Evidence map›Paper›PMID 30057114›Full record

ArticleCell2018

Cross-talk between Lysine-Modifying Enzymes Controls Site-Specific DNA Amplifications.

Sweta Mishra, Capucine Van Rechem, Sangita Pal, Thomas L Clarke, Damayanti Chakraborty, Sarah D Mahan, Joshua C Black, Sedona E Murphy, Michael S Lawrence, Danette L Daniels and 1 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
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  6. Review
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  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Observational
  15. Article
  16. Article
  17. Mechanistic insights into KDM4A driven genomic instability.Biochemical Society transactions · 2021
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Sweta MishraMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Capucine Van RechemMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Sangita PalMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Thomas L ClarkeMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Damayanti ChakrabortyMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Sarah D MahanPromega Corporation, 2800 Woods Hollow Road, Madison, WI 53711, USA.
Joshua C BlackMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Sedona E MurphyMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
Michael S LawrenceMassachusetts General Hospital Cancer Center and Department of Pathology, Harvard Medical School, 13th Street, Charlestown, MA 02129, USA; Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, MA 02142, USA.
Danette L DanielsPromega Corporation, 2800 Woods Hollow Road, Madison, WI 53711, USA.
Johnathan R WhetstineMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA. Electronic address: jwhetstine@hms.harvard.edu.

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
Understanding the Role of Histone Demethylases and Heterochromatin in Cell CycleR01GM097360 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI WHETSTINE, JOHNATHAN R. · 2012 to 2020
$3.4M
NCATS NIH HHS UL1 TR001102NIGMS NIH HHS R01 GM097360
6 · The paper itself

Abstract

Acquired chromosomal DNA amplifications are features of many tumors. Although overexpression and stabilization of the histone H3 lysine 9/36 (H3K9/36) tri-demethylase KDM4A generates transient site-specific copy number gains (TSSGs), additional mechanisms directly controlling site-specific DNA copy gains are not well defined. In this study, we uncover a collection of H3K4-modifying chromatin regulators that function with H3K9 and H3K36 regulators to orchestrate TSSGs. Specifically, the H3K4 tri-demethylase KDM5A and specific COMPASS/KMT2 H3K4 methyltransferases modulate different TSSG loci through H3K4 methylation states and KDM4A recruitment. Furthermore, a distinct chromatin modifier network, MLL1-KDM4B-KDM5B, controls copy number regulation at a specific genomic locus in a KDM4A-independent manner. These pathways comprise an epigenetic addressing system for defining site-specific DNA rereplication and amplifications.

Indexed as

DNA Copy Number VariationsDNA MethylationCell CycleChromatinHEK293 CellsHistonesHumansLysineRetinoblastoma-Binding Protein 2ChromatinHistonesKDM5A protein, humanLysineRetinoblastoma-Binding Protein 2amplificationchromatinepigeneticsH3K36H3K4H3K9histoneJmjCK36MKDMKDM4KDM5KMTMLLrereplicationSETD1BTSSG

Identifiers

PMID30057114
PMCPMC6212369

What OpenQuestion holds

Textmetadata
LicenceTDM
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.