Evidence map›Paper›PMID 24982761›Full record

ArticleJournal for immunotherapy of cancer2014

Combination therapy targeting toll like receptors 7, 8 and 9 eliminates large established tumors.

By Gan Zhao, John P Vasilakos, Debra Tross, Dmitri Smirnov, Dennis M Klinman

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-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

43 citing papers in PubMed, 79 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

By Gan ZhaoCancer and Inflammation Program, National Cancer Institute, NIH, Frederick MD 21702, USA.
John P Vasilakos3M Drug Delivery Systems Division, St. Paul MN 55144, USA.
Debra TrossCancer and Inflammation Program, National Cancer Institute, NIH, Frederick MD 21702, USA.
Dmitri Smirnov3M Drug Delivery Systems Division, St. Paul MN 55144, USA.
Dennis M KlinmanCancer and Inflammation Program, National Cancer Institute, NIH, Frederick MD 21702, USA.
National Cancer Institute · MYKindeva Drug Delivery (United States) · US

Funding

Mechanism of action and therapeutic utility of stimulatory CpG oligonucleotidesZIABC010852 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KLINMAN, DENNIS · 2009 to 2019
$11.3M
6 · The paper itself

Abstract

backgroundThe TLR7/8 agonist 3M-052 and the TLR9 agonist CpG ODN both trigger innate immune responses that support the induction of tumor-specific immunity. Previous studies showed that these agonists used individually could improve the survival of mice challenged with small tumors but were of limited therapeutic benefit against large/advanced tumors.

methodsNormal mice were challenged with syngeneic tumors. Once these tumors reached clinically detectable size (500-800 mm(3)) they were treated by intra-tumoral injection with 3M-052 and/or CpG ODN. Anti-tumor immunity and tumor growth were evaluated.

resultsThe co-delivery of agonists targeting TLRs 7, 8 and 9 increased the number and tumoricidal activity of tumor infiltrating CTL and NK cells while reducing the frequency of immunosuppressive MDSC. The combination of 3M-052 plus CpG ODN (but not each agent alone) eradicated large primary tumors and established long-term protective immunity.

conclusionThe combination of agonists targeting TLRs 7/8 and 9 represents a significant improvement in cancer immunotherapy.

Indexed as

CancerCpG ODNInnate immunityTherapyTLR agonists

Identifiers

PMID24982761
PMCPMC4075973
OpenAlexW2105757811

What OpenQuestion holds

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LicenceCC BY
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.