Evidence map›Paper›PMID 31444833›Full record

ArticleCancer science2019

Indoleamine 2,3-dioxygenase 2 depletion suppresses tumor growth in a mouse model of Lewis lung carcinoma.

Wakana Yamasuge, Yasuko Yamamoto, Hidetsugu Fujigaki, Masato Hoshi, Kentaro Nakamoto, Kazuo Kunisawa, Akihiro Mouri, Toshitaka Nabeshima, Kuniaki Saito

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. 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
1.2field-weighted citation impact, top 24% 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, 31 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

9 authors at 1 institution in 1 country.

Wakana YamasugeDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.
Yasuko YamamotoDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.ORCID https://orcid.org/0000-0001-8825-9188
Hidetsugu FujigakiDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.
Masato HoshiDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.
Kentaro NakamotoDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.
Kazuo KunisawaGraduate School of Health Sciences, Advanced Diagnostic System Research Laboratory, Fujita Health University, Toyoake, Japan.
Akihiro MouriDepartment of Regulatory Science, Graduate School of Health Sciences, Fujita Health University, Toyoake, Japan.
Toshitaka NabeshimaGraduate School of Health Sciences, Advanced Diagnostic System Research Laboratory, Fujita Health University, Toyoake, Japan.
Kuniaki SaitoDepartment of Disease Control and Prevention, Fujita Health University Graduate School of Health Sciences, Toyoake, Japan.
Fujita Health University · JP

Funding

Japan Society for the Promotion of Science 15H03086 (KS), 17H04252 (TN), and 17H07222 (YY)Private University Research Branding Project from the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT)
6 · The paper itself

Abstract

Tryptophan metabolism is important to induce immune tolerance in tumors. To date, 3 types of tryptophan-metabolizing enzymes have been identified: indoleamine 2,3-dioxygenase 1 and 2 (IDO1 and IDO2) and tryptophan 2,3-dioxygenase 2. Numerous studies have focused on IDO1 as its expression is enhanced in various cancers. Recently, IDO2 has been identified as a tryptophan-metabolizing enzyme that is involved in several immune functions and expressed in cancers such as pancreatic cancer. However, the biological role of IDO2 in the induction of immune tolerance in tumors has not yet been reported. In the present study, we examined the effects of Ido2 depletion on tumor growth in a mouse model of Lewis lung carcinoma by using Ido2-knockout mice. Ido2-knockout mice had reduced tumor volumes compared to WT mice. Furthermore, Ido2 depletion altered the tumor microenvironment, such as tryptophan accumulation and kynurenine reduction, leading to enhancement of immune cell invasion. Finally, enzyme-linked immunospot assay revealed that Ido2 depletion enhanced γ-interferon secretion in the tumor. In conclusion, Ido2 is an important immune regulator in the tumor microenvironment. Our data indicate that IDO2 is a potential target for cancer treatment and drug development.

Indexed as

AnimalsCarcinoma, Lewis LungCell Line, TumorGene Knockout TechniquesIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaKynurenineMaleMiceTryptophanTumor BurdenTumor EscapeTumor MicroenvironmentXenograft Model Antitumor AssaysIDO2 protein, mouseIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaKynurenineTryptophanIDO2immune toleranceinterferon gammakynureninetryptophan metabolism

Identifiers

PMID31444833
PMCPMC6778659
OpenAlexW2969272535

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.