Evidence map›Paper›PMID 26385103›Full record

ReviewClinical & experimental metastasis2015

Targeting IL4/IL4R for the treatment of epithelial cancer metastasis.

Katherine Venmar Bankaitis, Barbara Fingleton

Open access · greenAbstract readReview
In one paragraph

Review in Clinical & experimental metastasis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Peptides as multifunctional players in cancer therapy.Experimental & molecular medicine · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

2 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

2 authors at 1 institution in 1 country.

Katherine Venmar BankaitisDepartment of Cancer Biology, Vanderbilt University, 771 PRB, 2220 Pierce Ave, Nashville, TN, 37233-6480, USA.
Barbara FingletonDepartment of Cancer Biology, Vanderbilt University, 771 PRB, 2220 Pierce Ave, Nashville, TN, 37233-6480, USA. barbara.fingleton@vanderbilt.edu.
Vanderbilt University · US

Funding

Epithelial IL4Ralpha Regulates Colon Tumor ProgressionR01CA157781 · NCI · VANDERBILT UNIVERSITY · PI FINGLETON, BARBARA · 2011 to 2015
$1.6M
IL4-Regulated Metabolic Changes Contribute to Metastatic CapabilityF31CA183539 · NCI · VANDERBILT UNIVERSITY · PI VENMAR, KATHERINE TAMARA · 2014 to 2015
$47k
NCI NIH HHS F31 CA183539NCI NIH HHS R01 CA157781
6 · The paper itself

Abstract

While progress has been made in treating primary epithelial tumors, metastatic tumors remain largely incurable and still account for 85-90 % of all cancer-related deaths. Interleukin-4 (IL4), a Th2 cytokine, and the IL4/IL4 receptor (IL4R) interaction have well defined roles in the immune system. Yet, IL4 receptors are over-expressed by many epithelial cancers and could be a promising target for metastatic tumor therapy. The IL4/IL4R signaling axis is a strong promoter of pro-metastatic phenotypes in epithelial cancer cells including enhanced migration, invasion, survival, and proliferation. The promotion of breast cancer growth specifically is also supported in part by IL4-induced glutamine metabolism, and we have shown that IL4 is also capable of inducing glucose metabolism in breast cancer cells. Importantly, there are several types of FDA approved medications for use in asthma patients that inhibit the IL4/IL4R signaling axis. However, these approved medications inhibit both the type I IL4 receptor found on immune cells, and the type II IL4 receptor that is predominantly expressed by some non-hematopoietic cells including epithelial cancer cells. This article reviews existing therapies targeting IL4, IL4R, or IL4/IL4R signaling, and recent findings guiding the creation of novel therapies that specifically inhibit the type II IL4R, while taking into consideration effects on immune cells within the tumor microenvironment. Some of these therapies are currently in clinical trials for cancer patients, and may be exploitable for the treatment of metastatic disease.

Indexed as

HumansInterleukin-4Janus Kinase 1Neoplasms, Glandular and EpithelialReceptors, Interleukin-4Signal TransductionSTAT6 Transcription FactorTumor MicroenvironmentInterleukin-4JAK1 protein, humanJanus Kinase 1Receptors, Interleukin-4STAT6 Transcription FactorCytokineIL4IL4 receptorMetastasisProliferationSurvival

Identifiers

PMID26385103
PMCPMC4651701
OpenAlexW2177617302

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.