睾丸生殖细胞肿瘤（TGCT）是睾丸癌最常见的类型，占90％-95％的病例，是年轻成年男性中最常见的实性恶性肿瘤。免疫浸润在肿瘤中起着重要的调节作用，但其在TGCT中的作用尚不清楚。分子亚型分型是提供精确个体化治疗和避免不必要毒性的一种有前途的方法。本研究调查了TGCT的免疫浸润、关键生物标志物和免疫亚型。在GSE3218中，鉴定了24个差异表达的免疫基因（immDEGs）。使用这些基因开发了一个由六个immDEGs组成的新的风险签名。高风险组的个体总体生存率较差（危险比为4.61，P值<0.001）。我们在纯精原细胞瘤和混合型TGCT中验证了这个六个immDEGs风险签名。使用ConsensusClusterPlus鉴定出两种不同的免疫模式（Cluster 1和Cluster 2），与Cluster 2相比，Cluster 1具有不利的总体生存率（危险比为2.56，P<0.001）。Cluster 1患者的初始B细胞、记忆B细胞、浆细胞、初始CD4 T细胞、γδ T细胞和活化树突状细胞显著低于Cluster 2患者。与TGCT相关的基因包括WNT信号通路、TGF-β信号通路、抗原处理和呈递以及NK细胞介导的细胞毒作用。STC1在TGCT组织中升高，其高表达与TGCT的进展和预后不良有关。我们的发现可能有助于增加对TGCT起病和进展的理解。本文受版权保护。版权所有。

Testicular germ cell tumors (TGCT) are the most common type of testicular cancer, comprising 90%-95% of cases and representing the most prevalent solid malignancy in young adult men. Immune infiltrates play important regulatory roles in tumors, but their role in TGCT remains unclear. Molecular subtyping is a promising way to provide precisely personalized treatment and avoid unnecessary toxicities. This study investigated immune infiltrates, key biomarkers, and immune subtyping of TGCT. In GSE3218, 24 differentially expressed immune genes (immDEGs) were identified. A new risk signature consisting of six immDEGs was developed using these genes. Individuals in the high-risk group had poor overall survival (OS) (hazard ratio of 4.61 and P-value <0.001). We validated the six-immDEGs risk signature in pure seminoma and mixed TGCT types. Two distinct immune patterns (Cluster 1 and Cluster 2) were identified using the ConsensusClusterPlus, and Cluster 1 possessed an unfavorable OS compared to Cluster 2 (hazard ratio, 2.56; P <0.001). Cluster 1 patients had significantly lower naive B cells, memory B cells, plasma cells, naive CD4 T cells, gamma delta T cells, and activated dendritic cells than Cluster 2 patients. Genes relating to the WNT signaling pathway, TGF-β signaling pathway, antigen processing and presentation, and NK cell-mediated cytotoxicity were associated with TGCT. STC1 was elevated in TGCT tissues, and its high expression showed advanced clinicopathological characteristics and poor prognosis of TGCT. Our findings may contribute to increased understanding of the onset and progression of TGCT.This article is protected by copyright. All rights reserved.