Evidence map›Paper›PMID 37072703›Full record

ArticleBMC bioinformatics2023

Integrative analysis of TP53 mutations in lung adenocarcinoma for immunotherapies and prognosis.

He Li, Lei Yang, Yuanyuan Wang, Lingchan Wang, Gang Chen, Li Zhang, Dongchang Wang

Open access · goldAbstract read
In one paragraph

Article in BMC bioinformatics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

He Li *Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Lei Yang *Department of Epidemiology and Statistics, School of Public Health, Hebei Key Laboratory of Environment and Human Health, Hebei Medical University, Shijiazhuang, China.
Yuanyuan Wang *Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Lingchan WangDepartment of Ultrasound, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Gang Chen *Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, China. chengang3605@163.com.
Li Zhang *Department of Geriatrics, The Third Hospital of Hebei Medical University, Shijiazhuang, China. daylight1981@126.com.
Dongchang Wang *Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, China. dongchangwang@hebmu.edu.cn.
Hebei Medical University · CNThird Hospital of Hebei Medical University · CN

Funding

This study was supported by Hebei Natural Science Foundation in China H2020206255This study was supported by Hebei Natural Science Foundation in China H2021206016
6 · The paper itself

Abstract

backgroundThe TP53 tumor suppressor gene is one of the most mutated genes in lung adenocarcinoma (LUAD) and plays a vital role in regulating the occurrence and progression of cancer. We aimed to elucidate the association between TP53 mutations, response to immunotherapies and the prognosis of LUAD.

methodsGenomic, transcriptomic, and clinical data of LUAD were downloaded from The Cancer Genome Atlas (TCGA) dataset. Gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, gene set enrichment analysis (GSEA). Gene set variation analysis (GSVA) were performed to determine the differences in biological pathways. A merged protein-protein interaction (PPI) network was constructed and analyzed. MSIpred was used to analyze the correlation between the expression of the TP53 gene, tumor mutation burden (TMB) and tumor microsatellite instability (MSI). CIBERSORT was used to calculate the abundance of immune cells. Univariate and multivariate Cox regression analyses were used to determine the prognostic value of TP53 mutations in LUAD.

resultsTP53 was the most frequently mutated in LUAD, with a mutational frequency of 48%. GO and KEGG enrichment analysis, GSEA, and GSVA results showed a significant upregulation of several signaling pathways, including PI3K-AKT mTOR (P < 0.05), Notch (P < 0.05), E2F target (NES = 1.8, P < 0.05), and G2M checkpoint (NES = 1.7, P < 0.05). Moreover, we found a significant correlation between T cells, plasma cells, and TP53 mutations (R

conclusionsTP53 may be an independent predictor of response to immunotherapy in LUAD, and patients with TP53 mutations have higher immunogenicity and immune cell infiltration.

Indexed as

Adenocarcinoma of LungLung NeoplasmsHumansImmunotherapyMutationPhosphatidylinositol 3-KinasesTumor Suppressor Protein p53Phosphatidylinositol 3-KinasesTP53 protein, humanTumor Suppressor Protein p53Immune checkpointLung adenocarcinomaSignaling pathwaysTP53Tumor microenvironment

Identifiers

PMID37072703
PMCPMC10114340
OpenAlexW4366276181

What OpenQuestion holds

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LicenceCC BY
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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.