Evidence map›Paper›PMID 37378292›Full record

ArticleFrontiers in microbiology2023

EZH1/2 dual inhibitors suppress HTLV-1-infected cell proliferation and hyperimmune response in HTLV-1-associated myelopathy.

Akihito Koseki, Natsumi Araya, Makoto Yamagishi, Junji Yamauchi, Naoko Yagishita, Naoki Takao, Katsunori Takahashi, Yasuo Kunitomo, Daisuke Honma, Kazushi Araki and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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  7. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
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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

13 authors at 4 institutions in 1 country.

Akihito KosekiDepartment of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan.
Natsumi ArayaDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Makoto YamagishiLaboratory of Tumor Cell Biology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Junji YamauchiDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Naoko YagishitaDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Naoki TakaoDepartment of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan.
Katsunori TakahashiDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Yasuo KunitomoDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Daisuke HonmaOncology Research Laboratories, Daiichi Sankyo, Co., Ltd., Tokyo, Japan.
Kazushi ArakiEarly Clinical Development Department, Daiichi Sankyo, Co., Ltd., Tokyo, Japan.
Kaoru UchimaruLaboratory of Tumor Cell Biology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Tomoo SatoDepartment of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan.
Yoshihisa YamanoDepartment of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan.
St. Marianna University School of Medicine · JPDaiichi-Sankyo (Japan) · JPThe University of Tokyo · JPShizuoka University of Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Human T-cell leukemia virus type 1 (HTLV-1) causes HTLV-1-associated myelopathy (HAM), adult T-cell leukemia/lymphoma (ATL), HTLV-1-associated uveitis, and pulmonary diseases. Although both HAM and ATL show proliferation of infected cells, their pathogeneses are quite different. In particular, the pathogenesis of HAM is characterized by hyperimmune responses to HTLV-1-infected cells. Recently, we demonstrated the overexpression of histone methyltransferase EZH2 in ATL cells and the cytotoxic effects of EZH2 inhibitors and EZH1/2 dual inhibitors on these cells. However, these phenomena have never been studied in HAM. Furthermore, what effect these agents have on the hyperimmune response seen in HAM is completely unknown. Methods: In this study, we investigated histone methyltransferase expression levels in infected cell populations (CD4 Results: We found elevated expression of EZH2 in CD4 Conclusion: This study showed that EZH1/2 inhibitors suppress HTLV-1-infected cell proliferation through apoptosis and the hyperimmune response in HAM. This indicates that EZH1/2 inhibitors may be effective in treating HAM.

Indexed as

epigenetic drugEZH2HTLV-1HTLV-1 associated myelopathy (HAM)HTLV-1-infected cellsvalemetostat

Identifiers

PMID37378292
PMCPMC10291084
OpenAlexW4380264762

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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.