Evidence map›Paper›PMID 20028856›Full record

ArticleCancer research2010

CCL2 blockade augments cancer immunotherapy.

Zvi G Fridlender, George Buchlis, Veena Kapoor, Guanjun Cheng, Jing Sun, Sunil Singhal, M Cecilia Crisanti, Cecilia Crisanti, Liang-Chuan S Wang, Daniel Heitjan and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

114 citing papers in PubMed, 185 citations in OpenAlex.

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54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
    Crisanti, Cecilia [corrected to Crisanti, M Cecilia]
5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Zvi G FridlenderThoracic Oncology Research Laboratory and Department of Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160, USA. gfrid@mail.med.upenn.edu
George Buchlis
Veena Kapoor
Guanjun Cheng
Jing Sun
Sunil Singhal
M Cecilia Crisanti
Cecilia Crisanti
Liang-Chuan S Wang
Daniel Heitjan
Linda A Snyder
Steven M Albelda
University of Pennsylvania · US

Funding

VECTOR DEVELOPMENT /PRECLINICAL TESTINGP01CA066726 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KALOS, MICHAEL D · 1995 to 2016
$18.2M
TRAINING IN PULMONARY IMMUNOLOGYT32HL007586 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MEYER, NUALA JENNINGS · 1985 to 2025
$8.8M
NCI NIH HHS P01 CA066726NCI NIH HHS P01 CA 66726NHLBI NIH HHS T32 HL007586
6 · The paper itself

Abstract

Altering the immunosuppressive microenvironment that exists within a tumor will likely be necessary for cancer vaccines to trigger an effective antitumor response. Monocyte chemoattractant proteins (such as CCL2) are produced by many tumors and have both direct and indirect immunoinhibitory effects. We hypothesized that CCL2 blockade would reduce immunosuppression and augment vaccine immunotherapy. Anti-murine CCL2/CCL12 monoclonal antibodies were administered in three immunotherapy models: one aimed at the human papillomavirus E7 antigen expressed by a non-small cell lung cancer (NSCLC) line, one targeted to mesothelin expressed by a mesothelioma cell line, and one using an adenovirus-expressing IFN-alpha to treat a nonimmunogenic NSCLC line. We evaluated the effect of the combination treatment on tumor growth and assessed the mechanism of these changes by evaluating cytotoxic T cells, immunosuppressive cells, and the tumor microenvironment. Administration of anti-CCL2/CCL12 antibodies along with the vaccines markedly augmented efficacy with enhanced reduction in tumor volume and cures of approximately half of the tumors. The combined treatment generated more total intratumoral CD8+ T cells that were more activated and more antitumor antigen-specific, as measured by tetramer evaluation. Another important potential mechanism was reduction in intratumoral T regulatory cells. CCL2 seems to be a key proximal cytokine mediating immunosuppression in tumors. Its blockade augments CD8+ T-cell immune response to tumors elicited by vaccines via multifactorial mechanisms. These observations suggest that combining CCL2 neutralization with vaccines should be considered in future immunotherapy trials.

Indexed as

AnimalsAntibodies, MonoclonalChemokine CCL2FemaleFlow CytometryImmunotherapyLymphocytes, Tumor-InfiltratingMesothelinMiceMonocyte Chemoattractant ProteinsNeoplasms, ExperimentalReverse Transcriptase Polymerase Chain ReactionT-LymphocytesT-Lymphocyte SubsetsAntibodies, MonoclonalCcl12 protein, mouseCcl2 protein, mouseChemokine CCL2MesothelinMonocyte Chemoattractant ProteinsMsln protein, mouse

Identifiers

PMID20028856
PMCPMC2821565
OpenAlexW1973759139

What OpenQuestion holds

Textmetadata
LicenceTDM
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.