Evidence map›Paper›PMID 42034869›Full record

ArticleOncogene2026

Genome-wide screening identifies ZFP91 as a key regulator of EVI1 in myeloid leukemia.

Hiroki Hayashida, Yosuke Masamoto, Takashi Oyama, Toshiya Hino, Ken Morita, Katsunori Fujiki, Ryuichiro Nakato, Katsuhiko Shirahige, Mineo Kurokawa

Abstract read
In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Hiroki HayashidaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0009-0003-6324-7916
Yosuke MasamotoDepartment of Blood Transfusion, The University of Tokyo Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8168-6459
Takashi OyamaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Toshiya HinoDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Ken MoritaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Katsunori FujikiLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Ryuichiro NakatoLaboratory of Computational Genomics, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-3019-5817
Katsuhiko ShirahigeLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Mineo KurokawaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. kurokawa@m.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-4034-2422

Funding

Japan Agency for Medical Research and Development (AMED) JP23ama121020MEXT | Japan Society for the Promotion of Science (JSPS) JP20H03708MEXT | Japan Society for the Promotion of Science (JSPS) JP21H04805MEXT | Japan Society for the Promotion of Science (JSPS) JP22K16299MEXT | Japan Society for the Promotion of Science (JSPS) JP22KJ0806MEXT | Japan Society for the Promotion of Science (JSPS) JP24K19194
6 · The paper itself

Abstract

Ecotropic viral integration site 1 (EVI1) is essential for hematopoietic stem cell maintenance, and its aberrant expression is a significant adverse prognostic indicator in myeloid leukemia. EVI1 overexpression typically occurs due to chromosomal rearrangement involving 3q26. However, aberrant EVI1 expression is still observed in numerous cases without 3q26 abnormalities, leading to similarly poor outcomes, while the mechanism behind EVI1 overexpression in these cases remains largely unknown. Here, we performed genome-wide CRISPR screening using cells with GFP knock-in at the EVI1 locus and identified zinc finger protein 91 (ZFP91) was the leading activator of EVI1. ZFP91 knockout significantly reduced EVI1 expression and cell proliferation. We also showed that ZFP91 binds to the EVI1 promoter, enhancing H3K4me3/H3K27ac and chromatin accessibility. Our data showed that the ZFP91-EVI1 axis plays a critical role for activation of EVI1 in myeloid leukemia. Our screening approach represents a powerful and unbiased method for identifying expression regulators that can be broadly applied across a range of contexts.

Indexed as

Leukemia, MyeloidMDS1 and EVI1 Complex Locus ProteinAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, LeukemicHumansPromoter Regions, GeneticMDS1 and EVI1 Complex Locus ProteinMECOM protein, human

Identifiers

PMID42034869
PMCPMC13246443

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Registered trials

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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.