A fatty acid metabolism-related genes model for predicting the prognosis and immunotherapy effect of lung adenocarcinoma.

IF 2.2 4区 医学 Q3 ONCOLOGY
Cancer Biomarkers Pub Date : 2024-12-01 Epub Date: 2025-03-17 DOI:10.1177/18758592241296285
Lingxue Tang, Tong Wang
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引用次数: 0

Abstract

ObjectiveLung adenocarcinoma (LUAD) is a common and highly heterogeneous malignancy cancer with increasing morbidity and mortality. Dysregulation of fatty acid metabolism (FAM) has been identified as a key regulator of LUAD progression. Our purpose was to establish a risk model of FAM-related genes to provide a reference for the prognosis prediction of LUAD.MethodsFirstly, we screened FAM-related differentially expressed genes (DEGs) based on the Cancer Genome Atlas (TCGA) database, and identified the prognostic signatures by Cox-regression analysis. The least absolute shrinkage and selection operator algorithm (LASSO) was used to obtain the formula for risk model. And the analysis of Gene Expression Omnibus (GEO) dataset used to verify. Nomogram was produced for individualized prediction in clinical treatment. Immune cell function and drug sensitivity analysis used to screen potential therapeutic drugs.ResultsPatients in low-risk had better overall survival (OS). High-risk patients exhibit higher TMB and lower TIDE scores, and they are more likely to benefit from immunotherapy. The analysis of GEO verified that risk model has a high prediction accuracy.ConclusionThe risk model based on 17 FAM-related DEGs is of great value in predicting the prognosis of LUAD, and these prognostic signatures may be potential therapeutic targets for LUAD.

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来源期刊
Cancer Biomarkers
Cancer Biomarkers ONCOLOGY-
CiteScore
5.20
自引率
3.20%
发文量
195
审稿时长
3 months
期刊介绍: Concentrating on molecular biomarkers in cancer research, Cancer Biomarkers publishes original research findings (and reviews solicited by the editor) on the subject of the identification of markers associated with the disease processes whether or not they are an integral part of the pathological lesion. The disease markers may include, but are not limited to, genomic, epigenomic, proteomics, cellular and morphologic, and genetic factors predisposing to the disease or indicating the occurrence of the disease. Manuscripts on these factors or biomarkers, either in altered forms, abnormal concentrations or with abnormal tissue distribution leading to disease causation will be accepted.
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