BRCA1/2 signaling and homologous recombination deficiency in breast and ovarian cancer

Patients who have mutations of the genes BRCA1 or BRCA2 are at an increased risk for developing breast and ovarian cancer. BRCA1/2 function as tumor suppressor genes, responsible for regulating DNA repair, and play an essential role in homologous recombination. Mutation of BRCA1/2 results in homologous recombination deficiency and genomic instability which drives oncogenesis and cancer proliferation. Recently, BRCA1/2 gene expression has been implicated in regulating immune response. Here we discuss the signaling pathway of BRCA1/2 in relation to breast and ovarian cancer, with emphasis on how dysregulation facilitates the path to malignancy and current treatment options.

Automated summary

Mutations in BRCA1 or BRCA2 genes increase the risk of breast and ovarian cancer by impacting DNA repair and homologous recombination. Dysregulation of BRCA1/2 not only drives oncogenesis and cancer proliferation, but also affects immune response, influencing disease progression.