Cells have several pathways to repair DNA damage, including base excision repair, nucleotide excision repair, and mismatch repair. Deficiencies in these pathways can lead to an accumulation of mutations, genomic instability, and the activation of oncogenes or inactivation of tumor suppressor genes, ultimately resulting in cancer. For example, mutations in the BRCA1 and BRCA2 genes, which are involved in the repair of double-strand breaks, are strongly associated with breast and ovarian cancers.
