Evidence map›Paper›PMID 24711084›Full record

ReviewCancer immunology, immunotherapy : CII2014

Indoleamine 2,3-dioxygenase pathways of pathogenic inflammation and immune escape in cancer.

George C Prendergast, Courtney Smith, Sunil Thomas, Laura Mandik-Nayak, Lisa Laury-Kleintop, Richard Metz, Alexander J Muller

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed, 1 pooled it
10.9field-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

265 citing papers in PubMed, 1 synthesis or guideline pooled it, 486 citations in OpenAlex.

  1. Pooled it
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  5. CD8Science China. Life sciences · 2026
    Review
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  20. PTPN2 Negatively Regulates Macrophage Immune Responses and Cellular Bioenergetics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article

205 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 4 institutions in 1 country.

George C PrendergastLankenau Institute for Medical Research (LIMR), 100 Lancaster Avenue, Wynnewood, PA, 19096, USA, prendergast@limr.org.
Courtney Smith
Sunil Thomas
Laura Mandik-Nayak
Lisa Laury-Kleintop
Richard Metz
Alexander J Muller
Lankenau Institute for Medical Research · USNewLink Genetics (United States) · USSidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

IDO Inhibitors for Combinatorial Cancer TherapyR01CA109542 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2005 to 2015
$2.0M
IDO2 Targeting for pancreatic cancer treatmentR21CA159337 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2011 to 2012
$401k
NCI NIH HHS R01 CA109542NCI NIH HHS R21 CA159337
6 · The paper itself

Abstract

Genetic and pharmacological studies of indoleamine 2,3-dioxygenase (IDO) have established this tryptophan catabolic enzyme as a central driver of malignant development and progression. IDO acts in tumor, stromal and immune cells to support pathogenic inflammatory processes that engender immune tolerance to tumor antigens. The multifaceted effects of IDO activation in cancer include the suppression of T and NK cells, the generation and activation of T regulatory cells and myeloid-derived suppressor cells, and the promotion of tumor angiogenesis. Mechanistic investigations have defined the aryl hydrocarbon receptor, the master metabolic regulator mTORC1 and the stress kinase Gcn2 as key effector signaling elements for IDO, which also exerts a non-catalytic role in TGF-β signaling. Small-molecule inhibitors of IDO exhibit anticancer activity and cooperate with immunotherapy, radiotherapy or chemotherapy to trigger rapid regression of aggressive tumors otherwise resistant to treatment. Notably, the dramatic antitumor activity of certain targeted therapeutics such as imatinib (Gleevec) in gastrointestinal stromal tumors has been traced in part to IDO downregulation. Further, antitumor responses to immune checkpoint inhibitors can be heightened safely by a clinical lead inhibitor of the IDO pathway that relieves IDO-mediated suppression of mTORC1 in T cells. In this personal perspective on IDO as a nodal mediator of pathogenic inflammation and immune escape in cancer, we provide a conceptual foundation for the clinical development of IDO inhibitors as a novel class of immunomodulators with broad application in the treatment of advanced human cancer.

Indexed as

Tumor EscapeAnimalsHumansImmune ToleranceImmunotherapyIndoleamine-Pyrrole 2,3,-DioxygenaseInflammationNeoplasmsSignal TransductionIndoleamine-Pyrrole 2,3,-Dioxygenase

Identifiers

PMID24711084
PMCPMC4384696
OpenAlexW2075094265

What OpenQuestion holds

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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.