Evidence map›Paper›PMID 38757752›Full record

ArticleThe clinical respiratory journal2024

Identification and analysis of prognostic immune cell homeostasis characteristics in lung adenocarcinoma.

Yidan Sun, Qianqian Ma, Yixun Chen, Dongying Liao, Fanming Kong

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Article in The clinical respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yidan SunDepartment of Oncology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.ORCID https://orcid.org/0000-0002-0055-4754
Qianqian MaAffiliated Women's Hospital of Jiangnan University, Wuxi, Jiangsu, China.
Yixun ChenResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Dongying LiaoDepartment of Oncology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Fanming KongDepartment of Oncology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Funding

Wuxi Medical Development Branch FZXK2021008
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is one of the most invasive malignant tumor of the respiratory system. It is also the common pathological type leading to the death of LUAD. Maintaining the homeostasis of immune cells is an important way for anti-tumor immunotherapy. However, the biological significance of maintaining immune homeostasis and immune therapeutic effect has not been well studied.

methodsWe constructed a diagnostic and prognostic model for LUAD based on B and T cells homeostasis-related genes. Minimum absolute contraction and selection operator (LASSO) analysis and multivariate Cox regression are used to identify the prognostic gene signatures. Based on the overall survival time and survival status of LUAD patients, a 10-gene prognostic model composed of ABL1, BAK1, IKBKB, PPP2R3C, CCNB2, CORO1A, FADD, P2RX7, TNFSF14, and ZC3H8 was subsequently identified as prognostic markers from The Cancer Genome Atlas (TCGA)-LUAD to develop a prognostic signature. This study constructed a gene prognosis model based on gene expression profiles and corresponding survival information through survival analysis, as well as 1-year, 3-year, and 5-year ROC curve analysis. Enrichment analysis attempted to reveal the potential mechanism of action and molecular pathway of prognostic genes. The CIBERSORT algorithm calculated the infiltration degree of 22 immune cells in each sample and compared the difference of immune cell infiltration between high-risk group and low-risk group. At the cellular level, PCR and CKK8 experiments were used to verify the differences in the expression of the constructed 10-gene model and its effects on cell viability, respectively. The experimental results supported the significant biological significance and potential application value of the molecular model in the prognosis of lung cancer. Enrichment analyses showed that these genes were mainly related to lymphocyte homeostasis.

conclusionWe identified a novel immune cell homeostasis prognostic signature. Targeting these immune cell homeostasis prognostic genes may be an alternative for LUAD treatment. The reliability of the prediction model was confirmed at bioinformatics level, cellular level, and gene level.

Indexed as

Adenocarcinoma of LungHomeostasisLung NeoplasmsBiomarkers, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisSurvival AnalysisBiomarkers, Tumorgene signatureimmune homeostasislung adenocarcinomaprognosisTCGA

Identifiers

PMID38757752
PMCPMC11099951

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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.