Evidence map›Paper›PMID 29746927›Full record

ArticleCancer letters2018

Indoleamine 2,3-dioxygenase 1 inhibition targets anti-PD1-resistant lung tumors by blocking myeloid-derived suppressor cells.

Ailin Li, Hampartsoum B Barsoumian, Jonathan E Schoenhals, Taylor R Cushman, Mauricio S Caetano, Xiaohong Wang, David R Valdecanas, Sharareh Niknam, Ahmed I Younes, Guang Li and 3 more

Abstract read
In one paragraph

Article in Cancer letters, 2018. 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
3.5field-weighted citation impact, top 7% 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, 91 citations in OpenAlex.

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  12. The significant role of amino acid metabolic reprogramming in cancer.Cell communication and signaling : CCS · 2024
    Review
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  18. [Advances of Immunotherapy Resistance and Coping Strategies 
in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Review
  19. Article
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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

13 authors at 2 institutions in 2 countries.

Ailin LiDepartment of Radiation Oncology, The First Hospital of China Medical University, China.
Hampartsoum B BarsoumianDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Jonathan E SchoenhalsDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Taylor R CushmanDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Mauricio S CaetanoDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Xiaohong WangDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
David R ValdecanasDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Sharareh NiknamDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Ahmed I YounesDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Guang LiDepartment of Radiation Oncology, The First Hospital of China Medical University, China.
Wendy A WoodwardDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
Maria Angelica CortezDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA.
James W WelshDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, USA. Electronic address: jwelsh@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USFirst Hospital of China Medical University · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Indoleamine 2,3-dioxygenase 1 (IDO1), involved in the catabolism of tryptophan (Trp) to kynurenine (Kyn) is an important regulator of tumor-mediated immunosuppression implicated in resistance to anti-PD1 immunotherapy. We investigated the role of IDO1 in an anti-PD1-resistant lung cancer model (344SQ_R) compared to the parental 344SQ tumors (344SQ_P). IDO1 was overexpressed in tumor-infiltrating leukocytes, and plasma Kyn levels were increased, in 344SQ_R vs. 344SQ_P. The IDO1 inhibitor INCB023843 retarded tumor growth and reduced lung metastases in 344SQ_R. IDO1 was expressed at higher levels in F4/80

Indexed as

AnimalsCell Line, TumorEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticImmunosuppression TherapyImmunosuppressive AgentsIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineLung NeoplasmsMiceMyeloid-Derived Suppressor CellsNeoplasm TransplantationTryptophanTumor MicroenvironmentEnzyme InhibitorsImmunosuppressive AgentsIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineTryptophanAnti-PD1 resistanceIDO1ImmunotherapyLung cancerMyeloid-derived suppressor cells

Identifiers

PMID29746927
PMCPMC6027590
OpenAlexW2800712256

What OpenQuestion holds

Textmetadata
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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.