Evidence map›Paper›PMID 31428579›Full record

ReviewFrontiers in oncology2019

The Emerging Role of H3K9me3 as a Potential Therapeutic Target in Acute Myeloid Leukemia.

Laura Monaghan, Matthew E Massett, Roderick P Bunschoten, Alex Hoose, Petrisor-Alin Pirvan, Robert M J Liskamp, Heather G Jørgensen, Xu Huang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 82 citations in OpenAlex.

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  11. Physical modeling of nucleosome clustering in euchromatin resulting from interactions between epigenetic reader proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Review
  13. InterpretingbioRxiv : the preprint server for biology · 2024
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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

8 authors at 1 institution in 1 country.

Laura MonaghanHaemato-Oncology/Systems Medicine Group, Paul O'Gorman Leukemia Research Center, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
Matthew E MassettHaemato-Oncology/Systems Medicine Group, Paul O'Gorman Leukemia Research Center, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
Roderick P BunschotenSchool of Chemistry, University of Glasgow, Glasgow, United Kingdom.
Alex HooseSchool of Chemistry, University of Glasgow, Glasgow, United Kingdom.
Petrisor-Alin PirvanSchool of Chemistry, University of Glasgow, Glasgow, United Kingdom.
Robert M J LiskampSchool of Chemistry, University of Glasgow, Glasgow, United Kingdom.
Heather G JørgensenHaemato-Oncology/Systems Medicine Group, Paul O'Gorman Leukemia Research Center, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
Xu HuangHaemato-Oncology/Systems Medicine Group, Paul O'Gorman Leukemia Research Center, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
University of Glasgow · GB

Funding

Chief Scientist Office CGA/19/63Medical Research Council MC_PC_18048Wellcome Trust
6 · The paper itself

Abstract

Growing evidence has demonstrated that epigenetic dysregulation is a common pathological feature in human cancer cells. Global alterations in the epigenetic landscape are prevalent in malignant cells across different solid tumors including, prostate cancer, non-small-cell lung cancer, renal cell carcinoma, and in haemopoietic malignancy. In particular, DNA hypomethylation and histone hypoacetylation have been observed in acute myeloid leukemia (AML) patient blasts, with histone methylation being an emerging area of study. Histone 3 lysine 9 trimethylation (H3K9me3) is a post-translational modification known to be involved in the regulation of a broad range of biological processes, including the formation of transcriptionally silent heterochromatin. Following the observation of its aberrant methylation status in hematological malignancy and several other cancer phenotypes, recent studies have associated H3K9me3 levels with patient outcome and highlighted key molecular mechanisms linking H3K9me3 profile with AML etiology in a number of large-scale meta-analysis. Consequently, the development and application of small molecule inhibitors which target the histone methyltransferases or demethylase enzymes known to participate in the oncogenic regulation of H3K9me3 in AML represents an advancing area of ongoing study. Here, we provide a comprehensive review on how this particular epigenetic mark is regulated within cells and its emerging role as a potential therapeutic target in AML, along with an update on the current research into advancing the generation of more potent and selective inhibitors against known H3K9 methyltransferases and demethylases.

Indexed as

acute myeloid leukemia (AML)gene suppressionheterochromatinHistone 3 lysine 9 trimethylation (H3K9me3)Leukaemic stem cell (LSC)lysine specific demethylase (KDM)

Identifiers

PMID31428579
PMCPMC6687838
OpenAlexW2962172119

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.