · JP

Funding

Japan Orthopaedics and Traumatology Foundation (JP) 332Japan society for the Promotion of Science 18K16627Japan Society for the Promotion of Science 18K09067Japan Society for the Promotion of Science 19K16802
6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) is the most common malignant bone tumor and the prognosis of advanced cases is still poor. Recently, there have been several reports suggesting the relationship between innate immunity and OS, but the detailed mechanism is unknown. We demonstrate the relationship between OS and Toll-like receptor 4 (TLR4) which is one of the most important factors in innate immunity.

methodsWe established a syngenic mouse tumor model using C3H/HeN, C3H/HeJ mouse and a highly metastatic OS cell line, LM8. TLR4 activation with lipopolysaccharide (LPS) was performed on both mice and its influence on the progression of OS was evaluated. We also performed CD8 + cells depletion to examine the influence on TLR4 activation effects.

resultsTumor volume of C3H/HeN mice was significantly smaller and overall survival of C3H/HeN mice was significantly longer than C3H/HeJ mice. We found more CD8+ cells infiltrating in lung metastases of C3H/HeN mice and depletion of CD8+ cells canceled the antitumor effects of LPS.

conclusionTLR4 activation by LPS increased CD8+ cells infiltrating into lung metastases and suppressed OS progression in the mouse model. TLR4 activation may suppress the progression of OS via stimulating CD8+ cells and can be expected as a novel treatment for OS.

Indexed as

Adjuvants, ImmunologicAdolescentAnimalsAntineoplastic Combined Chemotherapy ProtocolsBone NeoplasmsCell Line, TumorChemotherapy, AdjuvantChildChild, PreschoolDisease Models, AnimalDisease ProgressionFemaleHumansKaplan-Meier EstimateLipid ALipopolysaccharidesAdjuvants, ImmunologicLipid ALipopolysaccharidesmonophosphoryl lipid ATLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4CD8-positive lymphocytesInnate immunityOsteosarcomaPrognosisToll-like receptor 4

Identifiers

PMID32047957
PMCPMC11027819
OpenAlexW3006080178

What OpenQuestion holds

Textmetadata
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.