Germline pathogenic variants in BRCA1 and BRCA2 (BRCA1/2) cause hereditary breast and ovarian cancer syndrome (HBOC). The function of BRCA1/2 in homologous recombination (HR) repair is considered essential for their activity as tumor suppressors. At the same time, BRCA1/2 also contributes to multiple cellular processes, including the regulation of the centrosome. However, it remains unclear how the dysregulation of BRCA1/2 leads to tissue-specific carcinogenesis. Previously, we identified BRCA1-interacting proteins, Obg-like ATPase 1 (OLA1) and the receptor for activated C kinase 1 (RACK1), which function together with BRCA1 to regulate the number of centrosomes. In this chapter, we describe the possible mechanisms that cause tissue-specific carcinogenesis in the breasts and ovaries of women with BRCA1 deficiency. We found that the characteristics of centrosome duplication in mammary cells and the effect of estrogen stimulation on centrosome amplification induced by OLA1 deficiency. These regulatory mechanisms of centrosome number may increase the risk of breast and ovarian cancers in individuals with BRCA1 pathogenic variants.