Evidence map›Paper›PMID 32203145›Full record

ArticleLeukemia2021

Ectonucleotidase CD39 is highly expressed on ATLL cells and is responsible for their immunosuppressive function.

Yasuhiro Nagate, Sachiko Ezoe, Jiro Fujita, Daisuke Okuzaki, Daisuke Motooka, Tomohiko Ishibashi, Michiko Ichii, Akira Tanimura, Masako Kurashige, Eiichi Morii and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  13. Advancing to the era of cancer immunotherapy.Cancer communications (London, England) · 2021
    Review
  14. Article
  15. ATP and cancer immunosurveillance.The EMBO journal · 2021
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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

16 authors at 5 institutions in 1 country.

Yasuhiro NagateDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Sachiko EzoeDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan. sezoe@bldon.med.osaka-u.ac.jp.
Jiro FujitaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0002-4552-783X
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Tomohiko IshibashiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Michiko IchiiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Akira TanimuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Masako KurashigeDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka University, Suita, Japan.
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka University, Suita, Japan.
Takuya FukushimaLaboratory of Hematoimmunology, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, Nishihara, Japan.
Youko SuehiroDepartment of Hematology, National Kyushu Cancer, Fukuoka, Japan.
Takafumi YokotaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Hirohiko ShibayamaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Kenji OritaniDepartment of Hematology, Graduate School of Medical Sciences, International University of Health and Welfare Hospital, Narita, Japan.
Yuzuru KanakuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
The University of Osaka · JPInternational University of Health and Welfare · JPNational Cerebral and Cardiovascular Center · JPNational Hospital Organization Kyushu Cancer Center · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult T-cell leukemia/lymphoma (ATLL) patients have an extremely poor prognosis, partly due to their immunosuppressive state. The majority of ATLL patients have leukemic cells with phenotype similar to Tregs, prompting suggestions that ATLL cells themselves have immunosuppressive functions. In this study, we detected CD39 expression on ATLL cells, particularly frequent on aggressive subtypes. CD39 and CD73 convert extracellular adenosine triphosphate (ATP) into adenosine, a key player in Tregs' immunosuppression. In vitro culture, both CD39

Indexed as

Gene Expression Regulation, LeukemicAdenosine TriphosphateAnimalsAntigens, CDApyraseBiomarkersCell Line, TumorDisease Models, AnimalGene Expression ProfilingGene Knockdown TechniquesHeterograftsHigh-Throughput Nucleotide SequencingHumansImmune ToleranceImmunomodulationImmunophenotypingAdenosine TriphosphateAntigens, CDApyraseBiomarkersCD39 antigen

Identifiers

PMID32203145
PMCPMC7787980
OpenAlexW3010870074

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.