Evidence map›Paper›PMID 36058143›Full record

ReviewCancer treatment reviews2022

Indoleamine 2,3-dioxygenase (IDO) inhibitors and cancer immunotherapy.

Yu Fujiwara, Shumei Kato, Mary K Nesline, Jeffrey M Conroy, Paul DePietro, Sarabjot Pabla, Razelle Kurzrock

Open access · greenAbstract readReview
In one paragraph

Review in Cancer treatment reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed, 1 pooled it
16.0field-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

204 citing papers in PubMed, 1 synthesis or guideline pooled it, 262 citations in OpenAlex.

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144 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

7 authors at 3 institutions in 1 country.

Yu FujiwaraDepartment of Medicine, Icahn School of Medicine at Mount Sinai, Mount Sinai Beth Israel, New York, NY, United States. Electronic address: yu.fujiwara@mountsinai.org.
Shumei KatoCenter for Personalized Cancer Therapy, University of California San Diego, Moores Cancer Center, La Jolla, CA, United States. Electronic address: smkato@health.ucsd.edu.
Mary K NeslineOmniSeq Inc., Buffalo, NY, United States.
Jeffrey M ConroyOmniSeq Inc., Buffalo, NY, United States.
Paul DePietroOmniSeq Inc., Buffalo, NY, United States.
Sarabjot PablaOmniSeq Inc., Buffalo, NY, United States.
Razelle KurzrockMCW Cancer Center and Genomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI, United States.
Medical College of Wisconsin · USMount Sinai Beth Israel · USUniversity of California, San Diego · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jesse Nodora · 1985 to 2026
$124.9M
NCI NIH HHS P30 CA023100
6 · The paper itself

Abstract

Strategies for unlocking immunosuppression in the tumor microenvironment have been investigated to overcome resistance to first-generation immune checkpoint blockade with anti- programmed cell death protein 1 (PD-1)/ programmed death-ligand 1 (PD-L1) and anti-cytotoxic T-lymphocyte associated protein 4 (CTLA-4) agents. Indoleamine 2,3-dioxygenase (IDO) 1, an enzyme catabolizing tryptophan to kynurenine, creates an immunosuppressive environment in preclinical studies. Early phase clinical trials investigating inhibition of IDO1, especially together with checkpoint blockade, provided promising results. Unfortunately, the phase 3 trial of the IDO1 inhibitor epacadostat combined with the PD-1 inhibitor pembrolizumab did not show clinical benefit when compared with pembrolizumab monotherapy in patients with advanced malignant melanoma, which dampened enthusiasm for IDO inhibitors. Even so, several molecules, such as the aryl hydrocarbon receptor and tryptophan 2,3-dioxygenase, were reported as additional potential targets for the modulation of the tryptophan pathway, which might enhance clinical effectiveness. Furthermore, the combination of IDO pathway blockade with agents inhibiting other signals, such as those generated by PIK3CA mutations that may accompany IDO1 upregulation, may be a novel way to enhance activity. Importantly, IDO1 expression level varies by tumor type and among patients with the same tumor type, suggesting that patient selection based on expression levels of IDO1 may be warranted in clinical trials.

Indexed as

Indoleamine-Pyrrole 2,3,-DioxygenaseMelanomaB7-H1 AntigenClass I Phosphatidylinositol 3-KinasesCTLA-4 AntigenEnzyme InhibitorsHumansImmune Checkpoint InhibitorsImmunotherapyKynurenineProgrammed Cell Death 1 ReceptorReceptors, Aryl HydrocarbonTryptophanTryptophan OxygenaseTumor MicroenvironmentB7-H1 AntigenClass I Phosphatidylinositol 3-KinasesCTLA-4 AntigenEnzyme InhibitorsImmune Checkpoint InhibitorsIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineProgrammed Cell Death 1 ReceptorReceptors, Aryl HydrocarbonTryptophanTryptophan Oxygenase3-dioxygenaseAryl hydrocarbon receptorImmune checkpoint inhibitorImmuno-oncologyImmunotherapyIndoleamine 2Precision medicine

Identifiers

PMID36058143
PMCPMC12187009
OpenAlexW4293581628

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.