Evidence map›Paper›PMID 17053813›Full record

ArticleCancer gene therapy2007

The effects of FasL on inflammation and tumor survival are dependent on its expression levels.

A Wada, Y Tada, K Kawamura, Y Takiguchi, K Tatsumi, T Kuriyama, T Takenouchi, J O-Wang, M Tagawa

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 32% 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, 22 citations in OpenAlex.

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  9. The immunoregulatory mechanisms of carcinoma for its survival and development.Journal of experimental & clinical cancer research : CR · 2011
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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

9 authors at 3 institutions in 1 country.

A WadaDivision of Pathology, Chiba Cancer Center Research Institute, Chiba, Japan.
Y Tada
K Kawamura
Y Takiguchi
K Tatsumi
T Kuriyama
T Takenouchi
J O-Wang
M Tagawa
Chiba Cancer Center · JPChiba University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The apoptosis-inducing Fas ligand (FasL) is expressed in a variety of human cancers and has been implicated in tumor immune evasion. Paradoxically, ectopic expression of FasL in experimental tumors triggers a neutrophil-mediated inflammatory response and tumor rejection. To resolve these conflicting findings, we have established B16 melanoma and P29 Lewis lung carcinoma lines expressing different levels of FasL and examined their tumorigenicity in vivo. While tumors with a high level of FasL were rapidly rejected as previously reported, those expressing a low level of FasL were not rejected but grew faster than did FasL-negative parental cells. The growth enhancement of FasL(low) tumors was not observed in T-cell-deficient nude mice, suggesting that FasL expressed in tumors at low levels counteracted against T-cell-dependent antitumor responses. In support of this notion, FasL(low) tumors were found to grow faster than parental cells in mice that had acquired tumor-specific immunity. Furthermore, histological examinations revealed apoptosis of lymphocytes in tissue sections of FasL(low) tumors. These results collectively suggest that FasL on tumors is a double-edged sword: at high levels it triggers tumor rejection whereas at low levels it facilitates tumor growth possibly by suppressing antitumor immune responses.

Indexed as

AnimalsApoptosisCarcinoma, Lewis LungCD40 LigandCoculture TechniquesCytotoxicity, ImmunologicFas Ligand ProteinFemaleFlow CytometryHumansInflammationIn Situ Nick-End LabelingMelanoma, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLCD40 LigandFas Ligand ProteinFasl protein, mouse

Identifiers

PMID17053813
OpenAlexW2067218196

What OpenQuestion holds

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Registered trials

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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.