Evidence map›Paper›PMID 26751963›Full record

ReviewCancer science2016

Dysregulation of protein methyltransferases in human cancer: An emerging target class for anticancer therapy.

Ryuji Hamamoto, Yusuke Nakamura

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 80 citations in OpenAlex.

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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.

Ryuji HamamotoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
Yusuke NakamuraSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
University of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein methylation is one of the important post-translational modifications. Although its biological and physiological functions were unknown for a long time, we and others have characterized a number of protein methyltransferases, which have unveiled the critical functions of protein methylation in various cellular processes, in particular, in epigenetic regulation. In addition, it had been believed that protein methylation is an irreversible phenomenon, but through identification of a variety of protein demethylases, protein methylation is now considered to be dynamically regulated similar to protein phosphorylation. A large amount of evidence indicated that protein methylation has a pivotal role in post-translational modification of histone proteins as well as non-histone proteins and is involved in various processes of cancer development and progression. As dysregulation of this modification has been observed frequently in various types of cancer, small-molecule inhibitors targeting protein methyltransferases and demethylases have been actively developed as anticancer drugs; clinical trials for some of these drugs have already begun. In this review, we discuss the biological and physiological importance of protein methylation in human cancer, especially focusing on the significance of protein methyltransferases as emerging targets for anticancer therapy.

Indexed as

MethylationMolecular Targeted TherapyAntineoplastic AgentsEpigenesis, GeneticHistonesHumansNeoplasmsProtein MethyltransferasesProtein Processing, Post-TranslationalAntineoplastic AgentsHistonesProtein MethyltransferasesAnticancer drugarginine methylationepigeneticslysine methylationpost-translational modification

Identifiers

PMID26751963
PMCPMC4832871
OpenAlexW2229161608

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.