Evidence map›Paper›PMID 42402603›Full record

ArticleClinical epigenetics2026

TCA-controlled histone succinylation identifies IDH3B as a prognostic and therapeutic target in AML.

Minhui Shi, Kepeng Yang, Hao Ding, Na Zhao, Jiewen Ma, Aijie Huang, Yun Wang, Xiaoyu Zhu, Domenico Iuso, Mengqing Gao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Minhui Shi *Department of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Kepeng Yang *Department of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Hao Ding *Department of Statistics and Finance, School of Management, University of Science and Technology of China, Hefei, 230026, China.
Na ZhaoDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Jiewen MaDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Aijie HuangDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Yun WangNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Xiaoyu ZhuDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China. xiaoyuz@ustc.edu.cn.
Domenico IusoDepartment of Veterinary Medicine, University of Teramo, 64100, Teramo, Italy. diuso@unite.it.
Mengqing GaoDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China. mengqinggao@ustc.edu.cn.

Funding

Anhui Provincial Department of Education Scientific Research Project 2023AH010079Anhui Provincial Natural Science Foundation 2308085J09International Cooperation Projects in Anhui Province 2023h11020005National Natural Science Foundation of China 12201601, U23A20453, 82270223 and 82170209National Natural Science Foundation of China 82200197PRIN 2022 PNRR P20225KJ5Lthe Gusu Talent Program GSWS2023083the NHC Key Laboratory of Thrombosis and Hemostasis, the First Affiliated Hospital of Soochow University KJS2420USTC Research Funds of the Double First-Class Initiative YD9110002047
6 · The paper itself

Abstract

backgroundMitochondrial metabolism-driven epigenetic modifications have emerged as crucial regulators for acute myeloid leukemia (AML) progression, linking metabolic activity in leukemic stem cells to epigenetically controlled transcriptional programs that drive oncogenic gene expression.

resultsHere, by integrating proteomic and transcriptomic data, we identified six genes whose expression were able to predict outcome in AML. Among these, IDH3B was highly expressed in leukemic stem cells and associated with poor prognosis. Functional studies revealed that IDH3B deletion in KMT2A-rearranged AML increased global protein succinylation, reduced acetylation, and sensitized cells to the menin-KMT2A inhibitor, both in vitro and in vivo. Mechanistically, loss of IDH3B, by increasing histone succinylation and reducing H3K79 methylation at the MYC promoter, amplified Revumenib-induced transcriptional repression of MYC.

conclusionsThese findings establish IDH3B as a key metabolic-epigenetic regulator in AML and highlight it as a potential synergistic target to enhance menin inhibition therapy.

Indexed as

HistonesIsocitrate DehydrogenaseLeukemia, Myeloid, AcuteAnimalsCell Line, TumorEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, LeukemicHistone-Lysine N-MethyltransferaseHumansMiceMyeloid-Lymphoid Leukemia ProteinPrognosisProteomicsHistone-Lysine N-MethyltransferaseHistonesIsocitrate DehydrogenaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinAcute myeloid leukemiaIDH3BMenin–KMT2A inhibitionMitochondrial metabolismSuccinylation

Identifiers

PMID42402603
PMCPMC13617953

What Socratic holds

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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 Socratic graph.