Evidence map›Paper›PMID 28530640›Full record

ArticleThe Journal of clinical investigation2017

Genetic regulation of the RUNX transcription factor family has antitumor effects.

Ken Morita, Kensho Suzuki, Shintaro Maeda, Akihiko Matsuo, Yoshihide Mitsuda, Chieko Tokushige, Gengo Kashiwazaki, Junichi Taniguchi, Rina Maeda, Mina Noura and 19 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 131 citations in OpenAlex.

  1. Targeting Runx1 Slows Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Current drug discovery technologies · 2025
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18 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

29 authors at 7 institutions in 2 countries.

Ken MoritaDepartment of Human Health Sciences, Graduate School of Medicine.
Kensho SuzukiDepartment of Human Health Sciences, Graduate School of Medicine.
Shintaro MaedaDepartment of Human Health Sciences, Graduate School of Medicine.
Akihiko MatsuoDepartment of Human Health Sciences, Graduate School of Medicine.
Yoshihide MitsudaDepartment of Human Health Sciences, Graduate School of Medicine.
Chieko TokushigeDepartment of Human Health Sciences, Graduate School of Medicine.
Gengo KashiwazakiDepartment of Chemistry, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, Japan.
Junichi TaniguchiDepartment of Chemistry, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, Japan.
Rina MaedaDepartment of Chemistry, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, Japan.
Mina NouraDepartment of Human Health Sciences, Graduate School of Medicine.
Masahiro HirataDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Tatsuki KataokaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Ayaka YanoDepartment of Human Health Sciences, Graduate School of Medicine.
Yoshimi YamadaDepartment of Human Health Sciences, Graduate School of Medicine.
Hiroki KiyoseDepartment of Human Health Sciences, Graduate School of Medicine.
Mayu TokumasuDepartment of Human Health Sciences, Graduate School of Medicine.
Hidemasa MatsuoDepartment of Human Health Sciences, Graduate School of Medicine.
Sunao TanakaDepartment of Human Health Sciences, Graduate School of Medicine.
Yasushi OkunoDepartment of Human Health Sciences, Graduate School of Medicine.
Manabu MutoDepartment of Therapeutic Oncology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kazuhito NakaResearch Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Kosei ItoDepartment of Molecular Bone Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Toshio KitamuraDivision of Cellular Therapy and Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yasufumi KanedaDivision of Gene Therapy Science, Department of Genome Biology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Paul P LiuOncogenesis and Development Section, National Human Genome Research Institute, NIH, Bethesda, Maryland, USA.
Toshikazu BandoDepartment of Chemistry, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, Japan.
Souichi AdachiDepartment of Human Health Sciences, Graduate School of Medicine.
Hiroshi SugiyamaDepartment of Chemistry, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, Japan.
Yasuhiko KamikuboDepartment of Human Health Sciences, Graduate School of Medicine.
Kyoto University · JPGraduate School USA · USKyoto University Hospital · JPHiroshima University · JPNagasaki University · JPOsaka University · JPThe University of Tokyo · JP

Funding

GENETIC ANALYSIS OF ZEBRAFISH EMBRYO DEVELOPMENTZIAHG000102 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI LIU, PAUL · 2009 to 2025
$17.1M
MOLECULAR PATHOGENESIS OF CHROMOSOME 16 INVERSION INHUMAN LEUKEMIAZIAHG000030 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI LIU, PAUL · 2009 to 2025
$15.8M
6 · The paper itself

Abstract

Runt-related transcription factor 1 (RUNX1) is generally considered to function as a tumor suppressor in the development of leukemia, but a growing body of evidence suggests that it has pro-oncogenic properties in acute myeloid leukemia (AML). Here we have demonstrated that the antileukemic effect mediated by RUNX1 depletion is highly dependent on a functional p53-mediated cell death pathway. Increased expression of other RUNX family members, including RUNX2 and RUNX3, compensated for the antitumor effect elicited by RUNX1 silencing, and simultaneous attenuation of all RUNX family members as a cluster led to a much stronger antitumor effect relative to suppression of individual RUNX members. Switching off the RUNX cluster using alkylating agent-conjugated pyrrole-imidazole (PI) polyamides, which were designed to specifically bind to consensus RUNX-binding sequences, was highly effective against AML cells and against several poor-prognosis solid tumors in a xenograft mouse model of AML without notable adverse events. Taken together, these results identify a crucial role for the RUNX cluster in the maintenance and progression of cancer cells and suggest that modulation of the RUNX cluster using the PI polyamide gene-switch technology is a potential strategy to control malignancies.

Indexed as

Core Binding Factor alpha SubunitsLeukemia, Myeloid, AcuteAnimalsAntineoplastic Agents, AlkylatingCell Line, TumorHumansMiceMice, Inbred NODNylonsPyrrolesTumor Suppressor Protein p53Xenograft Model Antitumor AssaysAntineoplastic Agents, AlkylatingCore Binding Factor alpha SubunitsNylonsPyrrolesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28530640
PMCPMC5490777
OpenAlexW2614655279

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.