Evidence map›Paper›PMID 23481183›Full record

ArticleBritish journal of cancer2013

Using macrophage activation to augment immunotherapy of established tumours.

Z G Fridlender, A Jassar, I Mishalian, L-Cs Wang, V Kapoor, G Cheng, J Sun, S Singhal, L Levy, S M Albelda

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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  19. Pro-Tumoral Inflammatory Myeloid Cells as Emerging Therapeutic Targets.International journal of molecular sciences · 2016
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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

10 authors at 3 institutions in 2 countries.

Z G FridlenderInstitute of Pulmonary Medicine, Hadassah-Hebrew University Medical Center, POB 12000, Jerusalem 91120, Israel. fridlender@hadassah.org.il
A Jassar
I Mishalian
L-Cs Wang
V Kapoor
G Cheng
J Sun
S Singhal
L Levy
S M Albelda
University of Pennsylvania · USHebrew University of Jerusalem · ILHadassah Medical Center · IL

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
VECTOR DEVELOPMENT /PRECLINICAL TESTINGP01CA066726 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KALOS, MICHAEL D · 1995 to 2016
$18.2M
NCI NIH HHS P01 CA066726NCI NIH HHS P01 CA 66726NCI NIH HHS P30 CA016520NIEHS NIH HHS ES013508-02NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

backgroundSuccessful immunotherapy will require alteration of the tumour microenvironment and/or decreased immune suppression. Tumour-associated macrophages (TAMs) are one major factor affecting tumour microenvironment. We hypothesised that altering TAM phenotype would augment the efficacy of immunotherapy.

methodsWe and others have reported that 5,6-Dimethylxanthenone-4-acetic-acid (DMXAA, Vadimezan) has the ability to change TAM phenotypes, inducing a tumour microenvironment conducive to antitumour immune responses. We therefore combined DMXAA with active immunotherapies, and evaluated anti-tumour efficacy, immune cell phenotypes (flow cytometry), and tumour microenvironment (RT-PCR).

resultsIn several different murine models of immunotherapy for lung cancer, DMXAA-induced macrophage activation significantly augmented the therapeutic effects of immunotherapy. By increasing influx of neutrophils and anti-tumour (M1) macrophages to the tumour, DMXAA altered myeloid cell phenotypes, thus changing the intratumoural M2/non-M2 TAM immunoinhibitory ratio. It also altered the tumour microenvironment to be more pro-inflammatory. Modulating macrophages during immunotherapy resulted in increased numbers, activity, and antigen-specificity of intratumoural CD8(+) T cells. Macrophage depletion reduced the effect of combining immunotherapy with macrophage activation, supporting the importance of TAMs in the combined effect.

conclusionModulating intratumoural macrophages dramatically augmented the effect of immunotherapy. Our observations suggest that addition of agents that activate TAMs to immunotherapy should be considered in future trials.

Indexed as

ImmunotherapyAdenocarcinoma, Bronchiolo-AlveolarAnimalsAntineoplastic AgentsCarcinoma, Lewis LungCD8-Positive T-LymphocytesCombined Modality TherapyFemaleLung NeoplasmsMacrophage ActivationMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMyeloid CellsNeutrophilsAntineoplastic AgentsvadimezanXanthones

Identifiers

PMID23481183
PMCPMC3619255
OpenAlexW2079588331

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.