ArticleBMC pulmonary medicine2021
Differences in genetics and microenvironment of lung adenocarcinoma patients with or without TP53 mutation.
Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
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- Multi-omics profiling reveals PLEKHA6 as a modulator of β-catenin signaling and therapeutic vulnerability in lung adenocarcinoma.American journal of cancer research · 2025Article
- Machine Learning and Weighted Gene Coexpression Network-Based Identification of Biomarkers Predicting Immune Profiling and Drug Resistance in Lung Adenocarcinoma.International journal of genomics · 2025Article
- Next generation sequencing and genomic mapping: towards precision molecular diagnosis of lung cancer in Morocco.The Pan African medical journal · 2024Article
- Construction and validation of an efferocytosis-related prognostic signature in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Neuropeptide Y Peptide Family and Cancer: Antitumor Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Integrative analysis of TP53 mutations in lung adenocarcinoma for immunotherapies and prognosis.BMC bioinformatics · 2023Article
- LINC02126 is a potential diagnostic, prognostic and immunotherapeutic target for lung adenocarcinoma.BMC pulmonary medicine · 2022Article
- Mechanism of Shishiwei Wendan Decoction in the Prevention and Treatment of Lung Adenocarcinoma Using Network Pharmacology and Molecular Docking.BioMed research international · 2022Article
- Lung Adenocarcinoma With Bone Metastases: Clinicogenomic Profiling and Insights Into Prognostic Factors.Cancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDifferences in genetics and microenvironment of LUAD patients with or without TP53 mutation were analyzed to illustrate the role of TP53 mutation within the carcinogenesis of LUAD, which will provide new concepts for the treatment of LUAD.
methodsIn this study, we used genetics and clinical info from the TCGA database, including somatic mutations data, RNA-seq, miRNA-seq, and clinical data. More than one bioinformatics tools were used to analyze the unique genomic pattern of TP53-related LUAD.
resultsAccording to TP53 gene mutation status, we divided the LUAD patients into two groups, including 265 in the mutant group (MU) and 295 in the wild-type group (WT). 787 significant somatic mutations were detected between the groups, including mutations in titin (TTN), type 2 ryanodine receptor (RYR2) and CUB and Sushi multiple domains 3(CSMD3), which were up-regulated in the MU. However, no significant survival difference was observed. At the RNA level, we obtained 923 significantly differentially expressed genes; in the MU, α-defensin 5(DEFA5), pregnancy-specific glycoprotein 5(PSG5) and neuropeptide Y(NPY) were the most up-regulated genes, glucose-6-phosphatase (G6PC), alpha-fetoprotein (AFP) and carry gametocidal (GC) were the most down-regulated genes. GSVA analysis revealed 30 significant pathways. Compared with the WT, the expression of 12 pathways in the mutant group was up-regulated, most of which pointed to cell division. There were significant differences in tumor immune infiltrating cells, such as Macrophages M1, T cells CD4 memory activated, Mast cells resting, and Dendritic cells resting. In terms of immune genes, a total of 35 immune-related genes were screened, of which VGF (VGF nerve growth factor inducible) and PGC (peroxisome proliferator-activated receptor gamma coactivator) were the most significant up-regulated and down-regulated genes, respectively. Research on the expression pattern of immunomodulators found that 9 immune checkpoint molecules and 6 immune costimulatory molecules were considerably wholly different between the two groups.
conclusionsTaking the mutant group as a reference, LUAD patients in the mutant group had significant differences in somatic mutations, mRNA-seq, miRNA-seq, immune infiltration, and immunomodulators, indicating that TP53 mutation plays a crucial role in the occurrence and development of LUAD.
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