Abstract
Patients with spread through air spaces (STAS) have worse postoperative survival and a higher recurrence rate in lung adenocarcinoma, even in the earliest phases of the disease. At present, the molecular pathogenesis of STAS is not well understood. Therefore, to illustrate the underlying pathogenic mechanism of STAS, we accomplished a comprehensive analysis of a microarray dataset of STAS. Differential expression analysis revealed 841 differentially expressed genes (DEGs) between STAS_positive and STAS_negative groups. Additionally, we acquired two hub genes associated with survival. Gene set variation analysis (GSVA) confirmed that the main differential signaling pathways between the two groups were hypoxia VHL targets, PKC, and pyrimidine metabolism pathways. Analysis of immune activity showed that the increased expression of MHC-class-Ⅰ was observed in the STAS_positive group. These findings provided novel insights for a better knowledge of pathogenic mechanisms and potential therapeutic markers for STAS treatment.