Evidence map›Paper›PMID 39377228›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

ASH1L in Hepatoma Cells and Hepatic Stellate Cells Promotes Fibrosis-Associated Hepatocellular Carcinoma by Modulating Tumor-Associated Macrophages.

Yuyang Du, Shasha Wu, Shaoyan Xi, Wei Xu, Liangzhan Sun, Jingsong Yan, Han Gao, Yanchen Wang, Jingyi Zheng, Fenfen Wang and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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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

16 authors.

Yuyang DuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Shasha WuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Shaoyan XiDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, 510275, China.
Wei XuGMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou, 511436, China.
Liangzhan SunDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Jingsong YanDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Han GaoDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Yanchen WangShenzhen Hospital, Southern Medical University, Shenzhen, 518000, China.
Jingyi ZhengShenzhen Hospital, Southern Medical University, Shenzhen, 518000, China.
Fenfen WangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Hui YangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Dan XieState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510080, China.
Xi ChenDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Xijun OuSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Xin-Yuan GuanDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, 999077, China.
Yan LiShenzhen Hospital, Southern Medical University, Shenzhen, 518000, China.ORCID 0000-0003-1146-5578

Funding

National Natural Science Foundation of China 82073127National Natural Science Foundation of China 82372768Natural Science Foundation of Guangdong Province 2022A1515012284Shenzhen Science and Technology Innovation Program JCYJ20220530115204011
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) often occurs in the context of fibrosis or cirrhosis. Methylation of histone is an important epigenetic mechanism, but it is unclear whether histone methyltransferases are potent targets for fibrosis-associated HCC therapy. ASH1L, an H3K4 methyltransferase, is found at higher levels in activated hepatic stellate cells (HSCs) and hepatoma cells. To determine the role of ASH1L in vivo, transgenic mice with conditional Ash1l depletion in the hepatocyte cell lineage (Ash1l

Indexed as

Carcinoma, HepatocellularDisease Models, AnimalHepatic Stellate CellsLiver CirrhosisLiver NeoplasmsMice, TransgenicTumor-Associated MacrophagesAnimalsDiethylnitrosamineHistone-Lysine N-MethyltransferaseHumansMiceDiethylnitrosamineHistone-Lysine N-MethyltransferaseASH1Lfibrosishepatic stellate cells (HSCs)hepatocellular carcinoma (HCC)macrophage

Identifiers

PMID39377228
PMCPMC11615825

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.