Evidence map›Paper›PMID 40341256›Full record

ArticleLeukemia2025

Regulation of H3K4me3 breadth and MYC expression by the SETD1B catalytic domain in MLL-rearranged leukemia.

Shintaro Izumi, Ko Ohtani, Makoto Matsumoto, Seito Shibata, Bahityar Rahmutulla, Masaki Fukuyo, Mitsutaka Nishimoto, Hideo Miyagawa, Emiko Sakaida, Koutaro Yokote and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
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

14 authors.

Shintaro IzumiDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.ORCID 0009-0003-8107-6532
Ko OhtaniDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.
Makoto MatsumotoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.ORCID 0009-0006-5365-8975
Seito ShibataDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.ORCID 0009-0002-7271-0346
Bahityar RahmutullaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.ORCID 0000-0002-4014-2789
Masaki FukuyoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.
Mitsutaka NishimotoDepartment of Hematology, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan.ORCID 0000-0002-0388-3836
Hideo MiyagawaPreventive Medicine and Environmental Health, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Emiko SakaidaDepartment of Endocrinology, Hematology and Gerontology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-7254-1928
Koutaro YokoteDepartment of Endocrinology, Hematology and Gerontology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Issay KitabayashiOncology Innovation Center/ Center for Translational Research, Fujita Health University, Aichi, Japan.ORCID 0000-0002-8409-0407
Kimi ArakiDivision of Developmental Genetics, Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan.ORCID 0000-0002-6980-5515
Takayuki HoshiiDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba-shi, Chiba, Japan. hoshiit@chiba-u.jp.ORCID 0000-0002-5418-1981

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP19K22399MEXT | Japan Society for the Promotion of Science (JSPS) JP22H03099MEXT | Japan Society for the Promotion of Science (JSPS) JP22H04684
6 · The paper itself

Abstract

Histone H3 lysine 4 trimethylation (H3K4me3) is abundant in mixed-lineage leukemia-rearranged (MLL-r) acute myeloid leukemia (AML) cells; however, the responsible enzymes and their roles remain unclear. This study aimed to identify the modifier responsible for high H3K4me3 modification in MLL-r leukemia and its downstream targets essential for the cell proliferation. Here, we performed a CRISPR-tiling screen against known H3K4 methylation modifiers in an MLL-r AML model. Disrupting the SETD1B catalytic SET domain caused depletion of FLT3-ITD or Nras

Indexed as

Gene Expression Regulation, LeukemicGene RearrangementHistone-Lysine N-MethyltransferaseHistonesLeukemia, Myeloid, AcuteMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Proteins c-mycCatalytic DomainCell Line, TumorCell ProliferationHumansMethylationhistone H3 trimethyl Lys4Histone-Lysine N-MethyltransferaseHistonesKMT2A protein, humanMYC protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Proteins c-myc

Identifiers

PMID40341256
PMCPMC12208907

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.