Evidence map›Paper›PMID 20179192›Full record

ArticleCancer research2010

CD73 on tumor cells impairs antitumor T-cell responses: a novel mechanism of tumor-induced immune suppression.

Dachuan Jin, Jie Fan, Long Wang, Linda F Thompson, Aijie Liu, Benjamin J Daniel, Tahiro Shin, Tyler J Curiel, Bin Zhang

Open 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. Cited by 246 papers.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed
18.0field-weighted citation impact, top 1% 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

246 citing papers in PubMed, 434 citations in OpenAlex.

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  15. Insights from Clinical Trials on AACS pharmacology & translational science · 2025
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186 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Dachuan JinCancer Therapy and Research Center, Department of Medicine, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
Jie Fan
Long Wang
Linda F Thompson
Aijie Liu
Benjamin J Daniel
Tahiro Shin
Tyler J Curiel
Bin Zhang
Oklahoma Medical Research Foundation · USThe University of Texas Health Science Center at San Antonio · US

Funding

INSTITUTE FOR INTEGRATION OF MEDICINE & SCIENCE: A PARTNERSHIP TO IMPROVE HEALTHUL1RR025767 · NCRR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2008 to 2011
$23.8M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR000149 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2012 to 2013
$6.8M
The Regulation of Inflammatory Responses by CD73R01AI018220 · NIAID · SCRIPPS CLINIC AND RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 1985 to 2012
$3.1M
CD73 and Tumor Immunity-CD73 and CTLA-4 combination Blockade in Ovarian CancerR01CA149669 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZHANG, BIN · 2011 to 2015
$1.7M
NCATS NIH HHS UL1 TR000149NCI NIH HHS R01 CA149669NCRR NIH HHS UL1 RR025767NIAID NIH HHS R01 AI018220
6 · The paper itself

Abstract

CD73, originally defined as a lymphocyte differentiation antigen, is thought to function as a cosignaling molecule on T lymphocytes and an adhesion molecule that is required for lymphocyte binding to endothelium. We show here that CD73 is widely expressed on many tumor cell lines and is upregulated in cancerous tissues. Because the ecto-5'-nucleotidase activity of CD73 catalyzes AMP breakdown to immunosuppressive adenosine, we hypothesized that CD73-generated adenosine prevents tumor destruction by inhibiting antitumor immunity. We confirmed this hypothesis by showing that combining tumor CD73 knockdown and tumor-specific T-cell transfer cured all tumor-bearing mice. In striking contrast, there was no therapeutic benefit of adoptive T-cell immunotherapy in mice bearing tumors without CD73 knockdown. Moreover, blockade of the A2A adenosine receptor with a selective antagonist also augmented the efficacy of adoptive T-cell therapy. These findings identify a potential mechanism for CD73-mediated tumor immune evasion and point to a novel cancer immunotherapy strategy by targeting the enzymatic activity of tumor CD73.

Indexed as

5'-NucleotidaseAdenosineAdenosine A2 Receptor AntagonistsAnimalsApoptosisFemaleFlow CytometryImmunotherapy, AdoptiveMiceMice, Inbred C57BLMice, KnockoutOvarian NeoplasmsPyrimidinesReceptor, Adenosine A2ARNA, Small InterferingT-Lymphocytes5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine5'-NucleotidaseAdenosineAdenosine A2 Receptor AntagonistsPyrimidinesReceptor, Adenosine A2ARNA, Small InterferingTriazoles

Identifiers

PMID20179192
PMCPMC2883609
OpenAlexW2102478114

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.