Evidence map›Paper›PMID 41951577›Full record

ArticleCell death & disease2026

ARID1A deficiency-driven reprogramming of polyamine metabolism promotes endometrial cancer malignancy and immune escape.

Han Tao, Xiaojun Wang, Zhiyi Hu, Yiran Li, Mengwen Kong, Yeli Sun, Kun Gao, Xiaoping Wan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Han Tao *Department of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.ORCID http://orcid.org/0009-0009-9131-9909
Xiaojun Wang *Department of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Zhiyi HuDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Yiran LiDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Mengwen KongDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Yeli SunDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Kun GaoShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. kungao@tongji.edu.cn.ORCID http://orcid.org/0000-0001-9060-3881
Xiaoping WanDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. wanxiaoping@tongji.edu.cn.ORCID http://orcid.org/0000-0001-6079-631X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81872109National Natural Science Foundation of China (National Science Foundation of China) 81972438National Natural Science Foundation of China (National Science Foundation of China) 82172975National Natural Science Foundation of China (National Science Foundation of China) 82272992National Natural Science Foundation of China (National Science Foundation of China) 82372841National Natural Science Foundation of China (National Science Foundation of China) 91954106
6 · The paper itself

Abstract

Metabolic reprogramming is crucial in developing endometrial cancer (EC); however, the mechanisms through which tumor suppressors control metabolites that drive cell proliferation and tumor growth remain unclear. ARID1A, an SWI/SNF chromatin remodeling complex subunit, is frequently mutated in endometrium-related malignancies. Here, EC tumors with ARID1A deleted exhibit increased polyamine production, which enhances malignant proliferative capacity while inhibiting the efficacy of functional CD8

Indexed as

DNA-Binding ProteinsEndometrial NeoplasmsMetabolic ReprogrammingPolyaminesTranscription FactorsTumor EscapeAnimalsCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationEflornithineFemaleGene DeletionGene Knockout TechniquesHistone DemethylasesHumansARID1A protein, humanDNA-Binding ProteinsEflornithineHistone DemethylasesKDM1A protein, humanPolyaminesTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID41951577
PMCPMC13186965

What OpenQuestion holds

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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.