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

Katalin Hegyi, Kristf Egervári, Zsuzsa Sándor, G. Méhes

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background: Mitotic deregulations may contribute significantly to cell division errors and the development of aggressive tumor cells. The mitotic kinase Aurora B is essential for chromosome segregation. Its gene is located at 17p13 in close proximity to the TP53 gene. Although the frequent alteration of this locus is well known, the information about the AURKB status and protein expression is limited. Methods: 50 breast carcinoma cases were evaluated for 17p13 status and chromosome 17 ploidy by FISH and for Aurora B protein by immunohistochemistry. Results: Aurora B protein expression showed a strong correlation with cell proliferation (regression coefficient = 0.77). Therefore, the Aurora B/MIB-1 index was used as a measure of expression, which showed a wide range (1-35%, mean 0.32, SD ± 0.28). A gain in the 17p13 chromosome locus could not be shown while a deletion was stated in 10/50 cases including a subset with TP53 and AURKB codeletion in 6/10 cases. The loss of TP53/AURKB loci strongly correlated with aneusomy (p <0.0001). Conclusion: Elevated Aurora B expression frequently occurs due to an increased cell proliferation rate in breast carcinoma. Codeletion of TP53 and AURKB at 17p13 indicates a concerted mechanism leading to the survival of cell clones with deficient mitotic kinase function which could contribute to the formation of aneuploid cells and an aggressive tumor phenotype.

Original languageEnglish
Pages (from-to)314-322
Number of pages9
JournalPathobiology
Volume79
Issue number6
DOIs
Publication statusPublished - Jul 2012

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Aurora Kinase B
Cell Proliferation
Breast Neoplasms
Chromosome Segregation
Chromosomes, Human, Pair 17
Ploidies
p53 Genes
Aneuploidy
Cell Division
Neoplasms
Cell Survival
Phosphotransferases
Clone Cells
Chromosomes
Immunohistochemistry
Phenotype
Genes
Proteins
IgA receptor

Keywords

  • Aneuploidy
  • Aurora kinase B
  • Cell proliferation
  • Kinase deregulation
  • p53 antigens

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Cite this

Aurora kinase B expression in breast carcinoma : Cell kinetic and genetic aspects. / Hegyi, Katalin; Egervári, Kristf; Sándor, Zsuzsa; Méhes, G.

In: Pathobiology, Vol. 79, No. 6, 07.2012, p. 314-322.

Research output: Contribution to journalArticle

Hegyi, Katalin ; Egervári, Kristf ; Sándor, Zsuzsa ; Méhes, G. / Aurora kinase B expression in breast carcinoma : Cell kinetic and genetic aspects. In: Pathobiology. 2012 ; Vol. 79, No. 6. pp. 314-322.
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abstract = "Background: Mitotic deregulations may contribute significantly to cell division errors and the development of aggressive tumor cells. The mitotic kinase Aurora B is essential for chromosome segregation. Its gene is located at 17p13 in close proximity to the TP53 gene. Although the frequent alteration of this locus is well known, the information about the AURKB status and protein expression is limited. Methods: 50 breast carcinoma cases were evaluated for 17p13 status and chromosome 17 ploidy by FISH and for Aurora B protein by immunohistochemistry. Results: Aurora B protein expression showed a strong correlation with cell proliferation (regression coefficient = 0.77). Therefore, the Aurora B/MIB-1 index was used as a measure of expression, which showed a wide range (1-35{\%}, mean 0.32, SD ± 0.28). A gain in the 17p13 chromosome locus could not be shown while a deletion was stated in 10/50 cases including a subset with TP53 and AURKB codeletion in 6/10 cases. The loss of TP53/AURKB loci strongly correlated with aneusomy (p <0.0001). Conclusion: Elevated Aurora B expression frequently occurs due to an increased cell proliferation rate in breast carcinoma. Codeletion of TP53 and AURKB at 17p13 indicates a concerted mechanism leading to the survival of cell clones with deficient mitotic kinase function which could contribute to the formation of aneuploid cells and an aggressive tumor phenotype.",
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