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Aurora kinase B expression in breast carcinoma: cell kinetic and genetic aspects

Katalin Hegyi1, Kristóf Egervári, Zsuzsa Sándor

  • 1Department of Pathology, University of Debrecen Medical and Health Science Center, Debrecen, Hungary.

Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology
|June 13, 2012
PubMed
Abstract

Insights

Elevated Aurora B expression in breast cancer correlates with increased cell proliferation. Codeletion of TP53 and AURKB genes at 17p13 may drive aneuploidy and aggressive tumor behavior.

Area of Science:

  • Oncology
  • Genetics
  • Cell Biology

Background:

  • Mitotic errors are linked to aggressive cancers.
  • Aurora B kinase is crucial for chromosome segregation and its gene (AURKB) is near TP53 at 17p13.
  • Information on AURKB status and expression in breast cancer is limited.

Purpose of the Study:

  • To investigate the status and protein expression of Aurora B in breast carcinoma.
  • To explore the correlation between Aurora B expression, cell proliferation, and chromosomal alterations at 17p13.

Main Methods:

  • Evaluated 50 breast carcinoma cases using fluorescence in situ hybridization (FISH) for 17p13 status and chromosome 17 ploidy.
  • Assessed Aurora B protein expression via immunohistochemistry.
  • Utilized the Aurora B/MIB-1 index to quantify expression levels.

Main Results:

  • Aurora B protein expression strongly correlated with cell proliferation (regression coefficient = 0.77).
  • No gain at the 17p13 locus was observed; deletions occurred in 10/50 cases.
  • A subset of deletions (6/10) involved codeletion of TP53 and AURKB, strongly correlating with aneusomy (p < 0.0001).

Conclusions:

  • Increased Aurora B expression in breast cancer is often due to higher cell proliferation rates.
  • Codeletion of TP53 and AURKB at 17p13 suggests a mechanism promoting survival of cells with faulty mitotic kinases.
  • This concerted genetic alteration may contribute to aneuploidy and the development of aggressive breast tumors.

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