Evidence map›Paper›PMID 38195889›Full record

ArticleBritish journal of cancer2024

Med23 deficiency reprograms the tumor microenvironment to promote lung tumorigenesis.

Xiaobo Fu, Siming Liu, Dan Cao, Chonghui Li, Hongbin Ji, Gang Wang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Central Med23 deficiency leads to malformation of dentate gyrus and ADHD-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  6. 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

6 authors at 3 institutions in 1 country.

Xiaobo Fu *State Key Laboratory of Genetic Engineering, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Siming Liu *Shanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Dan CaoState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Chonghui LiState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Hongbin JiState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.ORCID 0000-0003-0891-6390
Gang WangState Key Laboratory of Genetic Engineering, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China. gwang_fd@fudan.edu.cn.ORCID 0000-0002-4582-501X
Center for Excellence in Molecular Cell Science · CNFudan University · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32030028National Natural Science Foundation of China (National Science Foundation of China) 32170735
6 · The paper itself

Abstract

backgroundLung cancer is the leading cause of cancer-related death worldwide. We previously found that Mediator complex subunit 23 (MED23) is important for the tumourigenicity of lung cancer cells with hyperactive Ras activity in vitro, although the in vivo function of MED23 in lung tumourigenesis remains to be explored.

methodsIn this study, we utilized well-characterized Kras

resultsWe observed that lung epithelial Med23 deletion by adeno-Cre resulted in a significant increase in Kras

conclusionsCollectively, these findings revealed that MED23 may negatively regulate Kras-induced lung tumourigenesis in vivo, which would improve the precise classification of KRAS-mutant lung cancer patients and provide new insights for clinical interventions.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsCarcinogenesisCD8-Positive T-LymphocytesCell Transformation, NeoplasticHumansLungMediator ComplexMiceProto-Oncogene Proteins p21(ras)Tumor MicroenvironmentMed23 protein, mouseMediator ComplexProto-Oncogene Proteins p21(ras)

Identifiers

PMID38195889
PMCPMC10912217
OpenAlexW4390706486

What OpenQuestion holds

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LicenceCC BY
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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.