Ovarian high grade serous carcinoma (HGSC) is the commonest subtype of ovarian cancer, and the cause of approximately 80% ovarian cancer deaths. Genomically, HGSC is marked by ubiquitious mutations in TP53 and profound copy number aberrations, with very few classic driver oncogenic mutations. The extent of the copy number change has prevented effective genomic classification. To decode this complexity, we derived copy number signatures using shallow whole-genome sequencing of 117 HGSC cases from the BriTROC-1 study, which were validated on 527 independent cases. Our data show that HGSC comprises a continuum of genomes shaped by multiple mutational processes that result in known and reproducible patterns of genomic aberration. Copy number signature exposures at diagnosis predict both overall survival and the probability of platinum-resistant relapse. We have harnessed the BriTROC-1 samples to compare HGSC at diagnosis and relapse, showing that genomes are largely stable over the course of treatment. Finally, we have also utilised copy number signature analysis to compare cohorts of early- and late-stage HGSC, revealing that late-stage disease has distinct signature exposures consistent with whole genome duplication. These data suggest that early- and late-stage HGSC are genomically distinct and that diagnosis at early-stage might reflect biological differences and not fortuitous chance.