Prostate Cancer (PCa) is the most common type of cancer among men and 30 percent of these have amplifications in the q-arm of chromosome 8. Importantly, this region harbours the c-Myc (MYC) oncogene, which has is thought of as the sole contributor to poor outcome but dozens of other genes are gained/amplified and the functional consequence of these changes are unknown. Furthermore, stratification of patients based on high MYC mRNA alone is not prognostic. We therefore sought to evaluate the true impact of 8q amplification in prostate tumourigenesis. Using Computational analysis of whole genome sequencing data from localised PCa, we determined that amplifications of this region show a concurrent mRNA amplitude gradient across PCa risk categories for 34/66 genes in this region. Subsequent analysis of a subset of earlier stage (Node negative (N0) localised disease, Intermediate and high risk cohorts) showed concurrent mRNA overexpression in 23/43 genes. Furthermore, there is a marked BCR-free survival disadvantage in high-risk patients only carrying focal amplifications of this region. We assessed the transcriptional changes between MYC-diploid and MYC-amplified patients via co-expression analysis with MYC mRNA abundance. From the shortlisted genes, 10 showed no significant correlation to MYC-diploid patients with high MYC mRNA, thus suggesting independent activity. Furthermore, only two of these 10 genes are always co-expressed with MYC mRNA in patients with 8q-gains, suggesting high 8q amplification specificity. Analysis of high expression of these genes alone recapitulates 8q amplification associated survival and separation based on low MYC abundance indicates a potential oncogene function for these genes in driving disease progression. We have begun modelling “8q amplified” disease in immortalised, non-malignant prostate epithelial cells whereby cells overexpress MYC and our lead candidates in order to explore the role of these genes in tumourigenesis and disease recurrence. 8q-amplified prostate cancer represents a molecularly distinct group of patients and identifying targetable disease drivers in this cohort of patients could enable better treatment in early stage disease.