Evidence map›Paper›PMID 24787290›Full record

ReviewSeminars in oncology2014

Interferons and their stimulated genes in the tumor microenvironment.

Hyeonjoo Cheon, Ernest C Borden, George R Stark

Abstract readReview
In one paragraph

Review in Seminars in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

160 citing papers in PubMed, 257 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Interferon-Based Therapeutics in Cancer Therapy: Past, Present, and Future.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

100 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

3 authors at 2 institutions in 1 country.

Hyeonjoo CheonLerner Research Institute, Taussig Cancer Institute, and Case Comprehensive Cancer Center, Cleveland, OH. Electronic address: cheonh@ccf.org.
Ernest C BordenLerner Research Institute, Taussig Cancer Institute, and Case Comprehensive Cancer Center, Cleveland, OH.
George R StarkLerner Research Institute, Taussig Cancer Institute, and Case Comprehensive Cancer Center, Cleveland, OH.
Case Comprehensive Cancer CenterCleveland Clinic Lerner College of Medicine · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Amar Desai · 1987 to 2026
$142.3M
NCI NIH HHS P30 CA043703NCI NIH HHS P30CA043703
6 · The paper itself

Abstract

Constitutive expression of interferons (IFNs) and activation of their signaling pathways have pivotal roles in host responses to malignant cells in the tumor microenvironment. IFNs are induced by the innate immune system and in tumors through stimulation of Toll-like receptors (TLRs) and through other signaling pathways in response to specific cytokines. Although in the oncologic context IFNs have been thought of more as exogenous pharmaceuticals, the autocrine and paracrine actions of endogenous IFNs probably have even more critical effects on neoplastic disease outcomes. Through high-affinity cell surface receptors, IFNs modulate transcriptional signaling, leading to regulation of more than 2,000 genes with varying patterns of temporal expression. Induction of the gene products by both unphosphorylated and phosphorylated STAT1 after ligand binding results in alterations in tumor cell survival, inhibition of angiogenesis, and augmentation of actions of T, natural killer (NK), and dendritic cells. The interferon-stimulated gene (ISG) signature can be a favorable biomarker of immune response but, in a seemingly paradoxical finding, a specific subset of the full ISG signature indicates an unfavorable response to DNA-damaging interventions such as radiation. IFNs in the tumor microenvironment thus can alter the emergence, progression, and regression of malignancies.

Indexed as

Tumor MicroenvironmentAnimalsAntineoplastic AgentsApoptosisCytokinesDendritic CellsDNADNA DamageGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, p53HumansImmunity, InnateInterferonsMiceMice, TransgenicAntineoplastic AgentsCytokinesDNAInterferonsSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID24787290
PMCPMC4118773
OpenAlexW2128402485

What OpenQuestion holds

Textmetadata
LicenceTDM
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.