我们进行了一项初步研究来分析 20 种原发性肺部腺泡腺癌的差异甲基化状态。这些腺癌在突变分析中必须是野生型，并且具有高（TPS > 50%；n = 10）或阴性（TPS < 1%；n = 10）PD-L1 状态才能纳入我们的研究。为了检查 866,895 个特定位点的甲基化，我们使用了 Illumina Infinium EPIC 微珠芯片阵列。高甲基化和低甲基化在肿瘤的发生、进展和转移中都发挥着重要作用。它们还影响肿瘤微环境的形成，在肿瘤分化、表观遗传学、传播和免疫逃避中起着决定性作用。获得的甲基化模式与PD-L1表达相关。我们的分析确定了 PD-L1 高表达和阴性表达的肺腺癌中不同的甲基化模式。通过分析基因和启动子的甲基化结果与其病理学的相关性，我们发现PD-L1高表达的肿瘤往往通过高甲基化表现出致癌作用。另一方面，PD-L1 表达阴性的肿瘤通过低甲基化表现出抑制功能的丧失。与同时激活的显性致癌机制相比，高甲基化基因和启动子的抑制功能无效。肿瘤微环境支持两组的肿瘤生长。

We conducted a pilot study to analyze the differential methylation status of 20 primary acinar adenocarcinomas of the lungs. These adenocarcinomas had to be wild type in mutation analysis and had either high (TPS > 50%; n = 10) or negative (TPS < 1%; n = 10) PD-L1 status to be integrated into our study. To examine the methylation of 866,895 specific sites, we utilized the Illumina Infinium EPIC bead chip array. Both hypermethylation and hypomethylation play significant roles in tumor development, progression, and metastasis. They also impact the formation of the tumor microenvironment, which plays a decisive role in tumor differentiation, epigenetics, dissemination, and immune evasion. The gained methylation patterns were correlated with PD-L1 expression. Our analysis has identified distinct methylation patterns in lung adenocarcinomas with high and negative PD-L1 expression. After analyzing the correlation between the methylation results of genes and promoters with their pathobiology, we found that tumors with high expression of PD-L1 tend to exhibit oncogenic effects through hypermethylation. On the other hand, tumors with negative PD-L1 expression show loss of their suppressor functions through hypomethylation. The suppressor functions of hypermethylated genes and promoters are ineffective compared to simultaneously activated dominant oncogenic mechanisms. The tumor microenvironment supports tumor growth in both groups.