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Chronic lymphocytic leukemia (CLL) is characterized by repeated growth of malignant B-cells. An accumulation of p53 protein in the malignant cells is one of the hallmarks of CLL. This accumulation is determined by p53 gene mutations which are found in a significant number of CLL cases. While it is clear that in CLL p53 loses its functional activity for triggering cell cycle arrest or apoptosis, it is less well understood which of the disease-inducing events on one hand and the genetic defects in the tumor suppressor on the other hand are responsible for the observed phenotype in the CLL cells. The p53 gene product is a sequence-specific DNA binding protein which negatively regulates a number of target genes. To determine if CLL-initiating events are related to these target genes, we developed CLL cell lines, which are p53wt and have a constitutive expression of a p53 dominant-negative mutant, delta p53, similar to that found in CLL malignant cells. In this model system, we could show that delta p53 was able to suppress a majority of p53-mediated cell cycle arrest and apoptosis, indicating that the previously documented proliferative advantage of CLL cells is not mediated by the mutation of the p53 gene. However, delta p53 was unable to suppress cell death induced by the microtubule-stabilizing agent paclitaxel. In contrast, the cytotoxicity of the caspase-activating agent TRAIL (tumor necrosis factor-related apoptosis inducing ligand) was not significantly different in cells expressing either p53wt or delta p53. Caspase-3 cleavage was examined in control CLL cells and CLL cell lines expressing p53wt or delta p53 and the results correlated well with the cytotoxic results. p53wt cells showed basal caspase-3 levels in contrast to the CLL cell lines expressing delta p53 which showed a higher expression of activated c

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NOT FOR PUBLICATION NOV 13 2015

MOLLY C. DWYER, CLERK
UNITED STATES COURT OF APPEALS U.S. COURT OF APPEALS



FOR THE NINTH CIRCUIT


ZHU JIAHONG, No. 10-73669

Petitioner,
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