Mitotic Kinase Aurora B is Frequently Overexpressed in Aggressive B-Cell Lymphoma
Katalin Hegyi, Judit Bedekovics, Otto Docs, Gabor Irsai, Lajos Gergely, Livia Beke and Gabor Mehes
World Journal of Pathology 2015, 4:4
Aurora B is a mitotic kinase responsible for the proper organization of chromosomes and scheduling during cell division. This study aimed to examine the alterations in Aurora B expression in relation with major up- and downstream cell kinetic proteins (survivin, phospho-histone H3, Ki-67) in aggressive B-cell lymphoma. The potential cytogenetic background of kinase overexpression was also studied.
Fifty patients with aggressive B-cell lymphoma were recruited to the study. Reactive lymph node samples were used as non-neoplastic control. Protein expression was studied by immunohistochemistry, AURKB gene locus at 17p13.1 and chromosome 17 copy numbers were determined by fluorescence in situ hybridization.
We observed that Aurora B expression is strongly influenced by overall cell proliferation capacity. Cell cycle related Aurora B overexpression was determined by the Aurora B/MIB-1 index (AMI) and was stated in 13 cases (26.0%). Kinase overexpression (AMI>0.5) in aggressive lymphoma was associated with induced mitotic activity determined by phospho-histone H3 labelling. Copy number changes of AURKB locus (17p13.1) did not influence kinase expression. High AMI was not associated with significant chromosome 17 copy number alterations in this setting.
Aurora B is overexpressed in a significant portion of aggressive B-cell lymphoma. Since Aurora B expression is strongly dependent on the cell proliferation rate, total proliferative capacity should be considered in a quantitative assay. As a consequence of kinase upregulation the mitotic process is potentially accelerated disabling proper repair function at the G2/M checkpoint and enabling incomplete chromosomal segregation and movements leading to a more aggressive phenotype in diffuse B-cell lymphoma.
aggressive B-cell lymphoma, Aurora B, kinase deregulation, genetic instability