The treatment options for clinically localized prostate cancer include radical prostatectomy (RP) and/or radiation therapy. While curative in majority of the patients, up to ~15-30% of men experience a rise in blood prostate-specific antigen (PSA) levels after definitive local therapies, which reflects potential disease recurrence. The time until a patient experiences this post-treatment rise in PSA—defined as time to biochemical recurrence (BCR)—is an important marker as it can provide insights into risk for clinical progression amongst a proportion of such patients (prognosis). We aim to use tBCR to investigate transcriptomic signatures pertaining to the underlying tumor biology. Among 501 men undergoing RP in the TCGA Firehose Prostate Adenocarcinoma dataset, 70 experienced biochemical recurrence post RP. We studied the PC transcriptomic data of these 70 men. Patients were stratified into quartiles based on “Days to BCR” and their gene expression profiles were analyzed using Gene Set Variation Analysis, K-means clustering, Principal Component Analysis (PCA), Over-Representation Analysis (ORA), and overall survival was assessed for patients with and without genomic and/or transcriptomic alterations. K-means clustering identified a cluster of interest (Cluster 2) based on a linear expression pattern that distinguished early from late recurrence. ORA of Cluster 2 identified immune cell signatures related to tumor-associated macrophages (TAMs), dendritic cells (DCs), and natural killer (NK) cells, which shared an overlap of 6 genes: NSMCE2, DCAF13, RNF139, NDUFAF6, CHMP4C, and RAD21. PCA of Cluster 2 was performed to identify the individual contribution of genes in splitting early recurrent patients, particularity the six shared immune genes. Ultimately, dysregulation within the tumor microenvironment (TME) may compromise immune surveillance and promote increased susceptibility to cancer progression. Hence, further clinical analysis was performed to identify the impact of the six gene signature in patient outcomes. Building on this further, we will examine single cell data in independent cohorts of radical prostatectomy specimens to further understand the role of immune dysregulation in prostate cancer.