Evidence map›Paper›PMID 27717710›Full record

ReviewMolecular oncology2016

Dysregulation of histone methyltransferases in breast cancer - Opportunities for new targeted therapies?

Ewa M Michalak, Jane E Visvader

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

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  13. DOT1L Is a Novel Cancer Stem Cell Target for Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    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

2 authors at 1 institution in 1 country.

Ewa M MichalakACRF Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: michalak@wehi.edu.au.
Jane E VisvaderACRF Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: visvader@wehi.edu.au.
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone methyltransferases (HMTs) catalyze the methylation of lysine and arginine residues on histone tails and non-histone targets. These important post-translational modifications are exquisitely regulated and affect chromatin compaction and transcriptional programs leading to diverse biological outcomes. There is accumulating evidence that genetic alterations of several HMTs impinge on oncogenic or tumor-suppressor functions and influence both cancer initiation and progression. HMTs therefore represent an opportunity for therapeutic targeting in those patients with tumors in which HMTs are dysregulated, to reverse the histone marks and transcriptional programs associated with aggressive tumor behavior. In this review, we describe the known histone methyltransferases and their emerging roles in breast cancer tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsBreastBreast NeoplasmsDrug DiscoveryEnzyme InhibitorsEpigenesis, GeneticFemaleHistone CodeHistone-Lysine N-MethyltransferaseHumansMolecular Targeted TherapyProtein-Arginine N-MethyltransferasesTranscriptional ActivationAntineoplastic AgentsEnzyme InhibitorsHistone-Lysine N-MethyltransferaseProtein-Arginine N-MethyltransferasesBreast cancerChromatinHistone methyltransferaseInhibitorsTranscription

Identifiers

PMID27717710
PMCPMC5423136
OpenAlexW2523679195

What OpenQuestion holds

Textmetadata
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.