Evidence map›Paper›PMID 40319143›Full record

ArticleOncogene2025

Loss of NUMB promotes hepatomegaly and hepatocellular carcinoma through the AKT/glycogen/hippo signaling.

Yuke Shu, Qing Tao, Qing Xu, Yuwei Chen, Yahong Xu, Tingting Ma, Zhiqi Zhu, Xinyu Wei, Fei Liu, Zhenru Wu and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. 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

18 authors.

Yuke Shu *Department of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Qing Tao *Department of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Qing XuDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.ORCID http://orcid.org/0009-0009-6885-9392
Yuwei ChenDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yahong XuInstitute of Transplantation, Key Laboratory of Transplant Engineering and Immunology, NHC, West China Hospital, Sichuan University, Chengdu, 610041, China.
Tingting MaDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhiqi ZhuDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Xinyu WeiDepartment of Liver Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Fei LiuDepartment of Biliary Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhenru WuDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yuting ZengDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Menglin ChenDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Mingyang ShaoDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Xiaoyue CaoDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yongjie ZhouInstitute of Transplantation, Key Laboratory of Transplant Engineering and Immunology, NHC, West China Hospital, Sichuan University, Chengdu, 610041, China.
Wei PengDepartment of Liver Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Chuan LiDepartment of Liver Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China. lichuan85@163.com.ORCID http://orcid.org/0000-0002-1482-9480
Yujun ShiDepartment of Pathology & Institute of Clinical Pathology, West China Hospital, Sichuan University, Chengdu, 610041, China. shiyujun@scu.edu.cn.ORCID http://orcid.org/0000-0003-0494-6023

Funding

National Natural Science Foundation of China (National Science Foundation of China) 2024NSFSC0637National Natural Science Foundation of China (National Science Foundation of China) 82200691National Natural Science Foundation of China (National Science Foundation of China) 82404060National Natural Science Foundation of China (National Science Foundation of China) U22A20343
6 · The paper itself

Abstract

Excessive glycogen deposition is a common feature of liver enlargement, liver adenoma, and liver cancer, yet the underlying mechanisms remain poorly understood. In this study, we found that NUMB, a well-known cell fate determinant, is downregulated in glycogen-rich adenomas and hepatocellular carcinoma (HCC). NUMB-deficient livers developed excessive glycogen accumulation and adenoma formation particularly in aged mice. Surprisingly, the Alb-Cre:Trp53

Indexed as

Carcinoma, HepatocellularGlycogenHepatomegalyLiver NeoplasmsMembrane ProteinsNerve Tissue ProteinsProto-Oncogene Proteins c-aktAnimalsHippo Signaling PathwayHumansMaleMiceMice, KnockoutSignal TransductionTumor Suppressor Protein p53GlycogenMembrane ProteinsNerve Tissue ProteinsNUMB protein, humanNumb protein, mouseProto-Oncogene Proteins c-aktTumor Suppressor Protein p53

Identifiers

PMID40319143

What OpenQuestion holds

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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.