A comprehensive analysis of 560 breast cancer whole genome sequences identified 93 protein-coding genes with likely driver mutations. Non-coding regions showed high mutation frequencies but were unlikely to harbor driver mutations. Mutational signature analysis revealed 12 base substitution and six rearrangement signatures. Three rearrangement signatures, associated with defective homologous recombination DNA repair, were identified. These signatures include those with BRCA1 or BRCA2 dysfunction. The analysis highlights the repertoire of cancer genes and mutational processes in breast cancer. Mutational signatures were analyzed across exons, introns, and intergenic regions. Recurrent somatic mutations in non-coding regions were identified, including in the promoters of PLEKHS1 and TBC1D12. Mutational signatures were also found in long non-coding RNAs. Mutational signatures were analyzed for their DNA replication strand bias, with signatures 2 and 13 showing lagging strand bias. Mutational signatures associated with BRCA1 and BRCA2 mutations were identified, with signature 3 and 8 linked to BRCA1 and BRCA2 dysfunction. The study provides insights into the somatic genetic basis of breast cancer and highlights the importance of understanding mutational processes and driver mutations in cancer development. The findings contribute to a comprehensive understanding of the origins and consequences of somatic mutations in breast cancer.A comprehensive analysis of 560 breast cancer whole genome sequences identified 93 protein-coding genes with likely driver mutations. Non-coding regions showed high mutation frequencies but were unlikely to harbor driver mutations. Mutational signature analysis revealed 12 base substitution and six rearrangement signatures. Three rearrangement signatures, associated with defective homologous recombination DNA repair, were identified. These signatures include those with BRCA1 or BRCA2 dysfunction. The analysis highlights the repertoire of cancer genes and mutational processes in breast cancer. Mutational signatures were analyzed across exons, introns, and intergenic regions. Recurrent somatic mutations in non-coding regions were identified, including in the promoters of PLEKHS1 and TBC1D12. Mutational signatures were also found in long non-coding RNAs. Mutational signatures were analyzed for their DNA replication strand bias, with signatures 2 and 13 showing lagging strand bias. Mutational signatures associated with BRCA1 and BRCA2 mutations were identified, with signature 3 and 8 linked to BRCA1 and BRCA2 dysfunction. The study provides insights into the somatic genetic basis of breast cancer and highlights the importance of understanding mutational processes and driver mutations in cancer development. The findings contribute to a comprehensive understanding of the origins and consequences of somatic mutations in breast cancer.