Evidence map›Paper›PMID 27063195›Full record

ReviewPigment cell & melanoma research2016

EZH2 as a mediator of treatment resistance in melanoma.

Jessamy C Tiffen, Stuart J Gallagher, Hsin-Yi Tseng, Fabian V Filipp, Barbara Fazekas de St. Groth, Peter Hersey

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pigment cell & melanoma research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. X and Y Differences in Melanoma Survival Between the Sexes.Pigment cell & melanoma research · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.JID innovations : skin science from molecules to population health · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

6 authors at 3 institutions in 2 countries.

Jessamy C TiffenMelanoma Immunology and Oncology Group, The Centenary Institute, University of Sydney, Camperdown, NSW, Australia.
Stuart J GallagherMelanoma Immunology and Oncology Group, The Centenary Institute, University of Sydney, Camperdown, NSW, Australia.
Hsin-Yi TsengMelanoma Immunology and Oncology Group, The Centenary Institute, University of Sydney, Camperdown, NSW, Australia.
Fabian V FilippSystems Biology and Cancer Metabolism, Program for Quantitative Systems Biology, University of California Merced, Merced, CA, USA.
Barbara Fazekas de St. GrothT Cell Biology Program, The Centenary Institute, University of Sydney, Camperdown, NSW, Australia.
Peter HerseyMelanoma Immunology and Oncology Group, The Centenary Institute, University of Sydney, Camperdown, NSW, Australia. peter.hersey@centenary.org.au.
University of Sydney · AUCentenary Institute · AUUniversity of California, Merced · US

Funding

Tumor pyruvate kinase as key regulator of cancer metabolismR00CA154887 · NCI · UNIVERSITY OF CALIFORNIA, MERCED · PI FILIPP, FABIAN VOLKER · 2012 to 2014
$725k
Tumor pyruvate kinase as key regulator of cancer metabolismK99CA154887 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FILIPP, FABIAN VOLKER · 2011 to 2012
$177k
NCI NIH HHS K99 CA154887NCI NIH HHS R00 CA154887
6 · The paper itself

Abstract

Direct treatments of cancer such as chemotherapy, radiotherapy and targeted therapy have been shown to depend on recruitment of the immune system for their effectiveness. Recent studies have shown that development of resistance to direct therapies such as BRAF inhibitors in melanoma is associated with suppression of immune responses. We point to emerging data that implicate activation of the polycomb repressive complex 2 (PRC2) and its catalytic component-enhancer of zeste homolog 2 (EZH2)-in progression of melanoma and suppression of immune responses. EZH2 appears to have an important role in differentiation of CD4 T cells and particularly in the function of T regulatory cells, which suppress immune responses to melanoma. We review mechanisms of EZH2 activation at the genomic level and from activation of the MAP kinase, E2F or NF-kB2 pathways. These studies are consistent with activation of EZH2 as a common mechanism for induction of immune suppression in patients failing direct therapies and suggest EZH2 inhibitors may have a role in combination with immunotherapy and targeted therapies to prevent development of immunosuppression.

Indexed as

Epigenesis, GeneticDrug Resistance, NeoplasmEnhancer of Zeste Homolog 2 ProteinHumansMelanomaEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanenhancer of zeste homolog 2epigeneticimmune suppressionmelanomatreatment resistance

Identifiers

PMID27063195
PMCPMC5021620
OpenAlexW2326014866

What OpenQuestion holds

Textmetadata
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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.