kDa pleiotropic protein that participates in multiple biological pathways, including DNA damage repair, transcription, cell growth, and apoptosis [11, 12]. Evidence in support of a tumor suppressor role for BRCA1 was indirectly provided by studies showing somatic allelic loss of 17q21 in breast and ovarian tumors [13, 14]. Direct evidence for its tumor suppressor activity was provided by experiments showing that BRCA1 arrested growth of breast and ovarian cancer cells whereas inactivation of the endogenous BRCA1 gene accelerated the growth of normal and malignant cells and induced cellular transformation [15]. While clearly inactivating, BRCA1 germline mutations substantially increase breast and / or ovarian cancer risk, little information is available regarding the cellular and secreted factors involved in regulation of BRCA1 gene expression [11, 16]. Given the intimate involvement of both BRCA1 and the IGF system in normal cell cycle progression as well as in breast cancer cell proliferation, we hypothesized that the regulatory mechanisms controlling BRCA1 and IGF-IR gene expression