Evidence map›Paper›PMID 26822709›Full record

ReviewCytokine2017

Anti-metastatic functions of type 1 interferons: Foundation for the adjuvant therapy of cancer.

Angélica Ortiz, Serge Y Fuchs

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Malignancy in Idiopathic Inflammatory Myopathies: Recent Insights.Clinical reviews in allergy & immunology · 2025
    Review
  5. Review
  6. Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Metastatic triple negative breast cancer adapts its metabolism to destination tissues while retaining key metabolic signatures.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Extracellular vesicles in cancer progression.Seminars in cancer biology · 2021
    Review
  13. Review
  14. Molecular therapy oncolytics · 2020
    Article
  15. Article
  16. Article
  17. My journey from tyrosine phosphorylation inhibitors to targeted immune therapy as strategies to combat cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Angélica OrtizDepartment of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: anortiz@vet.upenn.edu.
Serge Y FuchsDepartment of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: syfuchs@vet.upenn.edu.
University of Pennsylvania · US

Funding

UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DIEHL, JOHN ALAN · 2013 to 2023
$10.9M
Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
NCI NIH HHS P01 CA165997NCI NIH HHS R01 CA092900
6 · The paper itself

Abstract

The anti-tumorigenic effects that type 1 interferons (IFN1) elicited in the in vitro studies prompted consideration of IFN1 as a potent candidate for clinical treatment. Though not all patients responded to IFN1, clinical trials have shown that patients with high risk melanoma, a highly refractory solid malignancy, benefit greatly from intermediate IFN1 treatment in regards to relapse-free and distant-metastasis-free survival. The mechanisms by which IFN1 treatment at early stages of disease suppress tumor recurrence or metastatic incidence are not fully understood. Intracellular IFN1 signaling is known to affect cell differentiation, proliferation, and apoptosis. Moreover, recent studies have revealed specific IFN1-regulated genes that may contribute to IFN1-mediated suppression of cancer progression and metastasis. In concert, expression of these different IFN1 stimulated genes may impede numerous mechanisms that mediate metastatic process. Though, IFN1 treatment is still utilized as part of standard care for metastatic melanoma (alone or in combination with other therapies), cancers find the ways to develop insensitivity to IFN1 treatment allowing for unconstrained disease progression. To determine how and when IFN1 treatment would be most efficacious during disease progression, we must understand how IFN1 signaling affects different metastasis steps. Here, we specifically focus on the anti-metastatic role of endogenous IFN1 and parameters that may help to use pharmaceutical IFN1 in the adjuvant treatment to prevent cancer recurrence and metastatic disease.

Indexed as

AnimalsApoptosisCell DifferentiationHumansInterferon Type IMelanomaNeoplasm MetastasisSignal TransductionInterferon Type ICancer metastasisColonizationInterferonInvasion

Identifiers

PMID26822709
PMCPMC4959969
OpenAlexW2251798475

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.