[Biologic mechanisms of @entity854 and chromosome number changes in XXXX ].

@entity2007 @entity0 @entity706 @entity5 @entity876 @entity1892 @entity16511 @entity854 @entity942 @entity2246
UNASSIGNED: The main goal of this work was to study the effect of Aurora kinase expression on cell ploidy and tumorigenesis. Fifty invasive @entity0 , 50 diffuse large @entity1892 and 10 reactive lymph node samples were recruited in the study. Because of the significant correlation with the overall cell proliferation rate, the overexpression of @entity16511 could not be stated on the basis of kinase expressing @entity5 cell fractions alone. The relative expression of @entity16511 kinase is better reflected by the AMI index which represents the @entity16511 expression in relation to the whole proliferative fraction of the @entity5 . A higher relative @entity16511 expression was associated with higher mitotic activity in @entity1892 . FISH analysis of the @entity16511 locus did not show any gains or amplifications in the samples analyzed. On the other hand, we have observed the loss of the gene in @entity0 and @entity706 samples as well. A strong correlation was shown between @entity16511 and @entity876 copy numbers: @entity16511 loss was associated with @entity876 deletion in all samples. According to our results on @entity0 , losses at 17p13.1 and chromosome 17 aneusomy determined by FISH showed a statistically significant correlation. Our study presents the frequent occurrence of chromosome 17 aneusomy in @entity0 and @entity1892 samples. Chromosome 17 aneusomy evaluated by FISH correlated with @entity2007 determined by flow cytometry. Direct correlation between kinase expression and ploidy could not be shown. The highest AMI values were seen in B-ALCL samples, and it was associated with high chromosome 17 copy numbers and mitotic activity. The damaged @entity16511 kinase function results in @entity942 in the CPC complex leading to @entity2246 , while @entity876 deficiency helps malignant cells to survive due to insufficient activation of the intrinsic apoptotic pathways. The upregulation of @entity16511 function may cause error in an important mitotic checkpoint, thus resulting in induction of aneuploid cell populations. These parallel effects finally increase the complexity of @entity854 and generate aneuploid cell populations.
