This study analyzed whole genome sequences from 560 breast cancers to understand the driver mutations and mutational processes that contribute to the development of breast cancer. The analysis identified 93 protein-coding cancer genes with likely driver mutations, and non-coding regions with high mutation frequencies but no driver mutations. Mutational signature analysis revealed 12 base substitution and six rearrangement signatures, with three rearrangement signatures associated with defective homologous recombination-based DNA repair. The study highlights the diverse repertoire of cancer genes and mutational processes involved in breast cancer and advances the understanding of the somatic genetic basis of the disease. Key findings include the identification of recurrently mutated cancer genes, the role of genomic rearrangements as driver mutations, and the presence of hypermutable hotspots in non-coding regions. The analysis also explored the association between mutational signatures and BRCA1/2 mutations, suggesting that mutational signatures may be better biomarkers for defective homologous recombination-based DNA double-strand break repair and responsiveness to PARP inhibitors.This study analyzed whole genome sequences from 560 breast cancers to understand the driver mutations and mutational processes that contribute to the development of breast cancer. The analysis identified 93 protein-coding cancer genes with likely driver mutations, and non-coding regions with high mutation frequencies but no driver mutations. Mutational signature analysis revealed 12 base substitution and six rearrangement signatures, with three rearrangement signatures associated with defective homologous recombination-based DNA repair. The study highlights the diverse repertoire of cancer genes and mutational processes involved in breast cancer and advances the understanding of the somatic genetic basis of the disease. Key findings include the identification of recurrently mutated cancer genes, the role of genomic rearrangements as driver mutations, and the presence of hypermutable hotspots in non-coding regions. The analysis also explored the association between mutational signatures and BRCA1/2 mutations, suggesting that mutational signatures may be better biomarkers for defective homologous recombination-based DNA double-strand break repair and responsiveness to PARP inhibitors.