Estrogen-Induced Breast Oncogenesis: Modulation by an Aurora Kinase Inhibitor

  • Sara Antonia Li
  • Luke K. T. Lam
  • Nayaz Ahmed
  • Adrianne E. Hontz
  • Jonathan J. Li
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 617)

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.


Aurora Kinase Centrosome Amplification Aurora Kinase Inhibitor Combine Hormone Replacement Therapy Mammary Gland Biol Neoplasia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer 2008

Authors and Affiliations

  • Sara Antonia Li
    • 1
  • Luke K. T. Lam
  • Nayaz Ahmed
  • Adrianne E. Hontz
    • 1
  • Jonathan J. Li
    • 1
  1. 1.Department of PharmacologyUniversity of Kansas University Medical CenterKansas CityUSA

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