Evidence map›Paper›PMID 27191891›Full record

ReviewOncotarget2016

SETD2: an epigenetic modifier with tumor suppressor functionality.

Jun Li, Gerben Duns, Helga Westers, Rolf Sijmons, Anke van den Berg, Klaas Kok

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

100 citing papers in PubMed, 166 citations in OpenAlex.

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  8. Enhancing titers of therapeutic lentiviral vectors using PKC agonists.Molecular therapy. Methods & clinical development · 2025
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  19. A prognosis prediction chromatin regulator signature for patients with severe asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
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40 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

6 authors at 3 institutions in 2 countries.

Jun LiDepartment of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands.
Gerben DunsGenome Sciences Centre, British Columbia Cancer Agency, Vancouver, Canada.
Helga WestersDepartment of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands.
Rolf SijmonsDepartment of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands.
Anke van den BergDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, The Netherlands.
Klaas KokDepartment of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands.
University of Groningen · NLUniversity Medical Center Groningen · NLBC Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the past decade important progress has been made in our understanding of the epigenetic regulatory machinery. It has become clear that genetic aberrations in multiple epigenetic modifier proteins are associated with various types of cancer. Moreover, targeting the epigenome has emerged as a novel tool to treat cancer patients. Recently, the first drugs have been reported that specifically target SETD2-negative tumors. In this review we discuss the studies on the associated protein, Set domain containing 2 (SETD2), a histone modifier for which mutations have only recently been associated with cancer development. Our review starts with the structural characteristics of SETD2 and extends to its corresponding function by combining studies on SETD2 function in yeast, Drosophila, Caenorhabditis elegans, mice, and humans. SETD2 is now generally known as the single human gene responsible for trimethylation of lysine 36 of Histone H3 (H3K36). H3K36me3 readers that recruit protein complexes to carry out specific processes, including transcription elongation, RNA processing, and DNA repair, determine the impact of this histone modification. Finally, we describe the prevalence of SETD2-inactivating mutations in cancer, with the highest frequency in clear cell Renal Cell Cancer, and explore how SETD2-inactivation might contribute to tumor development.

Indexed as

Epigenesis, GeneticGenes, Tumor SuppressorAnimalsCaenorhabditis elegansChromosome AberrationsDrosophila melanogasterGenome, HumanHistone-Lysine N-MethyltransferaseHistonesHumansMiceMice, KnockoutMutationNeoplasmsProtein DomainsSignal TransductionHistone-Lysine N-MethyltransferaseHistonesSETD2 protein, humanccRCCH3K36me3histone modificationSETD2tumor suppressor gene

Identifiers

PMID27191891
PMCPMC5226616
OpenAlexW2361260139

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.