Evidence map›Paper›PMID 18317452›Full record

ReviewOncogene2008

Immune escape as a fundamental trait of cancer: focus on IDO.

G C Prendergast

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

159 citing papers in PubMed, 324 citations in OpenAlex.

  1. Article
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  10. The Functions and Mechanisms of Long Non-coding RNA SNHGs in Gastric Cancer.Combinatorial chemistry & high throughput screening · 2024
    Review
  11. Review
  12. A novel immunogenomic classification for prognosis in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2023
    Article
  13. Review
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99 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

1 author at 1 institution in 1 country.

G C PrendergastLankenau Institute for Medical Research, Wynnewood, PA 19096, USA. prendergast@limr.org
Lankenau Institute for Medical Research · US

Funding

ROLE OF RHO IN FARNESYLTRANSFERASE INHIBITOR RESPONSESR01CA082222 · NCI · WISTAR INSTITUTE · PI PRENDERGAST, GEORGE C · 1999 to 2008
$2.4M
IDO Inhibitors for Combinatorial Cancer TherapyR01CA109542 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2005 to 2015
$2.0M
RhoB Signaling in Cancer Suppression and Cell SuicideR01CA100123 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2003 to 2007
$1.7M
NCI NIH HHS R01 CA100123NCI NIH HHS R01 CA109542NCI NIH HHS R01 CA82222
6 · The paper itself

Abstract

Immune escape is a critical gateway to malignancy. The emergence of this fundamental trait of cancer represents the defeat of immune surveillance, a potent, multi-armed and essential mode of cancer suppression that may influence the ultimate clinical impact of an early stage tumor. Indeed, immune escape may be a central modifier of clinical outcomes, by affecting tumor dormancy versus progression, licensing invasion and metastasis and impacting therapeutic response. Although relatively little studied until recently, immune suppression and escape in tumors are now hot areas with clinical translation of several new therapeutic agents already under way. The interconnections between signaling pathways that control immune escape and those that control proliferation, senescence, apoptosis, metabolic alterations, angiogenesis, invasion and metastasis remain virtually unexplored, offering rich new areas for investigation. Here, an overview of this area is provided with a focus on the tryptophan catabolic enzyme indoleamine 2,3-dioxygenase (IDO) and its recently discovered relative IDO2 that are implicated in suppressing T-cell immunity in normal and pathological settings including cancer. Emerging evidence suggests that during cancer progression activation of the IDO pathway might act as a preferred nodal modifier pathway for immune escape, for example analogous to the PI3K pathway for survival or the VEGF pathway for angiogenesis. Small molecule inhibitors of IDO and IDO2 heighten chemotherapeutic efficacy in mouse models of cancer in a nontoxic fashion and an initial lead compound entered phase I clinical trials in late 2007. New modalities in this area offer promising ways to broaden the combinatorial attack on advanced cancers, where immune escape mechanisms likely provide pivotal support.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingCell ProliferationDisease ProgressionHumansImmunotherapyIndoleamine-Pyrrole 2,3,-DioxygenaseModels, BiologicalNeoplasmsNuclear ProteinsPhosphatidylinositol 3-KinasesPolymorphism, GeneticSignal TransductionTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBIN1 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseNuclear ProteinsPhosphatidylinositol 3-KinasesTumor Suppressor Proteins

Identifiers

PMID18317452
OpenAlexW2094530868

What OpenQuestion holds

Textmetadata
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.