Evidence map›Paper›PMID 26190263›Full record

ArticleCancer cell2015

The H3K4-Methyl Epigenome Regulates Leukemia Stem Cell Oncogenic Potential.

Stephen H K Wong, David L Goode, Masayuki Iwasaki, Michael C Wei, Hsu-Ping Kuo, Li Zhu, Dominik Schneidawind, Jesus Duque-Afonso, Ziming Weng, Michael L Cleary

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 139 citations in OpenAlex.

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  9. The WWP1-JARID1B axis sustains acute myeloid leukemia chemoresistance.Proceedings of the National Academy of Sciences of the United States of America · 2025
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24 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

10 authors at 3 institutions in 2 countries.

Stephen H K WongDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
David L GoodeDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA; Peter MacCallum Cancer Centre and University of Melbourne, Melbourne, VIC 3010, Australia.
Masayuki IwasakiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael C WeiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Hsu-Ping KuoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Li ZhuDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Dominik SchneidawindDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jesus Duque-AfonsoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ziming WengDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael L ClearyDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: mcleary@stanford.edu.
Stanford University · USStanford Medicine · USThe University of Melbourne · AU

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
Molecular Targeting of MLL and Associated FactorsR01CA116606 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 2005 to 2020
$4.7M
NCI NIH HHS CA116606NCI NIH HHS R01 CA116606NCI NIH HHS T32 CA009151NCI NIH HHS T32 CA009302
6 · The paper itself

Abstract

The genetic programs that maintain leukemia stem cell (LSC) self-renewal and oncogenic potential have been well defined; however, the comprehensive epigenetic landscape that sustains LSC cellular identity and functionality is less well established. We report that LSCs in MLL-associated leukemia reside in an epigenetic state of relative genome-wide high-level H3K4me3 and low-level H3K79me2. LSC differentiation is associated with reversal of these broad epigenetic profiles, with concomitant downregulation of crucial MLL target genes and the LSC maintenance transcriptional program that is driven by the loss of H3K4me3, but not H3K79me2. The H3K4-specific demethylase KDM5B negatively regulates leukemogenesis in murine and human MLL-rearranged AML cells, demonstrating a crucial role for the H3K4 global methylome in determining LSC fate.

Indexed as

Epigenesis, GeneticAnimalsCell Line, TumorCells, CulturedCell Transformation, NeoplasticGene Expression ProfilingGene Expression Regulation, LeukemicHEK293 CellsHistone-Lysine N-MethyltransferaseHistonesHumansInterleukin Receptor Common gamma SubunitJumonji Domain-Containing Histone DemethylasesLeukemiaLysineMethylationHistone-Lysine N-MethyltransferaseHistonesIl2rg protein, mouseInterleukin Receptor Common gamma SubunitJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanKMT2A protein, humanLysineMyeloid-Lymphoid Leukemia ProteinNuclear ProteinsRepressor Proteins

Identifiers

PMID26190263
PMCPMC4536132
OpenAlexW1680709572

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.