肺癌仍然是全球癌症患病率和死亡率最高的原因，过度诊断在患者的生活和健康中造成了各种不必要的损失。如何更有效地筛查肺癌患者及其潜在的预后风险成为我们当前研究的重点。通过分析癌症基因组图谱项目（The Cancer Genome Atlas，TCGA）中的LUAD表达谱，我们使用差异表达基因（DEGs）构建了一个加权基因共表达网络，以找到关键模块和关键基因。基于最小绝对值收缩和选择算子（LASSO）的COX比例危险回归模型用于评估该模型对LUAD患者预后的预测价值。本研究识别出了4107个上调的DEGs和2022个下调的DEGs，富集分析表明这些分析与细胞外基质和粘附有关。通过提取关键模块中的中心基因，建立了由LDHA、TOP2A、UBE2C、TYMS、TRIP13、EXO1、TTK、TPX2、ZWINT和UHRF1组成的十个基因标志物，这些基因的上调与患者的预后风险增加相伴。其中，LDHA、TRIP13和TTK在LUAD中的高表达与较短的总生存期相关，并可作为独立的预后因子参与肿瘤NAD等代谢过程。本研究为LUAD预后研究提供了一个强大的分子靶点，并为LUAD的诊断和治疗以及靶向抑制剂的研发提供了理论依据。

Lung cancer remains the leading cause of cancer morbidity and mortality worldwide, and over-diagnosis causes various unnecessary losses in patients' lives and health. How to more effectively screen lung cancer patients and their potential prognostic risk become the focus of our current study. By analyzing the LUAD expression profile in The Cancer Genome Atlas (TCGA), we constructed a weighted gene co-expression network using differentially expressed genes (DEGs) to find the key modules and pivotal genes. A COX proportional risk regression model based on the least absolute shrinkage and selection operator (LASSO) was used to assess the predictive value of the model for the prognosis of LUAD patients. A total of 4107 up-regulated DEGs and 2022 down-regulated DEGs were identified in this study, and enrichment analysis showed that these analyzes were associated with the extracellular matrix of cells and adhesion. Ten gene markers consisting of LDHA, TOP2A, UBE2C, TYMS, TRIP13, EXO1, TTK, TPX2, ZWINT, and UHRF1 were established by extracting the central genes in the key modules, and the upregulation of these genes was accompanied by an increased prognostic risk of patients. Among them, high expression of LDHA, TRIP13, and TTK in LUAD was associated with shorter overall survival and could be used as independent prognostic factors to participate in metabolic processes such as tumor NAD. The present study provides a powerful molecular target for the study of LUAD prognosis and provides a theoretical basis for the diagnosis and treatment of LUAD and the development of targeted inhibitors.