Evidence map›Paper›PMID 40535071›Full record

ArticleTranslational lung cancer research2025

Impaired natural killer cell maturation in lung adenocarcinoma driven by

Hongxia Tian, Kezhen Li, Jing Chen, Weibang Guo, Zepeng Guo, Shuilian Zhang, Zhi Xie, Xin Huang, Sipei Wu, Wenzhao Zhong

Abstract read
In one paragraph

Article in Translational lung cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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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

Who cites it

5 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

10 authors.

Hongxia Tian *Department of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-3964-7947
Kezhen Li *Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Guangzhou, China.
Jing ChenDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Weibang GuoDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Zepeng GuoDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Shuilian ZhangDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Zhi XieDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Xin HuangDepartment of Hematology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Sipei WuDepartment of Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Wenzhao ZhongGuangdong Provincial Key Laboratory of Translational Medicine in Lung Cancer, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8917-8635

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Although natural killer (NK) cells play a crucial role in antitumor immunity, the metabolic changes driving their dysfunction in lung adenocarcinoma remain poorly understood. This study investigates how these metabolic modifications impact NK cell function within the lung adenocarcinoma microenvironment. Methods: A total of 13 pairs of lung adenocarcinoma samples were obtained from The Cancer Genome Atlas. Differential gene expression, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and single-cell metabolic quantification analyses were used to characterize the transcriptomic, pathway, and metabolic signatures of NK cells. The developmental trajectory was reconstructed via pseudotime analysis. The fatty acid-binding protein 4 ( Results: The number of NK cells was significantly decreased in the lung adenocarcinoma microenvironment. Conclusions: The study findings present new evidence showing that low

Indexed as

FABP4lipid metabolismLung adenocarcinomaNK cellSPON2

Identifiers

PMID40535071
PMCPMC12170238

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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.