Evidence map›Paper›PMID 42882478›Full record

ArticleCells2026

Cell Death Induction by MO2455, a Novel Potential Anti-Cancer Agent in Monocytic and T-Cell Leukemia Cells.

Ankitha Vadi Velu, Kenji Matsuno, Barkha Saraswat, Osamu Ohno, Yu Yingchun, Zhao Zhenkai, Ying Tong, Takahiro Tougan, Taiki Aoshi, Takeji Takamura and 2 more

Abstract read
In one paragraph

Article in Cells, 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

12 authors.

Ankitha Vadi VeluDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0000-0003-4136-6909
Kenji MatsunoDepartment of Pharmacy, Yasuda Women's University, Hiroshima 731-0153, Japan.
Barkha SaraswatDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0009-0005-4579-8348
Osamu OhnoDepartment of Chemistry and Life Science, School of Advanced Engineering, Kogakuin University, Tokyo 192-0015, Japan.ORCID 0000-0002-8147-6857
Yu YingchunDepartment of Immunology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Zhao ZhenkaiDepartment of Immunology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Ying TongDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0009-0004-9476-8359
Takahiro TouganDepartment of Immunology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Taiki AoshiDepartment of Immunology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Takeji TakamuraFaculty of Engineering, Kanagawa Institute of Technology, Atsugi 243-0292, Japan.ORCID 0000-0002-6740-2915
Fumiaki KoizumiDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.
Mitsuko MasutaniDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8523, Japan.ORCID 0000-0003-2631-4334

Funding

Japan Agency for Medical Research and Development 15Ack0106021, 17ck0106286Ministry of Education, Culture, Sports, Science and Technology KibanB 22300343, H23-Jitsuyoka (Gan)-004
6 · The paper itself

Abstract

Despite advances in targeted therapies, treatment resistance and disease recurrence remain major obstacles in leukemia management. Structural modification of clinically successful kinase inhibitors represents a promising approach for discovering novel anti-leukemic agents with improved biological activities. In the present study, we investigated the anti-leukemic activity and mechanism of action of MO2455, a newly synthesized imatinib-derived compound, in monocytic leukemia U937, THP-1, and T-cell leukemia CCRF-CEM cells. MO2455 showed substantial cytotoxic activity against all three cell lines, with IC

Indexed as

Antineoplastic AgentsImatinib MesylateLeukemia, T-CellApoptosisApoptosis Regulatory ProteinsCell DeathCell Line, TumorDNA FragmentationHistonesHumansMembrane Potential, MitochondrialMonocytesProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2U937 CellsAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanHistonesImatinib MesylateProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2apoptosiscell deathDNA damageimatinib derivativeleukemiamitochondrial dysfunction

Identifiers

PMID42882478
PMCPMC13664501

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.