Estrogen-Induced Breast Oncogenesis: Modulation by an Aurora Kinase Inhibitor
Breast cancer (BC) alone accounts for about 32% of all cancers occurring in women in industrialized countries, and thus, is clearly an immense world wide public health concern. More than 90% of all human BC cases are sporadic or nonfamilial with an equally high percentage of these cases being ductal breast carcinomas, the rest are lobular. This latter distinction is particularly important since ductal BCs are highly aneuploid, while lobular BCs are mainly diploid. While the presence of estrogen receptor (ERα) is nearly a ubiquitous feature of sporadic BCs; about 55–73%, aneuploidy, not the presence of ERα+, is its most defining characteristic (65–90%) (1–3). Moreover, the detection of high aneuploid frequencies in a preinvasive stage, ductal carcinoma in situ (DCIS), strongly implicates that this molecular alteration has a primary role in the ontogeny and progression of early sporadic ductal BCs.
KeywordsAurora Kinase Centrosome Amplification Aurora Kinase Inhibitor Combine Hormone Replacement Therapy Mammary Gland Biol Neoplasia
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